Narrative: In this review I first identify the conditions that may be assessed using Functional Neurology and then describe the neuron and the many processes associated with neuroplasticity and neural signalling.

Then I offer a comprehensive review of the effects of modalities upon neuroplasticity and neurogenesis, giving mechanisms and signalling pathways relevant to clinical observation. I finish with a discussion on nutrients found to affect cognitive function and propose mechanisms for their effectiveness. 

I conclude that the updated concept of functional neurology represents the neuron integrated into its environment and therefore susceptible to modulations of its signalling capacity by a vast array of external factors. These agents of change include both electrical and chemical phenomena triggered by such external interventions as rehabilitation, manual muscle therapy, acupuncture, biofeedback, aromatherapy, yoga, cognitive exercises, eye muscle exercises, mediation, exercise, diet, and botanical nutritional supplements.

Indexing terms: Chiropractic; functional neurology; neuroplasticity; clinical intervention; nutrients.

Cite: Rosner AL. Functional neurology: A review. Asia-Pac Chiropr J. 2026;7-1. https://www.apcj.site/RosnerFunctionalNeurology.pdf 

Introduction

    A discussion of the meaning and scope of functional neurology is perhaps best introduced with a quotation from the individual responsible for the origins of Chiropractic, DD Palmer:

‘Life is the expression of tone’. In that sentence is the basic principle of Chiropractic. Tone is the normal degree of nerve tension. Tone is the  expression of function by normal elasticity, activity, strength, and  excitability of the various organs as observed in a state of heath. Consequently, the cause of disease is any variation of tone, nerves too ‘tense’ or’ static’. (1)

    Specifically, functional neurology can be thought of as a master biomarker, in that it utilises an entity that acts as the origin of changes in health that, if left unattended, emerge as symptoms and ultimately as pathologies.

The neuron

    An understanding of functional neurology should begin with the neuron. (6) Here it is a matter of assessing the likelihood that the neuron will produce an action potential, depending upon its state of polarisation. This, in turn, depends upon the sum total of the excitatory and inhibitory stimuli that it encounters at any given moment. If the neuron is in a depolarised state, the cell has become more positive internally, minimising the potential difference across the membrane and thereby moving the neuron toward its firing threshold.

    This may be accomplished by the movement of positive sodium ions into the cell. Conversely, hyperpolarisation occurs when the cell interior has become more negative, increasing the potential difference across the membrane and causing the neuron to back away from its firing threshold. This state may be achieved by the efflux of positive potassium ions from the cell’s interior or by the entrance of negative chloride ions into the neuron.

    Calcium ions may also be involved in modulating membrane permeability and thus the firing threshold. Ion movements across the membrane are achieved through what are known as voltage gated channels. The depolarisation and hyperpolarisation cycle involving sodium and potassium ions is illustration in Figure 1. (7)

Neuroplasticity

    The reorganisation of nerve cells is the core concept of functional neurology; i.e., changes in the physiological function of the neuro-axis in response to changes in the immediate or external surroundings, was first identified anatomically in 1964 when the histology of the rat cerebral cortex was found to respond to environmental changes. (8) But indications of the brain’s ability to reorganise in response to the environment were reported over a century ago in the writings of Shepherd Ivory Franz, who first reported that monkeys that were subjected to mechanical stimulation of the peripheral nerves and muscles recovered from an induced paralysed condition of the arm to normal movement. (9) That same year, Franz and two coauthors reported in 5 subjects with paralysis of 5-20 years’ duration that voluntary motor control was restored with a rehabilitation program including massage, and shaking of the affected limb. (10)

    Franz speculated that ‘it is apparent that some possibility of functional adaptation exists in the brain for certain types of movements so that when a certain ‘centre’ and its connected muscles cannot be utilised, other ‘centres’ and their connecting muscles may be brought into play to bring about the desired result’. (11) It was just 30 years ago, however, that the World Health Organisation acknowledged that neuroplasticity could play a role in the repair of the central nervous system and thus might be a factor in effective healthcare interventions. (12) Not long afterward, these therapeutic interventions were soon deemed to be effective in counteracting lesions of the central nervous system regardless of whether they were applied acutely, sub-acutely, or late after injury. (13)

    More recently, Carrick demonstrated in a double blind randomised controlled trial that eye movement training produced changes in quantitative electroencephalogram patterns and in the NIH Stroke Scale in patients suffering from acute middle cerebral artery ischemic stroke, compared to a control group treated only with aspirin. The conclusion was that the eye movement training could induce altered brain activation to accompany the functionality of saccades. (14). Examples of plasticity at the synaptic level can be illustrated in Figure 2. (15)

    Neuroplasticity was shown to be not limited to neural injury and recovery. It includes dendritic remodelling, synapse turnover, long-term potentiation, and neurogenesis. In terms of human welfare, it encompasses brain development, the learning of skills, the formation and loss of memory, and self-repair from neural injuries. (16)

    For example, Carrick reported in a trial involving healthy volunteers that manipulation of the second cervical motion segment produced what was evidently an enlargement in the circumferential measurement of the blind-spot map associated with decreased cortical activity in only one cortical hemisphere. In other words, this particular intervention may have been associated with a change in brain function. (17)

    Even more intriguing was the observation that changes in hippocampal structure could be found in London taxi drivers as they became familiar with the city’s layout, shown by a redistribution of grey matter compared to controls. (18, 19)

    Because models in structural pathology fail to adequately account for several clinical and experimental findings in individuals with chronic musculoskeletal disorders, and because treatments guided by these models fail to effectively treat many chronic disorders, alternative paradigms are being sought.

The most prominent neurotransmitters involved in neural regulation at the molecular level in functional neurology are, as follows:

Acetylcholine

    A closer examination of the role of the neurotransmitters at the synapse provides a biochemical clue as to how the regulation of nerve signalling by molecular intermediates may occur. (32) Using acetylcholine as a typical neurotransmitter, Figure 3 illustrates how:

1. The action potential traveling down the length of the axon causes voltage-gated calcium channels to open, leading to the influx of Ca⁺² ions from the extracellular space.
2. By means of an exocytotic process, Ca⁺² releases a neurotransmitter (acetylcholine) from vesicle entrapment, allowing acetylcholine to enter the synaptic (cholinergic) cleft.
3. Acetylcholine binds to a specific nicotinic acetylcholine receptor on the neighbouring neuron, raising the resting potential of the postsynaptic nerve or muscle cell, opening a channel for sodium to enter the cell and trigger an action potential as discussed above.
4. Numerous poisons may either block acetylcholine from binding to its receptor (curare) or prevent its being recycled into its neuron of origin as acetate and choline (neurotoxins).

    This chain of events leads one to suspect that neurotransmitters may be the locus of the regulation of signalling between neurons. To qualify as a neurotransmitter, the chemical must satisfy five criteria: (32)

1. It must be produced by neurons
2. It must be stored in the synapses
3. It must be released into the synaptic cleft upon stimulation
4. It must bind specifically to receptors on the postsynaptic membrane of either another neuron or muscle cell, and
5. The binding must trigger an ion influx that governs the activity of the target cell.

What we illustrate in Figure 4 represents the basic essentials of but one of the abundant neurotransmitter-initiated pathways of nerve transmission.

    While acetylcholine is the best known neurotransmitter, amino acids, biogenic amines, purine derivatives from adenosine, peptides and proteins are also members of this neuromodulator. Other neurotransmitter-receptor complexes therefore need to be noted as well. The nicotinic receptor as a ligand-gated ion channel functions for gamma-amino butyric acid and glycine as well as for acetylcholine. Most neurotransmitter receptors control ion channels indirectly by binding to 7-helix receptors which transmit the signal via G proteins. The latter, consisting of three dissimilar subunits, allow an exchange of bound GDP for GTP and ultimately generates what is known as a second messenger. Second messengers include cyclic AMP (cAMP), cyclic GMP (cGMP), diacylglycerol, inositol triphosphate, calcium, and arachidonate. Among their other functions is the ability of second messengers to allow signal amplification within the cell.

    The end result of receptor stimulation at the synapse is to provoke DNA transcription of appropriate genes to produce proteins and neurotransmitters.

Other products to follow are cytoskeletons, membrane receptors and channels, and enzymes.

Gamma amino butyric acid

    A more representative and far more complex neurotransmitter in functional neurology is gamma-amino butyric acid (GABA), which acts as the primary inhibitory neurotransmitter in the mammalian central nervous system, playing a key role in modulating neuronal activity. No less than three classes of GABA receptors exist:

1. GABA_A: Electrophysiogical studies have indicated that the GABA_A-receptor complex rapidly mediates an increase in membrane conductance that is often accompanied by membrane hyperpolarisation. The result of this is an increase of the firing threshold and thus the reduction of spontaneous initiation, leading to overall neuronal inhibition with the membrane potential stabilised to near the resting level. With a damping of postsynaptic depolarisation achieved, there is the reduced likelihood of brain function from overreacting from excessive initiation of action potentials. The GABAergic synapse has been shown to have a far more complex structure than the acetylcholine receptor shown in Figure 4, although the basic mode of action in chemical transmission of signals across the synaptic cleft is essentially the same. (33)
2. GABA_B: These are guanine nucleotide-binding (G) protein coupled receptors, the function of which is to modulate Ca⁺² and K⁺ channels, capable of eliciting both presynaptic and postsynaptic inhibition. They have a broad range of expression in the nervous system:

• modulating synaptic excitability and placidity in the cerebral cortex
• generating rhythmic activity in cortical and thalamic circuits
• relaying primary afferent input to the spinal cord and brainstem, and affecting the activity of dopaminergic and other monoaminergic neurons. (34) Unlike the fast synaptic acting GABA_A receptors, GABA_B receptors exert a slow inhibitory potential. (35)

1. GABA_C: Like their GABA_A counterparts, GABA_C receptors are linked to chloride channels but are slow rather than fast-acting and also are insensitive to the benzodiazepines and anaesthetics that affect GABA_A receptors. (36, 37) Dopamine has been reported to modulate this receptor activity in both catfish cone-driven horizontal cells (38) and tiger salamander bipolar cell terminals. (39)

N methyl D-aspartate

    The leading molecular species for controlling synaptic plasticity and memory function has been identified as the N-methyl-D-aspartate (NMDA) receptor. (40) It is so named due to the selective binding of the agonist molecule NMDA to it and not to other glutamate receptors. It is an ion channel protein located in neurons, activated when both glutamate and glycine (or D-serine) bind to it. This allows positively charged ions, such as calcium (Ca⁺²), to flow through the cell membrane. (41, 42) (Figure 5) The increase of Ca⁺² within the cell allows it to function as a second messenger in a variety of signalling pathways. However, extracellular magnesium (Mg⁺²) (43) or zinc (Zn⁺²) can bind to specific sites and prevent Ca⁺² binding and activation. It is only with depolarisation of the cell that Mg⁺² or Zn⁺² can be dislodged from the pore, permitting a voltage-dependent flow of Ca⁺² or sodium (Na⁺) ions into the cell and potassium (K⁺) ions out of the cell. (44, 45)

    NMDA receptors are associated with synaptic plasticity, shown perhaps most directly by the demonstration that extra-synaptic NMDA receptors inhibit long term potentiation while producing long term depression, (46) while the inhibition is prevented by introducing an NMDA antagonist. (47) One of six subunits of the protein identified as NR2B has been pinpointed as a locus of plasticity since the ratio of NR2B to NR2A decreases with age in diverse animal species (including humans) starting on or before sexual maturity. In other words, the relative abundance of NR2B in the juvenile brain appears to confer upon it a greater plasticity than the adult brain.

    Interestingly, NMDARs have been identified outside as well as within the synapse. In research conducted over the past decade, the NMDARs outside of the synapse have been found to play a major role in excitotoxicity and cell death, while physiological activation of the NMDARs inside of the synapse can contribute to cell survival. This has led the authors of a review to suggest that preventing excessive activation of the extrasynaptic NMDARs could provide therapeutic benefit in such cases as Alzheimer disease or Huntington disease. (47)

Dopamine

    Dopamine belongs in both the catecholamine and phenethylamine families and plays a dual role, serving as 

1. the primary neurotransmitter in the brain, and 
2. a local chemical messenger outside of the nervous system. Able to cross the blood-brain barrier, dopamine is confined primarily to: (48)

    These regions are outlined in Figure 6. (49)

    As with most biologically active substances, dopamine exerts its effects by means of specific binding to and activating receptors. Two evolutionary and genetically different subtypes of receptors exist within the dopaminergic system (D1-like and D2-like) with a total of five distinct receptor classes in all. (50) The two receptor classes, when stimulated by a common agonist, produced an increase of intracellular calcium via a signalling pathway that was not activated by either receptor alone or when only one of the co-expressed receptors was activated by a selective agonist. (51) The consequences of the calcium stimulation produce changes in gene expression, protein production, enzyme levels, the cells’ firing rate, and the neuron’s sensitivity to dopamine itself. It begins as the cell uses calcium to build and strengthen synaptic connections to other neurons, releasing the calcium from vesicles stored within the neuron as shown in Figure 4.

    The physiological effects of dopamine expressed downstream include the following:

• Gene expression: Immediate early genes that are activated in dopaminergic neurons following stimulation include those of the fos family, (52, 53, 54) fos being a transcription factor that is upregulated in the brain following stimulation from drugs or other rewarding stimuli such as sexual behaviour or exercise. (54)
• Expression of numerous neuropeptides: Dopamine signalling has been shown to have direct effects upon the expressions of:

• Regulation of motor movement control: Purposeful exercise and/or movement that expends a significant amount of energy is regulated by the dopamine system. (59, 60) Derangements of the dopamine system play a central role in the development of Parkinson’s disease (61) and Attention Deficit Hyperactivity Disorder. (62)
• Mediation of behavioural responses to rewarding stimuli: It is generally accepted that the dopamine system is involved in reward and reinforcing mechanisms, as shown by the results of psychostimulant administration. (59, 63) It functions both as the centre of motivation or wanting as well as being directly affected by the physical activity involved in the pursuit of those entities desired. (64, 65, 66)

    Figure 7 presents an overview of the dopamine pathways in the brain and their downstream effects. (67)

Serotonin

    Serotonin (5-hydroxytryptamine, or 5-HT) is a monoamine neurotransmitter with multiple biological effects, synthesised from tryptophan. It is bound to a transporter protein known as 5-HTT located in the presynaptic cell membrane and responsible for the re-uptake of serotonin into its cell of origin after it has been released into the synaptic cleft to signal the adjacent neuron. The length of time that the chemical signal remains in the synapse is determined by the number and activity of the 5-HTT proteins. (68) Figure 8 illustrates these steps. (69)

    Many of serotonin’s function can be described at the molecular level as follows:

1. Regulator of mood: The popular conception of serotonin is that it enhances feelings of content and happiness. (70) Indeed, serotonin has a pervasive influence upon brain activity, being released from axons originating largely in the raphe nucleus of the brainstem but spreading into almost all brain areas. This diffuse mode of action differs from the rapid activity at the synapses, as shown in Figure 7, in which extracellular levels of serotonin will be highly sensitive to the rate at which it is removed.
2. Modulation of nitric oxide synthase: Numerous lines of evidence suggest that the production of nitric oxide is regulated by the 5-HTT transporter. (71)
3. Activation of hypothalamic-pituitary axis: Stimulation of the HPA axis in response to serotonin has been suggested in a mouse model, seen with the abundant expression of serotonin 2C receptors I the paraventricular nucleus of the hypothalamus linked to the activity of corticotropin-releasing hormone. (72)
4. Regulation of glucose balance: Serotonin 2C receptors have been shown to improve glucose tolerance and reduce plasma insulin in mouse models of obesity and type 2 diabetes. Downstream activation of melanocortin-4 receptors was identified as the mechanism involved, a matter of possible clinical significance since pro-opionmelanocortin neurons, found in the hypothalamus, are known to play a key role in suppressing appetite and inducing weight loss. (73)
5. Regulation of bone metabolism: Gut-derived serotonin regulates osteoblast proliferation and bone formation, while brain-derived serotonin regulates bone mass through the sympathetic nervous system. (74)

    In addition to those factors regulating neurotransmitter activity are those pertaining to the neuron itself. These would include an adequate supply of nutrients, cofactors, and essential compounds as well as assuring the sufficient exchange of oxygen and carbon dioxide. Lack of these compromises the production of protein as the result of what is known as transneural degeneration. Resulting from this is the neuron’s initial increase irritability, the elevation of its sensitivity to stimulation. But this hyperactivity can last for only a relatively short period of time in the face of deficient nutrients, so that the loss and degradation of microfilaments and microtubules as well as of membrane integrity allows calcium ions to enter unimpeded, resulting in cell death.

    These detrimental effects may then be transmitted downstream in a process known as diaschisis. (6)

    It is important to recognise that, while such receptors as those that respond to gravity or which maintain pacemaker depolarisation are constant in nature, most receptor systems are not and are thus periodically activated with surges of activity. The latter would include the cortical cells of vision or of memory which experience interruptions with disuse, such as in sleep or neglect. Yet these neurons are sustained to subthreshold activation by complex multineuron systems. (5) 

Neural networks: Excitation and inhibition

    Neurons are able to receive signals from up to 10,000 presynaptic neurons and likewise can deliver contacts to a like number of postsynaptic neurons. Understandably, this capability gives rise to enormously complex neuronal circuits. Some of the more basic circuit configurations are shown in Figure 9. (75)

Hyperexcited states of neurons, known as ‘wind-up’, suggests an inappropriate degree of output per unit input. Neuronal damage can result from: (30)

1. Overactivation of the NMDA receptors, resulting in cytotoxicity due to increased intracellular Ca⁺² concentrations.
2. Formation of free radicals from anaerobic energy production pathways, leading to damage to membranes and membrane receptor structures, or to mutations in DNA.
3. Transneural degeneration, occurring when intracellular protein and energy stores fall below the level needed to support the increased demands of hyperactivity.

    A translation of these networks onto a clinical platform is exemplified by the schematic in Figure 10, in which both the direct and indirect pathways of motor circuits of the basal ganglia are shown in both the normal and Parkinsonian states. (76, 77)

Figure 10: Direct and indirect pathways of the basal ganglia motor circuits in normal and Parkinsonian  states.

Red arrows: Inhibitory projections; Blue arrows: Excitatory projections; Changes in arrow thickness represent proposed increases (thicker) or decreases (thinner) in the firing rate activity of specific connections.

Dashed arrows labelling dopaminergic projections D1 and D2 from the SNc to the putamen in Parkinsonism indicate the partial lesion of that system.

Many connections have been omitted from this diagram.

Key: 

CM: centromedian nucleus

CMA: cingulate motor area

GPe: globus pallidus, external segment

GPi: globus pallidus, internal segment

M1: primary motor cortex; PMC: pre-motor cortex

PPN: pedunculopontine nucleus

SMA: supplementary motor area

SNc: substantia nigra pars compacta

SNr: substantia nigra pars reticulata

STN: subthalamic nucleus

VA/VL: ventral anterior/ventral lateral nucleus.

Brain hemisphericity

    Brain hemisphericity is based upon the finding that the human brain has been described as an asymmetric entity. (78, 79) However, the precise relationship between the brain’s asymmetric design and the functional control managed by each hemisphere remains a controversial subject. As to how much each hemisphere may function is deemed to relay upon its afferent stimulation from the periphery in addition to nutrient and oxygen supply. Current theory holds that hemisphericity is expressed in cortical modulations of the autonomic nervous system, sensory perceptions, cognitive, attentional, learning, and emotional processes. (80) Suggestive evidence was provided in a study of male adolescents of North American native ancestry subjected to a regimen of processing consonant-vowel combinations (CVs) and musical melodies. A laterality index suggested left hemisphere involvement for melodies and more for CV processing. (81) A further hint was provided in a study of normal young women compared to normal young men within a setting that emphasised hypnosis and partial sensory deprivation. 

    In these surroundings, the women’s reporting of a significantly stronger experience of a ‘presence’ correlated with their higher score on Vingiano’s right hemisphericity questionnaire. (82) Corroboration was offered by Lazure’s finding in a questionnaire administered to 50 boys and girls in grades 9 and 12 that a lower self-esteem score obtained on the Rosenberg questionnaire was associated with greater right hemisphericity, as measured by the Vingiano scale (r=0.52). (83)

    It has been suggested that an abundance of right- and left-sided structures in the brain besides the cortical hemispheres may be subject to asymmetric function. These would include the thalamus, amygdala, hippocampus, caudate, basal ganglia, substantia nigra, red nucleus, cerebellum, brainstem, and nuclei. To this assortment of structures might be added the peripheral nervous system.

    It has been further proposed that hemisphericity could lead to the dysfunction of major systems of the body, including the spine. Hemisphericity of the latter would include subluxation, spinal stiffness (increased extensor tone), spondylosis, intrinsic spinal weakness (decreased postural tone), decreased A-P curves in the cervical and lumbar spine, increased A-P curves in the thoracic spine, increased postural sway in sagittal or coronal planes, and pelvic floor weakness. (6)

Effects of modalities upon neuroplasticity and neurogenesis

    These interventions are built on the premise that functional synaptic connections are built involving cortical and subcortical (striatal and cerebellar) structures, following exposure to a variety of motor experiences. The connections are proposed to be highly dependent upon sensory information. (84)

Rehabilitation

    This approach addresses specific areas that are affected by a neurological deficit leading to over- or under-activation. The focus is upon the root cause rather than symptoms and includes the following forms suggested by one clinic specialising in functional neurology: (85)

Optokinetic (eye movement) exercises: 

    A trial involving patients with left-sided chronic neglect (impaired or lost ability to react to or process visual, auditory, tactile, or olfactory sensory stimuli) subjected to repetitive optokinetic stimulation with active pursuit eye movements (R- OKS) compared to a cohort undergoing conventional visual scanning (VST) revealed superior effects experienced by those in the former group in all tasks (digit cancellation, visuoperceptual and visuomotor line bisection and visual size distortion). (86) A larger randomised trial of healthy subjects found that those subjected to OKS exposure for five consecutive days displayed significant reductions of visual dependency, both at a perceptual and postural level, compared to a nonintervention control group. (87) A more elaborate follow-up clinical trial conducted by the same lead author found that patients with a clinical diagnosis of a peripheral vestibular disorder or chronic dizziness and/or unsteadiness responded positively to a more economical unsupervised DVD that provided an optokinetic rotating disc or drum, but only for vestibular-visual vertigo, and autonomic symptoms. Posturography and functional gait assessments were superior for groups trained with a full-field visual environmental rotator or supervised cohorts. In any case, optokinetic training provided improvements to individuals experiencing peripheral vestibular disorders. (88)

Balance and coordination therapy:

    The goal of this intervention is to provide a balance board or platform in order to increase the activation of the cerebellar structures controlling posture, head and eye yoked movements, and core stability. Support for this approach was offered by Rhyu, who analysed brain MRI scans of 16 male professional speed skaters, comparing those to scans of 18 non-skaters who did not engage in regular exercise. Skaters were shown to possess larger right hemispheres of the cerebellum and vermian lobules VI-VII (the lobes connecting the left and right parts of the cerebellum) than non-skaters, suggesting that the specialised abilities of balance and coordination in the skaters were associated with flexibility in the cerebellar structures.

    Specifically, the balance on the right foot required of speed skaters activated the right lobes of the cerebellum, in addition to the effects of learning a visually guided task believed to occur in the right side of the brain. (89) A second investigation involving traumatic brain injury patients found that balance training using PC-based portable balancers with real-time visual feedback induced plastic improvements in balance control which were associated with alterations in the cerebellar white matter microstructure. (90)

    Elsewhere, patients with cerebellar ataxia who participated in a home-based balance exercise program displayed significant rehabilitative improvements that were retained in most outcome measures one month later. (91)

Complex movement exercises:

    Because specific movements are targeted to specific areas of the brain, exercises which activate areas of the brain that are deficient or over-activated are indicated as a component of functional neurology rehabilitation. Intensive training, for example, is known to produce functional and structural neuro-adaptations. Professional handball players, for instance, displayed an increase in grey matter volume in hand areas, while ballet dancers revealed increases of the grey matter area in foot areas. Fractional anisotropy of the corticospinal tract (FA), on the other hand, showed lower FA in fibres connecting the foot compared to the hand areas of ballet dancers, while handball players revealed lower FA in fibres connecting the hand compared to their foot areas. (92)

    A separate investigation involving young adults aged 21-26 revealed modulations of the average activity in the alpha and beta frequencies in EEG patterns of the frontal and central brain regions when subjected to walking conditions combined with a cognitive or motor interference task, indicating an increased cognitive load during the walking In other words, impaired motor performance during dual-task walking was reflected by neural activation patterns of the brain. (93) 

    After the acquisition of visual motor skills in yet another trial, participants experiencing exercise regimens displayed improvements in procedural memory, but those increases diminished with increasing time lapses between the exercise and acquisition. (94)

    A fourth investigation found that moderate dancing activity compared to a non-sedentary control cohort without any dancing experience failed to display significant differences in four cognitive domains or brain volume, suggesting that a critical level of physical activity and fitness may have been attained in the control group. (95)

Vestibular rehabilitation:

    The vestibular system (inner ear and cerebellum) are the target areas of this aspect of functional neurological rehabilitation. Included in this type of therapy are a variety of forms of stability exercises, patterned movements of the extremities, rotational forms of movement, and eye exercises. (85) 

    A systematic review of 9 randomised controlled trials of varying quality revealed positive results in favour of vestibular rehabilitation regarding postural control, functional capacity, and quality of life in an elderly and middle-aged population with complaints of vestibular syndrome, lightheadedness or dizziness. Despite the fact that four studies were rated to be of adequate quality according to the PEDRO scale, they were subject to bias since they did not present allocation concealment or blinding of participants, therapists, or assessors. (96) 

    In a nonrandomised controlled trial with 20 patients diagnosed with vestibular diseases, cervical manual therapy and shoulder girdle exercises together with head movements, eye coordination tasks, and overall body movements and balance tasks produced improvements in quality of life, postural balance, and intensity of dizziness.These improvements were not associated with pharmacologic treatment. (97)

    A novel approach was offered by a team of investigators from Laval University, who determined that the presentation of virtual reality treatments of at least 150 minutes of cumulated exposure ensured symptom improvements in patients with vestibular disorders. The effect was dose-dependent and was based upon the Dizziness Handicap Index and perception of handicap symptoms. (98) A review of the literature led Lacour and Bernard-Demanze to propose a series of general recommendations regarding the timing, type, intensity, and duration of vestibular rehabilitation therapy. They proposed that: (99)

1. Therapeutic progression must proceed from the head to locomotion in a top-down sequence of exercises.
2. The therapy must address all facets of the vestibular syndrome; i.e., the postural, oculomotor, and perceptive symptoms following vestibular injury.
3. Prior to the therapy, nausea, vomiting, and vertigo need to be stopped or reduced.
4. Antiemetics and anti-vertigo drugs might be useful in the early (2-3 day) stage after vestibular injury but must be stopped thereafter.
5. Regaining eye motion control and eye-head coordination are the primary goals of the therapy.
6. Sensory substitution and sensory addition are tools for compensating vestibular loss.
7. Recovery of balance control and gaze stabilisation is attained differently among patients; therefore, a stereotyped vestibular rehabilitation protocol is to be avoided.

Developmental disorder rehabilitation:

    Areas of the brainstem which are origins of such developmental disorders as Autism Spectrum Disorders, ADHD, learning disabilities, and dyslexia may be targeted for rehabilitation approaches based on the principle of neuroplasticity. Treatments could include eye movement exercises, tracing therapy, complex movement exercises, hand-eye coordination exercises, music therapy, light stimulation, or balance or coordination work. In animal models, a large body of research has demonstrated the effects of environmental enrichment on both brain and behavioural development. Specific indicators have included the weight and thickness of the cortex, the density or affinity of neurotransmitter receptors, and increased numbers of synapses as well as the density of dendritic branching. 

    The literature has extended to aberrant genes coding for defective neurotransmitters and receptors in the brain leading to disorders of the synapse in autism, raising the possibility that interactions with environmental factors may influence these components and susceptibility to autism. (100)

    A closer inquiry into brain anatomy and the ability to learn nonnative speech sounds found that faster phonetic learners appeared to have more white matter in parietal regions of the brain, particularly in the left hemisphere. The authors concluded that morphological correlates of phonetic learning were related to the ability to process rapid temporal variation. (101) Further support of the neuroplastic responsiveness of the brain to interventions addressing developmental disorders was provided in a study of children with dyslexia. After training, performance on both oral language and reading tests significantly improved, bringing the dyslexic readers’ scores into the normal range. At the same time, increased metabolic activity was found in fMRI scans in the left hemisphere language regions, bringing brain activation in these regions closer to that seen in normal children with normal reading skills. (102)

    Virtually the same results were obtained in a second study involving dyslexic adults, likewise demonstrating how an external intervention (phonological training) produced increased fMRI signalling in the left hemisphere regions which are engaged by normal readers. (103) Results such as these have led researchers to introduce a cognitive training regimen as a treatment option for ADHD, called Online Neuroplasticity-based Training for the Remediation of ADHD in Children (ONTRRAC), currently under evaluation in a randomised controlled feasibility-efficacy trial. (104) Indeed, a similar brain-computer interface training program for adults with chronic hand hemiplegia after stroke has been shown in 3 patients to increase performance (moving a cursor on a screen) while enhancing MRI images reflecting the modulation of cortical activity, as demonstrated in Figure 11: (105)

Manual medicine (spinal manipulation and cranial therapy)

    Nearly 40 years ago, Korr proposed that biomechanically induced deformations of spinal nerves in spinal manipulation could alter axonal transport and with it, trophic influences upon target and effector cells. (106) Analgesia produced by stimulation of neurons outside the customary dermatomal and myotomal distributions used in musculoskeletal diagnosis has been labeled noxious inhibitory control. (107)

    The experiments of Sato and Swenson in rats showed that manual therapy could trigger changes in sympathetic function with the potential to alter pain through the sympathetic nervous system’s ability to change afferent input. (108) In healthy humans, diversified cervical adjustments appeared to result in parasympathetic responses seen to dominate the LH/HF ratio in heart rate variability measurements, whereas thoracic adjustments led to a reduction of pulse pressure suggesting a sympathetic response. (109) Depending upon which whether the ipsilateral or contralateral side is treated by manipulation and the cortical hemisphericity of the patient, an increase or decrease in brain function has been reported. (17) From these findings, it could be established that manual therapy activates endogenous analgesia systems.

Figure 11: Modulation of cortical activity in stroke patients by brain-computer interface training. Patients with chronic hand hemiplegia after stroke were trained to move a cursor on a screen via modulation of ipsilesional sensorimotor µ rhythm, which was recorded by magnetencephalography.

Successful trials lead to the brain-computer interact opening or closing the patient’s paralysed hand via a mechanised orthosis. 

(a) The performance of three patients across sessions indicates that the proportion of successful trials increased over time. The statistical maps for the correlations between sensorimotor µ rhythm amplitude, which was recorded from the sensors above the ipsilesional primary motor cortex, and successful performance at (b) early or (c) late training time points demonstrates modulation of sensorimotor rhythm with brain-computer interface training.

Red and yellow colours identify areas where there was a high degree of correlation. d Single axial images from T1-weighted, high-resolution MRI scans obtained from each patient. Each patient’s lesion is highlighted in red.

    Cranial sacral therapy, on the other hand, assumes that:

1. The human brain pulsates unrelated to heart rate at about 10-14 cycles per minute.
2. A person can feel these pulsations with one’s fingertips at given locations on the body.
3. The craniosacral system (cranium, joints, sutures, and sine) can move and be moved by touching and massaging.
4. Restrictions of the natural movements of the cranial system restrict or prevent the flow of cerebral spinal fluid.
5. Persons with increased inflammatory levels and neurological activation, such as with Autism Spectrum Disorder, experience restrictions that create learning disabilities, autistic symptoms (such as behavioural problems, poor social relationships, communication difficulties, and poor abstract thought), and other social and intellectual abnormalities.
6. With a pressure of about 5 grams, therapists can remove restrictions and generate movement of the cranial system that results in improved functioning.

    A publication from the Cambridge Centre for Behavioural Studies in 2011 concluded that the conceptual foundations upon which craniosacral therapy was based ‘have been shown to be flawed and are not substantiated by medical science. Its effectiveness in improving problems to which it has been applied has not been proven scientifically’. (110) More recent publications, however, beginning with a systematic review of 7 studies to assess the benefits of craniosacral therapy, (111) have arrived at a substantially more sanguine conclusion. A study of heart rate variability, for instance, found that patients with subjective discomforts treated with craniosacral therapy displayed increases of standard deviations of all RR-intervals as well as the total power of RR-interval variability in a given frequency range, indicative of a favourable effect of test subjects’ autonomic nervous system activity compared to untreated controls. (112)

    Furthermore, a survey of patients with Autism Spectrum Disorder published in 2017 disclosed positive responses from therapists, parents, and clients, establishing a basis for conducting further research addressing this encouraging result. (113) Within the space of just 6 years, further positive responses to craniosacral therapy were reported for patients with chronic neck pain, (114) chronic low back pain (the latter two investigations being randomised sham-controlled trials), (115) migraine headache, (116) and anxiety and depression in patients with fibromyalgia. (117)

The previous conclusion that craniosacral therapy lacks a foundation or scientific evidence to affect patient responses or influence the nervous system (110) thus appears to be premature.

Acupuncture

    Documentation of the relationship of neuroplasticity to acupuncture has reached the point at which an entire issue of the journal Neural Plasticity has been dedicated to that single topic. (16) Pathologies of a variety of disorders, such as stroke, Alzheimer’s disease, and pain are related to neural plasticity. The fact that these conditions have been documented to be relieved by environmental stimulation, as will be illustrated by the following examples, simply underscores the connection between acupuncture and neuroplasticity.

1. Stroke: In a comparison of 28 right-hemispheric stroke patients and 20 healthy subjects undergoing functional magnetic resonance imagining, stroke patients revealed a decreased functional connectivity between the bilateral motor cortices compared with healthy subjects. The decreased functional connectivity was significantly enhanced after acupuncture at the GB34 point, the most significant active point during the left passive thumb-to-index task. The result was thought to shed light upon the mechanism of neural plasticity for acupuncture therapy. (118) In a rat model of ischemic stroke produced by occlusion of the middle cerebral artery inducing cognitive deficit, lesions could be found by MRI analysis in the cortex, hippocampus, corpus striatum, and thalamus regions, accompanied by learning deficits in a water maze and reductions of the dendritic density in the spine and of synapses in the hippocampal pyramidal cells.. Electroacupuncture at the DU20 and DU24 acupoints reversed all of these changes, as well as increases in mRNA/LIMK1 signalling. It was apparent from these data that the mRNA/LIMK1 signalling mechanism was involved in the electroacupuncture-induced hippocampal synaptic plasticity, contributing to improving the learning and memory during the recovery stage of ischemic stroke in this animal model. (119)
   
2. Experimental spinal cord injury: After spinal cord injury was induced in experimental rats, the motor function of the hind limb was suppressed together with the level of a protein (neurotrophin 3 [NT-3]) essential to neuron survival and growth. Electroacupuncture at the Dazhu (GV 14) and Mingmen (GV acupoints, judged in Traditional Chinese Medicine to stimulate Yang meridians, restorations of both hind limb function and NT-3 levels were found. The conclusion was that the acupuncture treatment promoted neuronal function recovery which could have resulted from upregulating the expression of NT-3.120
   
3. Renal sympathetic activity: In experimental rats, daily acupuncture at the LR3 acupoint for 2 weeks attenuated increases of mean blood pressure that had previously been caused by enhanced renin release. It also increased the ratio of the low-frequency component compared to the high-frequency component in heart rate variability measures while reducing kidney epinephrine and norepinephrine, indicating the reduction of renal sympathetic activity. (121)
   
4. Pain memory: In yet another rat experimental model, electroacupuncture at the bilateral acupoint ST36 alleviated the retrieval of pain induced by the injection of carrageenan, while the NSAID drug indomethacin did not. Injection of a protein kinase (PKA) inhibitor into the anterior cingulate cortex likewise blocked the retrieval of pain memory. Electroacupuncture reduced the activation of PKA together with cyclic AMP (cAMP) and the signalling protein CREB. It thus appeared that electroacupuncture’s suppression of pain memory could be attributed at least partially to the inhibition of the cAMP/PKA/CREB signalling pathway. (122)
   
5. Downregulation of NMDA receptor: Previous data had shown that the N-methyl-d-aspartate receptors (NMDARs) are responsible for the glutamate-induced excitotoxicity in the postischemic brain. Expression of a subunit (NR1) of the NMDAR has been shown to be suppressed by electroacupuncture in a rat model of ischemic stroke, whereas a component of the cell signalling pathway (TrkA) leading to nerve growth factor, critically involved in cell survival and neuroprotective effects, is upregulated. These two factors may be components of the neuroplastic effects of acupuncture in alleviating stroke symptoms. (123)
   
6. Neuroplasticity changes in the human motor cortex: An acupuncture session involving 10 acupoints produced changes in potential amplitude measured by transcranial magnetic stimulation from both the ipsilateral and contralateral hemispheres compared to baseline. Thus, corticomotoneuronal excitability and interhemispheric competition could be modulated by acupuncture therapy in healthy subjects. (121)

Biofeedback

    Biofeedback is another mechanism by which environmental stimulation can be utilised to take advantage of the neuroplasticity that characterises human nervous systems. Whereas training and learning could involve numerous mechanisms and areas of the brain affected, biofeedback targets only a specific region of the brain, and thus permits insight into that specific area and how it contributes to behaviour. Several lines of evidence demonstrated the efficacy of biofeedback and its relationship to neuroplasticity:

1. Inductions of activity patterns achieved with a decoded functional magnetic resonance imagining (fMRI) signal as an online feedback method were able to accomplish the induction of activity patterns in the visual cortex of healthy adults. This indicated that the adult early visual cortex was so plastic that mere repetitions of the activity pattern corresponding to a specific feature of the cortex was sufficient to produce visual perceptive learning of a specific orientation, even without 

1. presentation of the stimulus
2. conscious awareness of the meaning of the neural patterns that subjects induced, or 
3. knowledge of the intention of the equipment utilised. (124)

1. A second trial, also using fMRI based neurofeedback using blood oxygenation signals from a circumscribed region of interest in the brain demonstrated that participants showed enhanced perceptual sensitivity only if they had undergone the previously learned regimen, and only for that region of the visual cortex. (125) Both studies thus demonstrated a causal relationship between the altered activity in the early visual cortex and the observed behavioural changes. (126)
2. A third investigation employing electroencephalogram (EEG) biofeedback administered to post-cancer patients with cognitive impairments showed reductions of the negative cognitive impairments and emotional sequelae of cancer treatment, in addition to improving fatigue and sleep patterns. (127)
3. Elsewhere, a neurofeedback training protocol designed to improve sustained attention induced increases of fractional anisotropy in white matter pathways and of the volume of gray matter in cerebral structures involved in the types of increased auditory and visual attention achieved. The authors reported that, after 50 years of research in the field of neurofeedback, this was the first empirical demonstration that neurofeedback training could lead to microstructural changes in white and gray matter. (128)
4. A Cochrane review of 13 trials involving 269 people subjected to electromyographic biofeedback showed a small amount of evidence suggesting that the procedure had a beneficial effect when used with standard physiotherapy techniques. Some studies, however, found no effect. (129)

Aromatherapy

    With its use of essential oils from plants, aromatherapy is postulated to work by stimulating olfactory receptors in the nose, communicating with the amygdala and hippocampus in the brain which controls emotions and memories. Aromatherapy also acts through the skin.

1. The presentation of three different odorants (spiced apple, eucalyptus, and lavender) to subjects produced widely differing alpha and theta activity of the electroencephalo-graphic (EEG) patterns in the left and right hemispheres. These did not agree with self-reports registered on questionnaires, indicating that the perceptual component of olfaction accounted for a limited part of the central nervous system changes produced by smelling an odor. (130)
2. Valeric acid (rated as unpleasant) and phenylethyl alcohol (rated as pleasant) were rated as to their effects upon the EEG frequency bands theta, alpha 1, alpha 2, and beta 1 at eight locations. Within 8 seconds after stimulus release, valeric acid increased alpha 2 power whereas phenylethyl alcohol did not. These data indicated that smelling an unpleasant odor led to a cortical deactivation. (131)
3. A 1.5-2.5-fold increase in relative sympathetic activity, representing the low frequency amplitude of systolic blood pressure, was produced in humans by the fragrance inhalation of essential oils, such a pepper oil, estragon oil, fennel oil, or grapefruit oil. On the other hand, the fragrance inhalation of rose oil of patchouli oil produced at 40% decrease in relative sympathetic activity. Inhalation of the odorless solvent triethyl citrate caused no change. Inhalation of pepper oil also caused a 1.7-fold increase in plasma adrenaline concentration, while the fragrance inhalation of rose oil led to a 30% decrease of the adrenaline levels. Thus, it was apparent that fragrance inhalation of essential oils could modulate sympathetic activity in adults. (132)
4. An early component (at 400-1000 ms) of the beta wave variation, part of an EEG method of  measuring the slow brain waves (>13 Hz) at the front of the scalp, was identified as responsive to odor while nearly independent of the subject’s psychological state, degree of arousal, sex, age, or level of consciousness. (133)
5. Elsewhere, inhalations of a variety of fragrances by healthy volunteers showed that prolonged inhalations of fragrances influenced autonomic nervous system parameters (as shown by systolic and diastolic blood pressures) as well as mental and emotional conditions. In addition, the chemical chirality of the odor molecules limonene and carvone produced differing physiological responses. (134)
6. In percutaneous artery intervention patients in an intensive care unit, aromatherapy oils effectively reduced their anxiety levels and increased the sleep quality, although blood pressure levels were not significantly affected. (135)

Functional neurology massage

    Using learning and feedback principles of neuroplasticity, functional neurology massage seeks to produce an improved congruence of the body, its emotions, and the nervous and endocrine systems. Unlike conventional massage, functional neurology massage may employ eye movements, aromatherapy, standing single leg exercises, massage to one side of the body, or light touch bodywork. (136) The purpose is to engage the nervous system, in which several lines of evidence either directly or indirectly suggest a neuroplastic response to massage:

1. A study of healthy adults subjected to pressure massage tracked the high- and low-frequency components (HF and LF) of heart rate variability as well as the LF/HF ratio as noninvasive markers of the autonomic nervous system. An increase of the HF ratio after moderate pressure massage suggested increased vagal efferent activity, while the decrease in the LF/HF ratio implied a shift from sympathetic to parasympathetic activity. Interestingly, light pressure massage produced precisely the opposite results. (137)
2. A combined regimen of massage and stretching in fibromyalgia patients after 18 sessions produced an increase of parasympathetic and decrease of sympathetic tone shown by heart rate variability. Joint flexibility also improved significantly. (138)
3. Similar results were found in children hospitalised in an intensive care unit. Foot and hand massage of 18 children produced a significant increase of parasympathetic activity as seen with a greater increase of HF compared to LF. Interestingly, the sum of HF + LF was positively correlated with clinical severity. (139)
4. The combined application of heat and massage for 40 minutes daily, 5 days a week for 2 weeks in 139 healthy subjects led to a significant increase of latency of a sympathetic skin response test, Plasma cortisol and norepinephrine levels also registered significant decreases, the sum total of indicators suggesting a relaxation of the autonomic nervous system. (140)
5. A more direct effect of massage was found with rats following facial nerve transection and immediate microsurgical repair. Those animals receiving 5 minutes of daily massage to the left whisker pad throughout the recovery period showed improved functional recovery in all whisking parameters compared to controls. In other words, massage produced an accelerated recovery. (141)
6. A similar investigation of the rat transected facial nerve model should that gentle stroking of the paralysed facial muscles resulted in full recovery of function, whereas electrical stimulation failed to improve vibrissal motor performance. (142)

Yoga

    Yoga is linked to neuroplasticity through habituation of the posture, breathing, guided imagery, and meditation that characterise this rapidly growing practice. It is essentially a training of the brain to focus as well as process positive thoughts, leading to activation of the parasympathetic nervous system with deeper breathing. The combination of breath control, posture, and presence practiced in yoga encourage a linkage between neural pathways, creating strong and complex neural networks, giving rise to the popular expression, ‘Neurons that fire together, wire together’. 

    Deep breathing, music, physical activity, communal experience, and music experienced in yoga stimulate the reward system characterised by dopamine and endorphin release which further amplify states of healing and well-being. Specific examples of the neuroplastic and neuro-protective effects of yoga include:

1. A study with non-suicidal outpatients of depression offered yoga showed correlated decreases of the Hamilton Depression Rating Scale and increase in serum brain-derived neurotrophic factor. These effects were not seen in groups receiving antidepressants alone or in combination with yoga. The conclusion was that neuroplastic mechanisms could be related to the therapeutic mechanisms of yoga in cases of depression. (143)
2. Yoga mediation practitioners were shown in another study to possess greater grey matter volume in frontal, limbic, temporal, occipital, and cerebellar regions compared to a matched control group. A dose-dependent effect was shown by the correlation of grey matter volume with the duration of yoga practice. Furthermore, the yoga practitioner group showed significantly fewer cognitive failures on the Cognitive Failures Questionnaire. From these results, it appeared that hatha yoga practice could be associated with the promotion of neuroplastic changes in executive brain systems, which could confer therapeutic benefits that accrue with repeated practice. (144)
3. Essentially the same result was obtained in a second study, in which subjects lacking yoga experience displayed the well-documented age-related global brain grey matter decline, while individuals taking yoga did not. Again, there was a dose-dependent correlation of years of yoga experience with grey matter volume differences in the left hemisphere (frontal operculum and orbital cortex), suggesting that yoga tuned the brain toward a parasympathetically driven mode and positive states. The combination of postures and meditation contributed mostly to the size of the hippocampus, precuneus/PCC, and S1/SLP, while the combination of mediation and breathing exercises contributed the most to V1 volume. The neuroprotective effects of yoga were suggested to provide a neural basis for its beneficial effects. (145)
4. In type 2 diabetic subjects aged 30-60 years, numerous types of yoga exercises conducted for 30-4 minutes every day for 40 days led to an increase of right hand and left hand median nerve conduction velocity, while the same parameters of the control groups deteriorated over the period of study. A neuroprotective role of yoga against the progressive decay of nerves in diabetes 2 was suggested by these data. (146)
5. In a randomised controlled trial, individuals engaged in yoga breathing compared to control subjects displayed an induction of salivary nerve growth factor, a trophic factor involved in the development, maintenance, and survival of the peripheral nervous system and cholinergic neurons of the central nervous system. (147)

Cognitive exercises, visualisation therapy, guided imagery

    Batteries of appropriately designed exercises encourage the creation of new synapses and neural circuits, a manifestation of the neuroplasticity thought to characterise areas of the brain. These approaches fall under the headings of cognitive exercises, visualisation therapy, or guided imagery.

    Among the exercises and actions suggested to increase cognitive ability are 8 proposed by Bergland:

1. physical activity
2. openness to experience
3. curiosity and creativity
4. social connections
5. mindfulness mediation
6. brain-training games
7. sufficient sleep, and 
8. reduction of chronic stress. (148)

    In terms of guided imagery, several investigations shed light upon the ability of such measures to promote neurological activity:

1. Perceptions of a visual cue stimulus were found to modify oscillations in the sensorimotor areas specific to hand movements as monitored by EEG patterns. (149)
2. Cued motor imagery enhanced motor evoked potentials of selected muscles in both healthy and stroke-affected individuals. Visual cueing was most effective in young people (20-35 years), while auditory cueing was most effective in both healthy and stroke-affected older people (over 55 years). (150)
3. A study of healthy volunteers revealed that an application of guided imagery and music stimuli produced increased activation seen by fRMI in five neural regions associated with negative emotional and episodic memory processing. Regions of the brain included the left amygdala, left anterior cingulate gurus, left insula, bilateral culmen, and left angular gyrus. (151)
4. Based on the hypothesis that neuropathic pain after spinal cord injury was based on a mismatch between motor commands and sensory feedback, investigators recruited five paraplegic patients to see whether a visual illusion aimed to correct this mismatch reduced pain. Guided imagery produced a slight reduction of pain, but not as great as that achieved by exposure to a mirror in which patients were exposed to virtual walking consisting of a mirror and a film of lower body walking. (152)
5. A six-week training in mental imagery for upper limb amputees produced significant reductions in the intensity and unpleasantness of constant pain and exacerbations. This was accompanied by reductions of cortical reorganisations of motor and somatosensory cortices expanding from the lip area to the hand area, as seen by fMRI. (153)
6. Interestingly, individuals who were hypnotised experienced the loss of autonomic (heart rate, respiratory frequency, tonic skin resistance, EEG patterns) responses expected during guided imagery that was considered to be neutral. However, the emotional valence of imagery that was judged to be unpleasant overrode the apparent hypnotic block, such that subjects exposed to such imagery experienced changes in the gamma, beta2 and beta 3 activities as well as in heart rate and respiratory frequency. (154)

Eye muscle exercises (Vision Therapy)

    The purpose of vision therapy is to improve visual abilities by training the eyes and brain to work together more effectively. Chinese eye exercises, in particular, were developed as a form of massage around peri-ocular acupoints and grounded in theories of traditional Chinese medicine.

1. Eye acupressure was believed to improve neural nutrition to the eyes, reducing eyestrain and the possibility of myopia as well as preventing migraine, neuralgia of the trigeminal nerve, conjunctivitis and facial paralysis. (155)
2. More recently, 190 schoolchildren aged 10-14 years underwent standard Chinese eye exercises and experienced a reduction in accommodative lag (ability to accommodate near and distant targets) in the short term compared to those who performed sham point eye exercises. It was unclear, however, whether such exercises were sufficient to prevent myopia progression in the long term. (156)
3. Exercises directed at accommodation, vergence, and convergence produced vergence and accommodation improvements in the vergence exercises only. (157)
4. Yogic eye exercises, consisting of palming, blinking sideways viewing, front and sideways viewing, rotational viewing, up and down viewing, preliminary nose tip gazing, and near and distant viewing, significantly reduced eye fatigue on a group of undergraduate nursing students. (158)
5. In terms of cognitive abilities applied to attention and memory, healthy volunteers subjected to rapid serial visual presentations showed greater accuracy in responding to target letters separated by one distractor, as well as in letter identification if they performed active eye exercises consisting of following a white square on a black background while making saccadic eye movements for 18.5 minutes. (159)
6. Elsewhere, a prospective randomised controlled trial found that patients with idiopathic cranial nerve VII paresis experienced a greater rate of recovery if they underwent eye exercises for a period of four weeks with improvements in oribicularis occuli muscle strengths. (160)
7. Evidence supporting the efficacy of eye exercises in managing convergence insufficiency, improving visual field remnants after brain damage, and developing fine stereoscopic skills was supported in a systematic review in 2005. (161)

Meditation

    Mindfulness meditation, defined by Jon-Kabat Zinn as ‘the ability to pay total attention to the present moment with a nonjudgmental awareness of the inner and/or outer experiences’, (162) raises an interesting paradox. Despite casual impressions, mediation actually appears to the neuroscientist as a complex task, involving what appear to be the contradictory tasks of intense concentration and openness to sensory experiences, emotions, and thoughts. Accordingly, meditation processes have been divided into those engaging focused attention (FA) and those involved in open monitoring (OM). FA, therefore, devotes full attention on a given object in a sustained fashion, while OM maintains an awareness of the content of experience from moment to moment, recognising emotional and cognitive patterns.

    Specific neural networks and instances supporting the occurrence of neuroplasticity are described as follows:

1. Activation of the dorsolateral prefrontal cortex, associated with executive decision making and attention, has been reported across a variety of mediation styles. Increased activation in the cingulate cortex, which plays a major role in integration of attention, motivation, and motor control, has also been noted, as has the activation of the anterior insula involved with the perception of visceral feelings (hunger, thirst, balance, detections of heart and breathing rates). (163)
2. In FA meditation, expert meditators with an average of 19,000 hours of practice showed more activation in a network of brain regions typically involved in sustained attention. However, expert meditators averaging 44,000 hours had less activation in response to distractor sounds used to probe the meditation. This inverted u-shaped learning curve suggested that, after extensive FA meditation training, minimal effort was needed to sustain attentional focus. Compared to novices, experts had less brain activation in regions related to discursive thoughts and emotion while showing more activation in the regions related to response inhibition and attention. These variations with hours of practice suggested plasticity in these mechanisms. (164)
3. Demonstrations of neural changes during OM meditation was provided by long-term Buddhist practitioners, who registered electroencephalograms with high-amplitude gamma-band oscillations and phase-synchrony during meditation, differing from controls. Specifically, the ratio of gamma-band activity (25-42 Hz) to slow oscillatory activity (4-13 Hz) was initially higher in the resting baseline before mediation for the practitioners compared to controls. During mediation, the difference between the two cohorts increased sharply. (165)
4. Differences in positive and negative responses to emotional sounds as shown by fMRI brain activation patterns of novices compared to experts in meditation are shown in Figure 12 from data from Lutz: (166)

Figure 12: Directionality of brain activation. Areas showing a negative (dark blue) or positive (orange) impulse response on average across 10 seconds in responses to all emotional sounds for 15 novices compared to 15 experts in meditation. Top row (A-D) represents one cross-section at Talalrach coordinate z="3" (a fMRI slice of the brain) and bottom row (E-H) represents another cross-section at the Talalrach coordinate z="13.

Narrative:  I report a patient with Hyperemesis Gravidarum. Her dilemma of constant vomiting, the frustration of seeking effective care, the use of AK methods and the resultant beneficial outcome is discussed and reviewed concluding with recommendations that may be helpful for other sufferers.

Indexing Terms:  Chiropractic; AK Applied Kinesiology; Hyperemesis Gravidarum; Vitamin K; Vitamin C.

Introduction

    This report reviews the dilemma of finding treatment for  patients suffering Hyperemesis Gravidarum (HG). A literature review of traditional care, methods of the applied kinesiology approach and a discussion of outcomes of two cases will be presented.

    Nausea of pregnancy (NVP) is common and not associated with an abnormal outcome if it finishes in the first trimester. HG is the worse case scenario for the nausea sufferer and may extend through the full term. Complications of Dehydration and malnutrition may create dangers for the mother and the baby. (1) It is estimated that 50-90% of pregnant women may suffer some form of nausea with only 0.3 to 2% having HG. However HG can account for 30% of hospital admissions before 20 weeks. (2) An overview of NVP indicates that 25% of pregnant women will have no symptoms, 25% will have nausea only and 50 % will have nausea and vomiting. It can be progressive leading to hospitalisation for dehydration, electrolyte disturbances, ketonuria, weight loss greater than 5% and malnutrition and can be compared to the nausea and vomiting of chemotherapy. (3, 4)

    HG has been associated with nulliparity, multiple births, previous history of an unsuccessful pregnancy, previous HG and obesity. Low risk is associated with advanced age, smoking and war. (5,6,7) The Maternal genes of the mother are more likely associated with 3x more risk for HG than the foetal paternal genes. (8) 

    Time lost from work is 14 days at a cost of about US$3,000 per patient with severe symptoms of NVP in the USA. (9) One study reported a loss of 62 hours of lost employed work and 32 hours of lost household work. (5)

    About 10% will not respond to remedies and usually medication will begin. The mildest medication is first accompanied by hospital care where metabolic problems are a risk and/or a greater than 5% weight loss or malnutrition has resulted. Foetal deformities are a risk with management by medication. (10) These deformities range from thalidomide as a cause of limb deformities to cleft palate associated with steroids.

    A Google search of principle proposed natural treatments include Acupuncture, hypnosis, ginger and vitamin B6, red raspberry, Vit C and Vit K. (11) Conservative medical management is recommended to begin with including Vit B-6, doxylamine and ginger capsules. Metoclopramide, Promethazine, Ondansetron and Methylprednisolone may be progressively added and used with caution. Emergency care for hydration, electrolyte and nutritional support may be parenteral, enteral or nasogastric with varying degrees of success and risk of bacteraemia, sepsis and thrombosis. (12)

    This case report is important as it is one of the few cases recorded that uses a novel approach to resolving HG as quickly as possible. It is also unusual in that it uses old research observations that showed promising results with relative safety but for some reason more extensive research was never conducted.

    The Null Hypothesis for this case study is that a method of using Vit K and Vit C will have no benefit for a patient suffering HG.

Case Report

    This report describes a 28 year old homemaking mother, 5’ 7½ (171.5cm tall, 72 kilo weight before her 2^nd pregnancy. She said she was referred by a family member to contact our clinic. She consulted by telephone describing her distress suffering the nausea of pregnancy diagnosed as hyperemesis gravidarum. She said her weight had dropped to 62 kg over the previous 13 weeks from constant vomiting.

    The patient had similar problems in the previous pregnancy 2 years earlier. She said that she hoped that she wouldn’t suffer the same with this pregnancy. She described hyperemesis gravidarum from 6 weeks to 20 weeks before it stopped at that time. This time it began earlier at 4 weeks with more intense symptoms prompting this consultation and treatment that eventually began at 13 weeks.

    During the first pregnancy the patient was prescribed Maxalon (metachlopromide) and Ondanzatron (4MG AND 8MG) and Cyclamine. The patient explained that she still felt sick it was only when she was throwing up uncontrollably or at least having consistent urges to throw up that the medications were working. She was recommended to take them consistently every 4-6 hrs(Maxalon) however when the medications were vomited, the ondanzatron was recommended.

    The patient was concerned that this was a chemotherapy drug but found it worked better, however none stopped the constant nausea feeling or even helped recover the dehydration. The dehydration that she experienced caused the condition to worsen. She found that when she was properly hydrated she was able to keep from vomiting however during both pregnancies she was never recommended fluids by either her doctor or the hospital staff. She was only ever given injections of Maxalon and Ondanzatron wafers as they were guaranteed not to reflux. She took all of the medication during the 6 weeks till 20 week term. Birth of a girl was normal with no complications.

    During the second pregnancy symptoms followed a similar pattern but more intense with constant vomiting. At 10 weeks her 10 kilo weight loss prompted compassionate help from friends and family motivating her to call our clinic for help. This time medical management included Maxalon plus Ondanzatron for additional help between weeks 5 - 8. The medication helped digest some food but the vomiting continued. Her request for fluids during hospital visits was refused due to lack of dehydration signs. Treatment in hospital included 2-3 Maxalon gluteal injections that temporarily stimulated vomiting until it was absorbed. It helped reduce the intensity of the vomiting. The patient travelled to Perth to be with family where similar treatment continued from Week 8 to Week 13.

Consultation and treatment

    I was unable to physically examine the patient. I advised the patient that I would complete a literature search and return her call after our telephone consultation. I conducted the search and could find little additional information to assist her outside of the medical care she was receiving.  I did advise her that hydration was important and attending a hospital for a saline drip may be necessary as a last resort. First aid measures involving sipping fluids, sucking ice and a salt water enema were all suggested. 

    I advised the patient to ask her doctor to give her Vitamin K and Vitamin C injections (due to vomiting oral supplements) according to Merkel’s advice, and included his paper. Her doctor kept delaying administration of the injections for 3 weeks until the patient ‘pestered’ him to do it. He explained that while Vitamin K is routinely given to eligible infants no one has given it to their mothers. Injections of Vit C were unobtainable, One injection of Vit K was administered at 13 weeks with 2 x 500mg tablets of Vit C. 

    Initially the nausea stopped for 24 hours with a return of normal appetite. Fatigue and nausea returned for 3-4 days without vomiting. Then the nausea stopped. 2 mild vomits have occurred when missing meals which the patient thought may be related to low blood sugar. Self management was now possible using liquid Chlorophyll (a source of Vit K) and 2 Vit C 500 mg tablets chewed daily for 3-4 weeks eliminating all signs of nausea. Based on the previous pregnancy following the same pattern, the patient was happy to have weeks 13 - 20 nausea free.

AK literature search

    A search of AK literature was conducted to find alternative methods of care for NVP and HG. George Goodheart, a Chiropractor, discussed his methods for helping this condition in 1987. (13) 

Goodheart’s Method

1. Oral Vit C diagnosed with lingual Vit C absorption test. Up to 25 mg 3x per day.
2. Vit K 5 mg per day 
3. Use liquid or tablet forms of Chlorophyl
4. Consider Psychological counselling
5. Use a protomorphogen (liver extract)
6. Diagnose lymphatic, vascular, neurological, acupuncture, and respiratory reflexes relating to the liver
7. Review Postural stress with foetal development needing mechanical treatment.

    Goodheart based this nutritional supplementation of Vit K and Vit C on current nutritional knowledge of that time and experience with manipulative skills as a Chiropractor.

    Goodheart described a paper that used Vit K and Vit C therapy published in 1952. (14) A search of Pubmed located the paper by Richard Merkel MD, who discussed the use of menadione bisulfite and ascorbic acid in the treatment of nausea and vomiting of pregnancy. This was described as a preliminary report.

    Merkel proposed a hypothesis resolving the problem of NVP and HG could be accomplished by decreasing placental capillary permeability preventing transfer of the ‘vomiting factor’ to the expectant mother. 

    He used this treatment in a series of seventy consecutive cases of nausea and/or vomiting of pregnancy, varying from mild to severe. Thirty-three of the women were primigravidae and thirty-seven multigravidae. Seven were Rh^- negative, and sixty-three Rh⁺. All were given orally each day 25mg of ascorbic acid and 5mg of menadione bisulfite without any attempt at psychotherapy or other supportive measures. The prothrombin levels in the blood and the bleeding time of each patient were determined both prior to medication and afterward.  

    Therapy, averaging thirty days, was continued until the withdrawal of medication produced no recurrence of symptoms. 64 had a remission of their symptoms within 72 hours. 3 were relieved of vomiting but continued with nausea, three had no relief and one advanced case into the 2^nd trimester found it was the only therapy that helped. Three patients continued therapy until delivery. Iron absorption improved with therapy. Vit C alone had no benefit. No dangers with the medication at these doses was observed. Merkel recommended further research to validate his preliminary report.

    Merkel’s study was followed up in 1958 by two Canadian researchers, M Ferron and H Gibeault with similar results. (15) Gerber describes his use of this therapy and the difficulty getting it published in a column in ‘The Townsend Report’, an online health newsletter. (16) He refers to a paper by Wright published in 1984. (17) Some evidence for Vit K deficiency was presented in a case study by Robinson et al in 1998. This study of a woman at 15 weeks gestation with HG and epistaxis concluded that Vit K deficiency and coagulopathy should be considered in women with HG who present with a bleeding diathesis. They recommended prophylactic Vit K replacement should be considered in cases where HG is severe and protracted. (18) They were not aware of previous studies and acknowledged that Vit K deficiency is a known complication of malnutrition and a known cause of coagulopathy.

    Of Goodheart’s methods, only 1, 2, and 3 were convenient with a telephone consultation. Unfortunately persistent vomiting by the patient was so severe, I suggested that the patient ask her doctor for injections of Vit K given that this was the current mode of medication being used for other vomiting medications. While Vit K injections are given routinely to prevent bleeding problems in babies at birth this deficiency may not correlate to the mother. (19)

    A grey literature search in the International College of Applied Kinesiology located another case study authored by Daniel Duffy titled Nausea of Pregnancy responds to Chiropractic care. (20) In this paper, Duffy reported patient management success using the following Applied Kinesiology protocol:

1. Flaccidity of the ileocecal valve (ICV)
2. 2Subluxation complex involving malposition of the Occiput and lack of proper lymphatic flow in the Right Upper Trapezius and Left Sterocleidomastoid
3. Subluxation complex involving the dorsal spine
4. Pelvic instability caused by a subluxation complex involving the sacroiliac joint and right piriformis muscle
5. Subluxation complex involving lymphatic drainage of the Sartorius muscle, including Whole Adrenal Gland-negated positive therapy localisation (FTL) of the Adrenal Neurolymphatic points. The source of Whole Adrenal Gland was Biotice. 

    Unfortunately this methodology needed a face to face consultation for the manual therapy interventions to be administered. I have added this protocol here for the benefit of the reader when opportunity arises.

Discussion

    This case illustrates the consultative management of a multigravida mother suffering hyperemesis gravidarum using AK research material. Goodheart’s observations published in his 1987 manual discussed this disabling condition of hyperemesis gravidarum and enabled location of historical research material relevant to this patient.

    Information for this case presentation was sourced from the diaries of the patient and personal interviews via text, email and telephone. Diagnosis of Hyperemesis Gravidarum was determined by medical examination.

    The patient determined that she needed more than usual care for the HG she was suffering based on her experience with her past pregnancy. Useful information in addition to current knowledge was found that posed little risk to the mother and foetus compared to the medications offered. Cooperative care by attending physicians may have been lacking given the mother’s observation of dehydration and malnutrition she felt she was suffering as well as including the delay in reviewing and using the presented research for proposed and relatively immediate relief. When treatment was finally given the mother perceived a benefit of a possible extra 7 weeks vomit free compared to her first baby. 

    At the time of writing the mother was well and not suffering HG.

Conclusion

    New knowledge from this application of historical data indicates that VNP and HG may have a cause related to an increase capillary permeability of the placental base releasing a ‘vomiting factor’.

    This case report illustrates that this cause may be helped by treatment with Vitamin K and Vitamin C administered either orally or injection. AK methods had sufficiently recorded the data and proposed other treatments that may be supportive of this theory. The null hypothesis was found false for this patient.

    This case adds to the sparse data for this method of treatment but should encourage further research. This data is specific to this patient and should not be taken as a general treatment for this condition.

Objective: The objective was to determine the effect of chiropractic care and Applied Kinesiology (AK) techniques to provide relief and range of motion restoration of the effects of right frozen shoulder syndrome.

Clinical Features:A 30-year-old male patient presented with complaints of chronic right shoulder pain that radiated into his right upper trapezius from surfing. 

Intervention and Outcomes: AK based techniques were utilised to in the areas of vertebral subluxation to help decrease the discomfort associated with the patient’s right frozen shoulder. Manual muscle testing (MMT) was also used to determine proper facilitation of reactive muscle testing. After two visits utilising Chiropractic care and AK based techniques, the patient’s shoulder pain had subsided his range of motion was restored.

Conclusions: This case report exemplifies a combination approach of care to a patient with adhesive capsulitis with a resolution of symptoms and a return to activity in a manner of 2 visits. A combination of Chiropractic care benefitted the patient by use of AK based analysis through global MMT, and also while working with chief complaints allowed the patient to return to surfing in a relatively quick manner. However, research involving one or two specific techniques would benefit to know the true potential of care involving the area of complaints.

Indexing Terms: Chiropractic; Applied Kinesiology; frozen shoulder; adhesive capsulitis; manual muscle testing.

Cite:  McBride AS. Resolution of Adhesive Capsulitis following Chiropractic care and Applied Kinesiology (AK): A case report. Asia-Pac Chiropr J. 2026;7.1. https://www.apcj.site/McBrideAdhesiveCapsulitis.pdf

Introduction

    Frozen shoulder syndrome (FSS) is a common condition presenting to variety of health care practitioners including Chiropractors, osteopaths, medical doctors, and physical therapists. Also referred to as adhesive capsulitis, FSS remains one of the most poorly understood shoulder conditions, (1) with its aetiology and pathogenesis largely disputed. (2) 

    Recently, a consensus definition of FSS was reached by the American Shoulder and Elbow Surgeons to be ‘a condition characterised by functional restriction of both active and passive shoulder motion for which radiographs of the glenohumeral joint are essentially unremarkable …’ (1)

• Proper positioning so the test muscle is the prime mover
• Adequate stabilisation of regional anatomy
• Observation of the manner in which the patient or subject assumes and maintains the test position
• Observation of the manner in which the patient or subject performs the test
• Consistent timing, pressure, and position
• Avoidance of preconceived impressions regarding the test outcome
• Nonpainful contacts and nonpainful execution of the test
• Contraindications due to age, debilitative disease, acute pain, and local pathology or inflammation’. (19)

    This technique was well utilised in the care of this patient for the treatments regarding a need for Chiropractic adjustments/manipulations, sacro-occipital technique (SOT) blocking needs, ocular lock technique, nutritional testing, soft tissue care, acupuncture meridian therapies, Therapy Localisation (TL) of care, and Ileocecal Valve (ICV) functioning.

Quantum Neurology (QN)

    Quantum Neurology^® Rehabilitation is a method of exercising and strengthening the Nervous System. This is done by incorporating neurological activation, physical mobilisation, and light therapy. Using a patented system of evaluation and correction, it enables the practitioner to find hidden neurological weaknesses in the body. Specific techniques allow practitioners to activate the Nervous System’s innate healing power so that the body can heal itself. (20) This technique was used in evaluating and treating various myotomes and cranial nerves and their associated inhibitory muscle tests.

Diversified technique

    Spinal manipulation is a passive and rapid movement of a joint beyond its active and passive limit of movement, but remaining within the limit of the joint’s anatomical integrity. This patient received one to two dynamic thrusts, applied with high velocity low amplitude force, directed at one or more restricted lumbar, thoracic or cervical spine segments. This approach to manipulation is commonly referred to as diversified technique. (21) This technique was applied to the correction of adjusting specific segments of the spine and pelvis.

Chiropractic and AK treatment

    The patient was seen for a total of 2 visits of the time period from November 2nd, 2022 to November 8^th, 2022. After the initial exams were conducted, the doctor undertook the initial Chiropractic analysis on the first visit as well.

    Upon the first visit, November 2^nd 2022, the doctor evaluated and adjusted based on AK analysis in a standing position by using the right deltoid muscles as a group evaluating the patient in a head forward and cervical flexion position, and it was determined to do a standing first thoracic (T1) adjustment. This was done by having the patient place his feet together, arms out horizontally and bilaterally to each side, and then the doctor placing their hands interlocked underneath the patient’s arms and hands on the back of his neck. This was followed by the patient placing their hands on the doctor’s interlocked hands, followed by the patient taking a deep inspiration and expiration, while slouching back into the supporting knee of the doctor and then the doctor would do a manual ‘traction’ of the cervicothoracic junctional area. The right deltoid muscle group was retested and shown to be facilitated.

    The doctor also performed Primary Atlas Technique (PAT)22 and AK analysis and it was determined that the left C1 segment had shifted laterally. This was adjusted in a supine position via a rotary Diversified Chiropractic high velocity-low amplitude (HVLA) adjustment in a superior to inferior and lateral to medial line of drive with an 2^nd digit (index finger) contact. The 5^th cervical vertebrae (C5) was also found via therapy localisation (TL) with the patient contacting the vertebrae to have a ‘vertebral body right’ rotation malposition, which was also adjusted via a rotary Diversified chiropractic high velocity-low amplitude (HVLA) adjusting C5 from right to left, counterclockwise with the head in slight flexion.

    In addition to the cervical spine segments being adjusted, the Lovett Reactor vertebrae (23) of L5 and L1 in the lumbar spine were also adjusted in side posture lying stance using HVLA as well.

    The patient was evaluated and treated based on findings from an inhibited muscle test via the Quantum Neurology (QN) model of analysis. The pubic bone was checked first. This was performed by the patient laying supine on the table with the knees bent, feet together while flat on the table. The doctor placed the hands on the patient’s distal femur heads, and the patient was instructed to approximate the knees while the doctor resisted. There was a failure/inhibition of the knees to approximate. The patient then TL’d each side of the pubic bone, and it was determined that the patient had a superior left pubic bone. This was corrected with the use of an Activator™instrument adjusting tool (24) with a line of drive of Superior to inferior on a superior pubic bone contact while a GRT™red light was placed at level of the patient’s brainstem. The muscle test was rechecked and showed a facilitation of the initial pubic bone test. The S1 myotome aka the peroneus tertius was also tested bilaterally, and shown to have an inhibition on the left foot. This was corrected with the doctor’s hands placing pressure on the patient’s left inguinal ligament and then a re-testing showed a facilitation of the peroneus tertius. This was also determined to showing a right sided rectus femoris inhibition on the right side, and was corrected with firm pressure applied to the space at 2” (5cm) above and 1” (2.5cm) lateral to the umbilicus. This was also shown to facilitate upon testing the muscle post-treatment.

    The doctor also checked the patient’s ileocecal valve (ICV), (22) and it was determined that the patient showed having an ‘Open’ ICV. This was shown by testing a strong indicator muscle, in this case the right pectoralis major-clavicular (PMC) division, and then having the patient TL the right lower quadrant of the abdomen just 1 - 2” (2.5-5cm)  above the right anterior superior iliac spine with his fist. This showed an inhibited PMC muscle. The test was then ‘challenged’ by having the patient pull the right lower quadrant abdominal tissue superior and medial towards the left shoulder, which did facilitate the PMC muscle. This was also further confirmed showing an inhibition of the right iliacus muscle. 

    From there, the various points addressed were the Bladder 58 acupuncture meridian point on the left, which is on the posterior border of the fibula; Kidney 4/5, which is posterior and inferior to the medial malleolus, in the depression medial to the attachment of the tendon of the calcaneus. This was also corrected with firm pressure within the patient’s right bicipital groove and over the lamina of the C3 vertebrae on the right. Following all of that treatment, the patient re-TL’d the ICV and the PMC showed strengthening as well as the right iliacus muscle.

    The patient also showed to have a right hyoid dysfunction as well, specifically his right omohyoid. This was tested by using the bilateral PMC muscles as indicator muscles, and then having the patient protrude the tongue out of his mouth, which showed an inhibition of the bilateral PMC muscles. This was then examined by moving the patient’s hyoid bone in various directions to stretch the muscles and testing a previously strong indicator muscle for weakening. It is assumed that a positive test is due to neuromuscular spindle cell dysfunction in the muscle being stretched. (22) When positive, the doctor evaluated the muscle being stretched with accurate (TL) by having the patient therapy localise to the muscle with the tip of his index finger, the area of dysfunction. The treatment was then directed to the neuromuscular spindle cell to push its ends together. The bilateral PMC muscles were then re-tested with the patient protruding his tongue showing a facilitation and no longer needing any treatment on the hyoid muscles.

    The patient’s pulse points were also checked as part of AK diagnosis. This test was performed by using the Rectus Femoris muscle as an indicator muscle, and then having the patient contact TL the various pulse points until there was an inhibition of the muscle noted. It was determined that he had a right-distal wrist crease point show up as an inhibited muscle test, indicating the most deficient meridian, which in Chinese medicine is designated as a ‘Metal Element’ point. The metal element related muscle that was checked was the tensor fascia latae (TFL) on the left side. This was correlated by the patient TL’ing the ‘alarm point’ for the TFL which is 1.5’ 4cm lateral to the patient’s umbilicus on each side of the abdomen, which facilitated the previously inhibited TFL.

    The doctor also held contact at the ‘tonification’ point of Large Intestine 11 (LI11). LI11 is a point located at the elbow, which is located at the end of the crease on the outer side of the bent elbow. (25) The doctor then retested the original left TFL muscle and there was a facilitation of the muscle.

    The patient was also adjusted prone on the T4-T6 as well as T8-10 vertebrae since they were also TL’ed and shown to have inhibition using the hamstrings as a group as an indicator muscle. This was also confirmed via bilateral teres major muscle testing showing fixations (22) in these various areas.

    The patient was also noted to have a left Category (CAT I) listing (22) with a confirmation of both his hands being placed on the left SI joint testing his left hamstring showing an inhibition. This was also confirmed with his left piriformis inhibiting upon being in a quadruped position. This was corrected with the patient prone, using blocks placed at the right ASIS and the left greater trochanter. This strengthened/facilitated the hamstring response, and the patient was left on these blocks for about 2 minutes until the hamstring was retested, showing a titration point where there was an inhibition and showing no more work was needed.

    The second and final visit took place on November 8^th 2022 with the patient having no pain in the right shoulder, but only some minor discomfort in the lower back. The doctor used PAT and found a right lateralisation of the C1 vertebrae, which was adjusted supine via a rotary Diversified Chiropractic high velocity-low amplitude (HVLA) adjusting in a superior to inferior and lateral to medial line of drive with an 2^nd digit (index finger) contact.

    The doctor also checked the patient’s ileocecal valve (ICV)22, and it was determined that the patient showed having an ‘Open’ ICV. It was corrected in the same manner as the first visit.

    This patient once again had a ‘Metal element’ distal wrist crease pulse point identified, which corresponded to an inhibited left TFL muscle, and was treated by holding the LI 11 point until a pulse was found on the left elbow crease, and the left TFL muscle was facilitated.

    The patient was also shown to have a CAT I listing on the left side once again, and was treated in the same manner as the first visit.

Chiropractic/AK outcomes

    SOAP (Subjective Objective Assessment Plan) notes were taken as a daily record keeping procedure to monitor patient progress. The notes explained the basic procedures mentioned on each subsequent visit and what was found upon chiropractic examination and what was adjusted or worked on with QN and AK therapies.

    Upon conclusion of the 2^nd and last visit of the patient, he had reported that his right shoulder pain had totally dissipated and was able to perform Apley’s Scratch test and Mazion’s test with no discomfort in the shoulder, and he was also able to lift furniture and surf in the 6 days between visits. The patient had mentioned that the incorporation of QN and AK treatments of the right shoulder from visit 1 had made a big difference in the recovery of the right shoulder.

Discussion

    The aim of this study was to determine the effect of several different AK based techniques with Chiropractic care on decreasing the frequency and duration of shoulder pain this patient had experienced over the last month when surfing. In this case report, the right frozen shoulder discomfort he had been experiencing was likely being caused because of overall body joint mechanics that made the right shoulder, specifically the humerus bone, compensate for the lack of overall motion and subsequent pain he was experiencing.

    In this particular case study, the patient responded rapidly with conservative AK and AK-based therapies addressing the entire body since the patient reported the mechanism of injury initially started from surfing. These symptoms were only present for a 1-month duration, so long-term

effects were not noted. The evaluation on the follow up appointment also showed that he had no range of motion issues including negative tests of both Mazion’s test and Apley’s scratch test on the right. This could indicate that it was more of an acute-based injury and that there was overall postural distortion causing shoulder compensation.

    In other types of treatments for FSS, there is a tendency to rely upon injections and/or physical/physiotherapy to aide in the recovery. Based on the available evidence, it appears that the use of an Intra-articular (IA) corticosteroid injections for patients with frozen shoulder of duration less than 1 year is associated with greater benefits compared with all other interventions, and its benefits may last as long as 6 months. (26) This has important treatment ramifications for the general and specialist musculoskeletal practitioner, providing them with an accessible, cost-effective, (27) and evidence-based treatment to supplement exercise regimes, which is anticipated will inform national guidelines on frozen shoulder treatments moving forward.

    In the short-term, IA corticosteroid appeared to be associated with better outcomes compared with no treatment in all outcome measures. Adding arthrographic distension to IA corticosteroid may be associated with positive effects that last at least as long as 12 weeks compared with IA corticosteroid alone; however, these benefits are probably not clinically significant. Compared with physiotherapy, IA corticosteroid seemed to be associated with better outcomes, with clinically significant differences. Combination therapy with IA corticosteroid plus physiotherapy may be associated with significant benefits compared with IA corticosteroid alone or physiotherapy alone for ER ROM and function, respectively, at 6 weeks. (25)

    Because of the paucity of robust evidence, no firm recommendations exist for clinical practice.

    The National Institute of Health and Care Excellence (NICE) guidelines,28 influenced in turn by the BESS/BOA recommendations, recommend a stepped approach, starting with physiotherapy and only considering IA corticosteroid if there is no, or slow, progress. Many treatments are available for frozen shoulder including both operative and non-operative.

    Operative procedures include manipulation under anaesthesia and arthroscopic surgeries. Surgery reduces the severe complications of frozen shoulder. Non-operative includes pain management through different modalities (Transcutaneous electrical nerve stimulation, Short wave diathermy, Interferential therapy etc.), mobilisation techniques, exercise plan and precautionary measures. All treatments just improve the functional time to recovery and increase the range of motion. (29)

    However, none of the treatment is authentic to totally eliminate the future chance of disease. Physical examinations are generally considered low-cost process and results can directly be obtained at the time of the consultation. On the other hand, precision is based upon doctor’s knowledge and practice.

    Today a frozen shoulder is diagnosed by clinical examination and imaging tests. (30) Firstly a doctor diagnoses the problem by asking the patient to rotate the shoulder in a different direction. If physicians are uncertain about the problem, then formal test such as magnetic resonance imaging (MRI) can be carried out for diagnosis. Arthrography is considered a standard test for the diagnosis of a frozen shoulder. It is having sensitivity 91 %, specificity 100 % and accuracy 92 %, but the test is an expensive and painful process. (31)

    As part of this case study, there was no advanced imaging taken due to the acute onset of the FSS symptoms as well as the patient’s fast response to care.                 There was also not a need for advanced imaging from a cost-perspective benefit for the patient as well. There is no existing fact, that any solitary check can diagnose a frozen shoulder problem. (32) Cost-effective treatment process is always dependent upon proper clinical assessment and diagnosis. The severity of the disease can be judged best by imaging tests as compared to clinical examination. According to the recent research if we make decision just on the basis of physical examination, it has sure chances that to give us false-positive ratio. Analysis made on the basis of physical examination always conflict with the imaging test. Due to this, we cannot make any decision just on the basis of clinical examination. (30)

    Physiotherapy is widely adopted as an initial treatment in many shoulder conditions including FS. (33, 34) Physiotherapy should include an exercise program that can restore shoulder motion. The patient should be placed on an exercise program with the goal of regaining and maintaining motion.

    Patients receiving exercise therapy should begin an active assisted ROM exercise program as well as gentle passive stretching exercises including forward elevation, internal and external rotation, and cross body adduction. These exercises should be performed five to six times per day. And it is important to perform multiple 5- to 10-minute sessions per day as the shoulder will become stiff again in the time between sessions. (35)

    Many studies have demonstrated physiotherapy as an adjunctive intervention that provides good results. NSAIDs were proven to be more effective when used in combination with physiotherapy as compared to NSAIDs alone. (36) Similarly, steroid injection used in combination with physiotherapy resulted in better outcomes compared to injection alone. (37, 38)

    Despite the self-limited natural history of the disease, some patients fail to achieve desired outcomes with non-operative management. (11, 39, 40) Factors that influence the decision on surgical management include severity and duration of symptoms as well as response to conservative treatment. (39, 41) General indications for surgery are persistent pain and limited motion despite a minimum 3 to 6 months of non-operative management including medication, local injections, or physiotherapy. (11, 29, 40) Levine et al. (42) reported that patients with more severe initial symptoms, younger age at the time of onset, and reduction in motion despite 4 months of compliance with therapy are most likely to require surgery.

    Another potential treatment for addressing FSS is Manipulation under Anaesthesia (MUA). MUA involves passive tearing of the thickened inflamed capsule and contracted ligaments. It is mainly performed under general anaesthesia, however, recent development of ultrasound technology enabled it with brachial plexus or cervical nerve root block. (43, 44) Magnetic resonance imaging after MUA shows capsular tears (mid-substance and humeral avulsion of glenohumeral ligaments), labral tears, or bone bruises of the humeral head. (44) And arthroscopic findings of post-MUA include hemarthrosis, tearing of the joint capsule or rotator cuff, superior labrum from anterior to posterior tear lesion, labral tear, middle glenohumeral ligament rupture. Even though the optimal timing of MUA has not yet been determined, Vastamaki et al. (45) suggested that if conservative management failed, the best time for MUA might be between 6 and 9 months from the onset of the symptom.

    They believed that too early manipulation (before 6 months after the onset of symptom) may lead to a recurrence because the disease is still at the inflammation stage. (45) MUA has been used extensively with satisfactory short- and long-term results. This particular case study also did not have a use for MUA regarding the patient.

    There is presently very little evidence to support chiropractic management of FSS. Murphy et. al (46) reported that that the OTZ Tension Adjustment restores normal function of C0-C1, trapezius, and SCM, thereby restoring normal glenohumeral mechanics, improving shoulder ROM, and reducing pain on elevation of the arm. It has been previously shown that some shoulder complaints resolve after practitioner-applied manipulation. (47 - 54)

    However, with regard to the efficacy of Chiropractic adjustments specifically for shoulder complaints, the current evidence is limited, (55) consisting of one small pilot study, (56) a qualitative study, (57) and a number of case reports. (55, 58 - 60)

    In AK based treatments of evaluation, it appears that the subclavius muscle is important in rotating the clavicle. In many cases of ‘frozen shoulder’, great improvement can be made by treating the subclavius muscle. (61) Since the subclavius muscle cannot be directly tested, it must be evaluated by observation of clavicle movement and therapy localiSation over the muscle.

    Treatment of the subclavius muscle is usually directed to the neuromuscular spindle cells, Golgi tendon organ, or origin/insertion. The digital pressure applied must be rather heavy to contact as much of the muscle as possible. (22) This was not addressed in this particular case study, but serves as a good indicator for future studies.

Conclusion

    This case study describes several AK based therapies for the treatment of frozen shoulder syndrome (FSS). It’s applicability to other patients with similar conditions should be explored.

More research is needed on the subject of AK care-based therapies with Chiropractic for the treatment of frozen shoulder. Specifically, focusing on one individual technique in the treatment of FSS or limited shoulder mobility for further research would be best.

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49. Leung M.S.F., Cheing G.L.Y. Effects of deep and superficial heating in the management of frozen shoulder. J Rehabil Med. 2008;40(2):145–150.
50. Buchbinder R., Youd J.M., Green S., Stein A., Forbes A., Harris A. Efficacy and cost-effectiveness of physiotherapy following glenohumeral joint distension for adhesive capsulitis: a randomized trial. Arthritis Care Res. 2007;57(6):1027–37.
51. Bergman G.J., Winter J.C., Van Tulder M.W., Meyboom-De Jong B., Postema K., Van Der Heijden G.J. Manipulative therapy in addition to usual medical care accelerates recovery of shoulder complaints at higher costs: economic outcomes of a randomized trial. BMC Musculoskelet Disord. 2010;11:200.
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Background:  A two year old male was presented for Chiropractic care by his mother with chief complaints of delayed speech, generalised low postural tone, persistent primitive reflexes, emotional dysregulation, and general fussiness.

Intervention:  The patient received a short course of Chiropractic care, with all interventions modified to be age appropriate. This included diversified, drop-piece, and activator-assisted spinal and pelvic adjustments, cranial releasing techniques, soft tissue work, and a prescribed home exercise programme targeting left-body stimulation, proprioceptive joint distraction, and gross motor activation.

Outcomes:  The patient’s mother noted fast and notable improvements in social engagement, speech, imaginative play, emotional regulation and gross motor competence, alongside the chiropractors observation of improvements in objective findings. The patients health index also rose from 58/100 to 82/100 (within the target range) over the course of care. 

Conclusion:  This case demonstrates an association between subluxation-based Chiropractic care and rapid improvement in speech, neurodevelopment, and emotional regulation in a two-year-old male with persistent primitive reflexes. This is consistent with the core Chiropractic paradigm, wherein subluxation may impact developmental maturation, and that Chiropractic care may facilitate improved nervous system function.

Indexing Terms:  Chiropractic; Subluxation; paediatrics; delayed speech; primitive reflexes; emotional dysregulation.

Cite: Godfrey J, Postlethwaite R, McIvor C. Improvement in Speech, Primitive Reflex Integration and Neurodevelopmental Dysregulation in a two-year-old male under Chiropractic care: A Chiropractic paediatric case report. Asia-Pac Chiropr J. 2026;7.1. https://www.apcj.site/GodfreySpeech.pdf

Introduction

    In the last decade Chiropractic researchers have made significant leaps in the evidence for the neurological impacts of Chiropractic, and the prevalence of neurodevelopmental disorders in children has increased by 40%. 

    We now have research indicating that Chiropractic care increases neural plasticity and sensorimotor integration. (Haavik and Murphy, 2007; Haavik and Niazi, 2024) While these studies were undertaken using adult populations, there is an increasing amount of case report data detailing individual cases of paediatric patients showing indications of neurodevelopmental improvement, including integration of retained primitive reflexes, concomitant with Chiropractic care. (Doyle, 2021; Fairest and Russell, 2019; Steinberg and Postlethwaite, 2022) 

    Additionally, a retrospective study of 37 paediatric patients with neurodeflective (also known as neurodevelopmental) disorders showed significant improvements in autonomic nervous system balance following subluxation based care. (Holt and Spoelstra, 2022) The study, which used clinical and educational tools to assess progress, revealed significant improvements in processing, engagement, learning and connection to surroundings across the cohort.

    But perhaps most notably, statistics emerging in 2022 have revealed that in the decade prior, diagnoses of autism and other neurodevelopmental disabilities increased by 40%. (Shaw and Williams, 2022) This represents a significant challenge for parents and health professionals alike. Moreover, it is a challenge for Chiropractors and Chiropractic researchers to enter the conversation when it comes to bringing these two worlds together and presenting Chiropractic as a potentially vital part of infant and paediatric neurodevelopment. 

Language

Bibliography

• Doyle M. (2021). Improvements in developmental delay in a female child following chiropractic care: a case report and selective review of the literature. Journal of Clinical Chiropractic Pediatrics. Vol. 20. Iss 2. https://jccponline.com/doyle20-02.pdf 
• Fairest C, Russell D. (2019), “Improvement in behavior and attention in a 7-year-old girl with ADHD receiving chiropractic care: a case report and review of the literature,” Journal Clinical Chiropractic Pediatrics, Volume 18, No 1. http://jccponline.com/ADHD.pdf  
• Goddard Blythe S, Duncombe R, Preedy P. et al. (2022). Neuromotor readiness for school: the primitive reflex status of young children at the start and end of their first year at school in the United Kingdom. Education 3-13, 50(5), 654–67. https://doi.org/10.1080/03004279.2021.1895276 
• Haavik-Taylor H, Murphy B. Cervical spine manipulation alters sensorimotor integration: A somatosensory evoked potential study.Clin Neurophysiol. 2007;118(2):391-402. DOI 10.1016/j.clinph.2006.09.014
• Haavik H, Niazi IK, Amjad I, et al. Neuroplastic Responses to Chiropractic Care: Broad Impacts on Pain, Mood, Sleep, and Quality of Life. Brain Sci. 2024, 14, 1124.
• Hock S, Spoelstra A. Improved Brain Development in 37 Children Undergoing Chiropractic Care for Correction of Vertebral Subluxation: A Retrospective Analysis of Health Outcomes. J. Pediatric, Maternal & Family Health. 2022;86-94.
• Johnson CJ, Beitchman JH, Brownlie EB. (2010). Twenty-year follow-up of children with and without speech-language impairments: Family, educational, occupational, and quality of life outcomes. American Journal of Speech-Language Pathology, 19(1), 51–65. https://doi.org/10.1044/1058-0360(2009/08-0083) 
• Law J, Boyle J, Harris F, et al. (2000). Prevalence and natural history of primary speech and language delay: findings from a systematic review of the literature. Int J Lang Commun Disord. Apr-Jun;35(2):165-88. DOI 10.1080/136828200247133.
• Martello J. (2023). Persistent Primitive Reflex and Developmental Delay in the School-Aged Child. The Journal For Nurse Practitioners. Vol. 19. Iss. 10. November 2023 DOI https://doi.org/10.1016/j.nurpra.2023.104767 
• Modrell AK, Tadi P. Primitive Reflexes. [Updated 2023 Mar 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554606/ 
• Shaw KA, Williams S, Patrick ME, et al. Prevalence and Early Identification of Autism Spectrum Disorder Among Children Aged 4 and 8 Years — Autism and Developmental Disabilities Monitoring Network, 16 Sites, United States, 2022. MMWR Surveill Summ 2025;74(No. SS-2):1–22. DOI: http://dx.doi.org/10.15585/mmwr.ss7402a1 
• Steinberg B, Postlethwaite R, McIvor C. Improvement in Physical Resilience and Management of ADHD in a 12-year-old Male under Chiropractic Care: A case report. Asia-Pac Chiropr J. 2022;2.6. apcj.net/papers-issue-2-6/#SteinbergResilience  

About the Case Report project

This Case Report is a part of the ASRF Case Report Project, a project designed to gather client studies from chiropractors and transform them into much-needed case reports, focused on the effects of chiropractic care on clinical presentations highly relevant to chiropractic, such as stress, immunity and adaptability.

This valuable project is made possible by the generous fundraising and contributions of ASRF supporters.

    Of note in this series is that from the top left, the initial plot shows a sparsity of readings, indicating that the brain initiated eye movements that were too slow to be recorded while the spread of the entire group represents the brain’s inability to reproduce an identical saccade to the same target with the same timing consistently. Clearly a sign of a dysfunctional nervous system.

    The top middle plot shows some green rightward looking preemptive saccades to the left of the main group, which are erroneously initiated by the superior colliculus of the brain stem. Again a dysfunctional reaction to a voluntary saccade. Throughout the treatment period there is a positive progression, however the disparity between sides represents a neurological conflict.

Force Plate Posturography

    Pre-treatment instrumented force plate posturography demonstrated impaired postural stability consistent with the persistent neuromotor control deficits documented in chronic PPCS. Force plate measures have been shown to detect ongoing functional impairment in PPCS populations (12) and to identify deficits not apparent on conventional clinical balance tests such as the Balance Error Scoring System. (11) Athletes and workers with mTBI history demonstrate significantly poorer stability than controls during balance perturbations and quiet stance, with differences accentuated in eyes-closed conditions, (11) a pattern consistent with the reliance on visual substitution for vestibular impairment observed clinically in PPCS. Pre- and post-treatment posturographic data are presented in Figure 2

Force Plate Analysis: Pre vs Post Treatment

Pre-treatment

Force Plate Posturography

    Pre-treatment force plate posturography confirmed objective postural instability consistent with persistent balance impairment in chronic PPCS. (11, 12) Post-treatment force plate posturography demonstrated objective improvement from baseline.

    This force plate analysis represents severe multi system postural control failure, characterised by critical visual dependency with near total postural collapse without vision on a firm surface. It indicates that proprioception alone on a firm surface is completely inadequate to maintain upright stability. He is entirely dependent on visual input for posture control on a firm surface. When vision is removed the postural control system fails rather than successfully switching to proprioceptive and/or vestibular references, as would normally occur. Recall that this chap, on initial presentation, had to lean against a wall in order to talk!

    The paradoxical relative preservation of performance on a soft platform compared to a firm platform without vision indicates that the patient cannot effectively use firm surface proprioceptive input as a postural reference when visual input is unavailable. This suggests disruption of the central integration of proprioceptive and vestibular signals, likely at the level of the vestibular nuclei and their cerebella connections, which are responsible for weighting and combining these inputs for postural control.

    The absence of within-trial adaption in each of the 4 testing conditions confirms that this patient has no postural adaptive reserve, every condition taxes the system to its absolute limit.

Diagnostic Assessment

Overview of Assessment Battery

    Both patients underwent comprehensive assessment structured across the objective domains: autonomic, saccadic, postural stability, cervical, neurological and physical examination with oculomotor assessment for convergence insufficiency (P2 only). The assessment battery reflects the multi-domain presentation of PPCS, encompassing vestibular, oculomotor, cognitive, autonomic, cervicogenic, and postural systems, (5, 7) and the recognised need for objective rather than purely symptom-based diagnostic approaches to this population given the absence of a consensus diagnostic standard. (21)

Saccadometry

    Saccadometry was performed in darkened conditions, consistent with published protocols. (9) The overlap (OVL) paradigm was assessed. Parameters recorded included bilateral latency (ms), amplitude (degrees), peak velocity (deg/s), and main sequence ratio (Q value) at each session. Latency distribution profiles and phase plots were generated for each paradigm to characterise trajectory variability.

    Pre-treatment saccadometry for P1 demonstrated elevated latency with bilateral asymmetry and high inter-trial trajectory variability, consistent with frontal-cerebellar circuit disruption. The latency was elevated relative to published normative data8 with wide latency scatter consistent with poor control of saccade initiation, a pattern that has been shown to correlate with corpus callosum white matter diffusivity, reduced executive function performance, and PPCS symptom burden. (9) 

    Post-treatment saccadometry demonstrated improvement from baseline. Pre-treatment saccadometry for P2 demonstrated elevated latency, reduced peak velocity, and disordered trajectory profiles consistent with the oculomotor circuit disruption characteristic of chronic PPCS.8,10 Post-treatment saccadometry demonstrated objective improvement.

Force Plate Posturography 

    Instrumented force plate posturography was used to quantify postural stability through measurement of centre-of-pressure displacement during standardised standing tasks. Force plate-based posturography has been shown to detect ongoing neuromotor control impairment in PPCS populations (12) and to identify deficits not apparent on clinical balance tests alone, with instrumented measures sensitive to postural abnormalities persisting well beyond symptomatic resolution in both acute and chronic mTBI. (11)

    Pre-treatment posturography for both P1 and P2 demonstrated impaired postural stability. Post-treatment posturography demonstrated objective improvement from baseline in both patients.

Oculomotor Assessment

    Both patients underwent assessment of Near Point Convergence (NPC). Convergence insufficiency was diagnosed on the basis of a receded NPC, consistent with the diagnostic criteria used in published PPCS convergence insufficiency studies. (18) The prevalence of symptomatic convergence insufficiency in adults with PPCS has been reported at 20.4%18 and at 23-42% in military populations, (19) placing the finding within an expected range for this diagnostic context.

Physical and Neurological Examination

    Both patients underwent physical examination including cervical range of motion assessment, segmental motion palpation, upper and lower limb neurological examination, and cranial nerve screening.

Both patients demonstrated cervical segmental restriction and dysfunction consistent with cervicogenic contribution to headache and dizziness. Neurological examination was otherwise consistent with multi-domain PPCS without focal lateralising deficit.

Diagnostic Challenges

    Several diagnostic challenges were present in both cases. There is currently no global consensus on the objective measures that establish a definitive diagnosis of PPCS in any age group, (21) and the diagnosis remains clinical rather than biomarker-confirmed. The objective assessment tools used in this series, quantitative saccadometry, and force plate posturography, are not universally available in primary or secondary care settings, creating inequity in access to this level of diagnostic evaluation for PPCS patients.

    Second, both patients presented beyond twelve months post-injury, at which point the neurological deficit profile reflects the compound effects of the initial injury, maladaptive neuroplasticity during the intervening period, physical deconditioning, and possible learned postural and behavioural compensatory strategies. Disentangling these contributions from the primary injury deficit was not possible from assessment data alone and was not required for treatment planning.

    Third, neuro-imaging was not performed at the time of assessment. Both patients had presented beyond the acute phase at which structural neuro-imaging was performed, clinical assessment did not reveal red flags warranting urgent imaging. The absence of neuro-imaging is a recognised limitation of clinical case series in this population and precludes characterisation of any structural correlates of the objective neurophysiological findings.

Diagnosis

    Both patients were diagnosed with persisting post-concussive syndrome (PPCS) on the basis of a documented history of mTBI, symptom duration exceeding three months, and the presence of three or more persistent post-concussive symptoms across multiple domains at the time of presentation. The diagnosis is consistent with the 2023 American Congress of Rehabilitation Medicine diagnostic criteria for concussion and mTBI, (21) which define mTBI as a traumatically induced physiological disruption of brain function with Glasgow Coma Score 13-15, loss of consciousness under 30 minutes where present, and post-traumatic amnesia under 24 hours.

    The multi-domain objective abnormalities documented across the assessment battery, saccadometric frontal-cerebellar disruption (both), postural instability (both), and convergence insufficiency (both), were interpreted as consistent with the distributed neurophysiological consequences of chronic mTBI affecting brainstem, cerebellar, oculomotor, and autonomic pathways, and as representing the objective substrate of the presenting symptom profile.

    Alternative diagnoses considered and excluded included: primary vestibular disorder (no unilateral peripheral pattern on examination, no BPPV features, no Menière’s disease features); functional neurological disorder (objective findings on quantitative instrumented assessment inconsistent with a purely functional aetiology); primary mood disorder driving somatic amplification (possible contributory factor not formally excluded but not the primary diagnosis given the objective neurophysiological profile); and cervicogenic syndrome as the primary diagnosis (cervicogenic pathology was identified in both patients and managed as a contributing factor, but the distributed multi-domain objective findings were not consistent with cervicogenic aetiology as the sole explanation).

Prognosis

    At the time of first assessment, the prognosis for each patient was guarded given the chronicity of their presentations, the multi-domain objective neurophysiological deficit profiles, and the documented difficulty of achieving recovery in PPCS beyond twelve months. (6, 7) The absence of a prior structured multimodal rehabilitation programme for either patient was noted as a prognostically relevant factor, as both had exhausted standard management without benefit prior to referral.

    For P1, the prognosis for functional improvement was considered reasonable given the absence of neurological red flags, the absence of a prior structured rehabilitation attempt targeting the documented objective deficit profile, and the patient’s motivation to return to his trade. The saccadometric dysmetria was a significant finding but was interpreted as reflecting a potentially reversible adaptive state rather than irreversible structural damage, on the basis of the absence of a focal deficit.

    For P2, the prognosis was also considered reasonable for functional improvement, though complicated by the orthostatic tachycardia, which required specific rehabilitation addressing the autonomic system, (19, 20) and the cervicogenic component requiring physical management. (15, 16) 

    Both patients were counselled that the rehabilitation program would be individualised, protracted, and progressively dosed, and that the primary target was functional recovery and occupational reintegration rather than normalisation of all objective neurophysiological parameters.

Therapeutic Intervention

Shared Intervention Principles

    Both patients received an individualised, assessment-driven, multimodal neurorehabilitation program. Interventions were selected and dosed on the basis of each patient’s specific objective deficit profile as identified at baseline assessment, consistent with the approach described by Ross et al (10) in which neuroplasticity and sensory entrainment created by rigorous, diagnostic- and problem-focused, structured neurorehabilitation are proposed as the mechanisms of efficacy in chronic PPCS.

    The principle of progressive loading, beginning at a level within the patient’s tolerance and advancing difficulty systematically with demonstrated capacity, was applied across all components. No adverse events were reported during either patient’s treatment course.

Patient 1: Clinic-Based interventions

    Vestibular stimulation via Orbital multi-axis rotational chair. The Orbital device delivers controlled rotation in sagittal roll, yaw, and pitch planes, providing vestibular stimulation patterns not reproducible through any natural daily activity. Multi-axis rotational therapy in the PPCS population has been associated with significant reductions in symptom severity, enhanced balance improvement, and faster recovery trajectories when added to standard neurorehabilitation protocols.

    Saccade and oculomotor training using a head-mounted weighted helmet with laser targeting computer-generated randomly selected LARP and RALP diagonal plane target panels. The weighted helmet increases the proprioceptive and motor demand of head movement, while the laser-to-target task requires active VOR engagement with immediate visual feedback on accuracy, a prerequisite for cerebellar VOR adaptation. (22, 23, 24, 25, 26)

    Sensorimotor integration as backwards treadmill walking with weighted ankles (0.5 kg per ankle) and concurrent juggling for five minutes per session. This dual-task paradigm diverts attentional resources from conscious postural control, training automatic vestibular-postural responses while the visual system is engaged in the juggling task. The backwards direction specifically challenges the vestibular system by removing the predictive visual flow available during forward locomotion.

    Lighted target panel tapping using random illuminated targets presented on a panel requiring rapid manual responses, beginning at slow presentation rates and progressively increasing in speed with demonstrated performance capacity. This trains upper limb reaction time, visuomotor processing speed, and hand-eye coordination.

    Rhythmic entrainment therapy using audiovisual feedback signal synchronised with bilateral hand clapping on cue. Entrainment-based timing training, consistent in principle with the Interactive Metronome paradigm, has been shown in a randomised controlled pilot trial to significantly improve attention, immediate memory, and delayed memory in patients with persistent cognitive complaints following TBI when added to standard rehabilitation care, with effect sizes in the medium-to-large range. (27)

    Spinal adjustments targeting identified cervical segmental dysfunction. Spinal manipulative therapy for cervicogenic headache has been supported by systematic review and meta-analysis with significant moderate-to-large short-term effects for headache frequency and intensity. (16)

Home program

    One leg teeth balance exercise: a standing single-leg balance task while teeth cleaning to engage the trigemino-cerebellar proprioceptive pathway.

Diaphragmatic breathing in a five-second rhythm for one minute, three times per day, slow respiratory rate breathing to modulate autonomic tone and reduce sympathetic hyperactivation consistent with the post-concussive autonomic dysregulation. (28) This was documented with pupillometry (29, 30) to assist with patient compliance.

    Vergence card: home vergence rehabilitation targeting the oculomotor convergence-divergence system.

    iPad App saccade and pursuit training: horizontal anti-saccade training and diagonal pursuit exercises (up-right and down-left) for three minutes twice daily.

    Breath-pause exercise: sudden full exhalation followed by maximal apnoea, progressively building toward one-minute sustained breath pause. This exercise modulates CO₂/O₂ balance and trains respiratory and autonomic regulation.

    Head-turn walking: rapid side-to-side yaw head movements while walking, within symptom tolerance, providing a low-level continuous horizontal VOR stimulus during functional activity. (31)

Administration of therapeutic intervention

    P1 completed 45 treatment sessions over 16 months. Clinic sessions were structured to deliver the full intervention battery with progressive task difficulty. The treatment table for P1 is presented in the Timeline section.

Changes in therapeutic intervention with rationale

    Treatment intensity and task difficulty were progressively advanced throughout the 16-month course as P1 demonstrated improved performance capacity. The primary adaptive change across the treatment period was systematic progression of all tasks toward greater speed, complexity, and cognitive-motor demand, in line with the principle of progressive neurological loading. No abrupt changes in treatment type or direction were required. The 16-month duration reflects the protracted nature of recovery in chronic PPCS beyond twelve months post-injury and the extended timeline required to produce cumulative neuroplastic change in the context of the documented objective deficit profile.

Patient 2: Clinic-Based interventions 

    Vestibular stimulation via Orbital multi-axis rotational chair, as described for P1, with axis selection and dosing determined by P2’s specific vestibular deficit profile on assessment. Beginning with Yaw and progressing to Yaw with Roll, P2 progressively tolerated the stimulation without adverse effects.

    Rhythmic entrainment therapy: bilateral hand clapping synchronised to a 54 Hz audiovisual beat. The 54 Hz frequency corresponds to the Interactive Metronome standard beat rate. Rhythmic entrainment therapy at this frequency trains sensorimotor synchronisation, neural timing, and frontal-cerebellar timing circuits implicated in cognitive processing speed, deficits consistently documented in PPCS. A randomised controlled pilot trial found that Interactive Metronome therapy added to standard rehabilitation care significantly improved attention, immediate memory, and delayed memory in soldiers with persistent cognitive complaints following blast-related TBI, with neuroplastic changes accounting for large proportions of the variance in neuropsychological outcomes. (27)

    Sensorimotor Integration Reaction Timer panel training with the ‘gap scenario’. The gap paradigm presents a temporal gap (400ms) between target offset and the next stimulus, reducing fixation-related suppression of the superior colliculus and producing shorter saccadic latencies. This specifically targets the saccadic latency elevation documented on saccadometry, addressing the neural timing deficit at the subcortical level.

    Head-mounted laser: tracing a wall map and navigating a maze at varying distances. This task requires sustained active head-eye coordination across spatial targets, engaging the VOR across the full range of head movement and demanding convergence and divergence across changing target distances, directly addressing P2’s convergence insufficiency in a functional movement context.

    Diagonal saccade and pursuit exercises: saccades and smooth pursuits performed diagonally across a wall target at arm’s length. Diagonal plane exercises engage the LARP and RALP canal and oculomotor planes simultaneously, combining vestibular and vergence rehabilitation demands.

    Repetitive Peripheral Somatosensory Evoked Potential (RPSEP) stimulation of the Trigeminal nerve (CN V) using a peripheral nerve stimulator applied at four locations along the Trigeminal distribution for one minute each. Trigeminal nerve stimulation produces somatosensory evoked potentials with cortical projections to the primary somatosensory cortex via brainstem relay, (32) and Trigeminal SEP provides an objective test of Trigeminal nerve function and its central connections through the brain-stem. (33) The Trigeminal nuclei in the pons are not anatomically contiguous with the vestibular nuclei but have direct functional interactions relevant to vestibular, autonomic, and oculomotor integration.

    Repetitive stimulation at peripheral Trigeminal locations was applied to drive afferent brainstem input through these interconnected circuits as a component of the broader neurorehabilitation strategy.

    Spinal adjustments targeting identified cervical segmental dysfunction, as described for P1.

Home program

    Cervical stretching exercises: addressing identified range of motion restriction and muscle tension.

    X2 VOR exercise performed slowly: active head movement while maintaining visual fixation on a moving target was performed at reduced speed consistent with P2’s tolerance, targeting gaze stabilisation through VOR adaptation.

    One leg teeth balance exercise: as described for P1.

    Isometric exercises five minutes daily to promote Myokine production while maintaining strength and joint loading without dynamic movement stress, appropriate for a patient with exercise intolerance in the early treatment phase.

    Vergence card: home vergence rehabilitation for the convergence insufficiency directly identified on assessment.

    Infinity Thumb exercise: looking firstly to the horizon then the tip of the outstretched thumb, followed by bringing the thumb to 6cm in front of the eyes and reversing, this trains convergence and divergence across the full range of binocular gaze, specifically addressing P2’s convergence deficit.

    Deep knee bends (squats) 25 repetitions three times daily: lower limb strengthening and repeated postural loading providing an orthostatic and proprioceptive training stimulus.

Administration of therapeutic intervention

    P2 completed 42 treatment sessions over 10 months. The treatment table for P2 is presented in the Timeline section.

Changes in therapeutic intervention with rationale

    As P2’s convergence insufficiency improved with directed oculomotor rehabilitation, the visual demands of the laser map and maze exercise were progressively increased to maintain challenge at the convergence and divergence system. The reaction timer panel speed was systematically advanced with demonstrated improvement in response latency and accuracy. The vestibular rotation components were adjusted across sessions in response to P2’s tolerance and symptomatic response. The vocational reorientation that occurred during the latter portion of treatment, P2 undertaking online distillery manufacturing courses, was not a treatment modification but an adaptive patient-led functional outcome that emerged from improving capacity during treatment, and was supported as a purposeful and motivationally significant recovery milestone.

    The 10-month treatment duration reflects P2’s rate of clinical progression within the constraints of his functional tolerance and the complexity of his multi-domain deficit profile.

Follow-up and outcomes

Patient 1

    Clinician-assessed outcomes were documented through serial objective re-assessment across the treatment period. Progressive improvement was noted throughout the 16 months of treatment across all assessed domains.

    Saccadometry: post-treatment data demonstrated improvement from baseline in latency, bilateral latency symmetry, and trajectory profile consistency in the overlap paradigm. Quantitative pre- and post-treatment saccadometric data are presented.

    Force plate posturography: assessment demonstrated improved postural stability from the pre-treatment baseline. Pre- and post-treatment data are presented.

    Patient-assessed outcome: at the completion of treatment, P1 reported feeling markedly recovered. This subjective assessment of recovery was consistent with the objective neurophysiological findings and directly preceded P1’s decision to seek re-employment in his trade. P1 subsequently returned to full-time employment as a qualified electrician. At the time of preparing this manuscript, P1 provided verbal confirmation that no exacerbations or recurrence of the initial signs or symptoms have occurred since resuming full-time work.

    The post-treatment assessments described above constitute the follow-up diagnostic data for P1. No further formal follow-up assessment was scheduled beyond the treatment completion assessment. Ongoing monitoring was not conducted through additional neurophysiological testing at the time of manuscript preparation, as P1 reported full functional recovery.

    P1 completed 45 sessions across a 16-month treatment period, indicating satisfactory adherence to the clinic-based program across an extended course. The sagittal roll component of the Orbital rotational chair, described as an atypical movement not reproducible in daily activity, was tolerated without vestibular exacerbation across the treatment period. Home program adherence was not formally measured by objective means; P1’s progressive improvement on all clinical and objective measures across sessions is consistent with adequate engagement with home exercise components between clinic visits. No tolerability concerns were documented during the treatment period.

    No adverse events attributable to the treatment program were reported or documented for P1. No unanticipated events affected the treatment course. The absence of symptom exacerbation beyond the typical post-session fatigue expected in neurological rehabilitation is consistent with the progressive loading approach applied across all interventions.

Patient 2

    Saccadometry: post-treatment assessment demonstrated improvement from the pre-treatment baseline across latency, peak velocity, and trajectory profile metrics in the overlap paradigms. Post-treatment data are presented in Figures 1 & 3.

    Force plate posturography: post-treatment force plate assessment demonstrated improved postural stability from the pre-treatment baseline. Post-treatment data are presented in Figure 2.

    Convergence: clinical convergence assessment at the completion of treatment demonstrated improvement in near point convergence (NPC=6cms) from the presenting deficit.

    Patient-assessed outcome: P2 reported a remarkable improvement in his ability to progress through life across the 10-month treatment period. Towards the treatment completion P2 was feeling well enough to undertake online courses and to pursue vocational reorientation. He was not entirely pain-free at treatment completion and acknowledged the potential benefit of further treatment; however, he reported sufficient functional capacity to sustain his new vocational activities independently. 

    The unanticipated functional endpoint of P2’s rehabilitation, transition from spray painting to founding, operating, and staffing a distillery manufacturing business, was not the originally intended outcome of treatment but represents a remarkable and clinically meaningful vocational reintegration in a patient who entered treatment unable to resume his prior occupation and unable to engage in any employment or retraining.

    The post-treatment assessments described above constitute the follow-up diagnostic data for P2. No further neurophysiological follow-up assessment was undertaken at the time of manuscript preparation. P2 remained engaged in his new vocational activities without scheduled clinical attendance, though he acknowledged the potential value of further treatment.

    P2 completed 42 sessions across a 10-month treatment period, indicating satisfactory adherence across a protracted outpatient course. The vestibular rotation, RPSEP stimulation, sensorimotor integration components including spinal manipulation, were tolerated across the treatment period without documented intolerance. Home program adherence was not formally measured by objective means.

    Progressive improvement of objective measures across sessions is consistent with sufficient engagement with home exercises to support the clinical gains documented. No significant tolerability concerns were documented during the treatment period.

    No adverse events attributable to the treatment program were reported or documented for P2.

Discussion

Strengths

    The primary strength of this case series is the use of serial objective neurophysiological assessment to document treatment response in parallel with the primary functional outcome of interest, occupational reintegration. The combination of quantitative saccadometry, and instrumented force plate posturography across the treatment period provides a multi-domain objective evidence base that is rarely reported alongside vocational outcomes in the PPCS literature. 

    Most published PPCS case series and retrospective studies rely on subjective symptom scales as primary outcome measures; the objective neurophysiological data presented here address a recognised gap in the evidence base. (5, 7)

    Both patients represent a chronicity of presentation, PPCS exceeding twelve months, that is associated with poor prognosis in the broader literature and that is underrepresented in rehabilitation trial populations. (6, 7) The occupational outcomes are clinically meaningful beyond the neurophysiological data: P1’s full return to a safety-critical skilled trade and P2’s novel vocational self-employment represent outcomes that carry direct economic, psychological, and social significance for the patients and their communities.

    A further strength is the explicit documentation of every intervention modality, its dosage, and its progression rationale, in compliance with CARE reporting standards, (34) which allows readers and future researchers to evaluate and potentially replicate the treatment approach.

Limitations

    The absence of a control condition is the primary methodological limitation inherent to case series design. It is not possible to determine from two cases whether the observed improvements reflect the specific treatment program, the passage of time, regression to the mean, placebo response, or some combination of these. The CARE guidelines acknowledge this limitation as intrinsic to case report methodology (34) and the cases are presented as clinical observations rather than as evidence of treatment efficacy.

    Neuro-imaging was not performed at either presentation. The absence of MRI data means that the structural correlates of the objective neurophysiological findings, including any white matter abnormalities consistent with diffuse axonal injury, or focal lesions that might explain the asymmetric components of the saccadometric data, cannot be characterised. This limits the mechanistic interpretation of the findings.

    Formal standardised symptom questionnaires, such as the Rivermead Post Concussion Symptoms Questionnaire or the Post-Concussion Symptom Scale, were not administered. The absence of validated symptom severity scoring precludes direct comparison of symptom trajectories with published normative data and with outcomes reported in other PPCS rehabilitation studies using these instruments.

    The contribution of individual treatment components to the overall outcome cannot be determined from the data available. Both patients received multimodal programs in which all interventions were delivered concurrently and progressively. The specific therapeutic mechanism responsible for the measured improvements cannot be isolated.

    Home program adherence was not objectively monitored. The assumption that home exercises contributed to outcomes rests on clinical inference rather than documented compliance.

    Finally, the asymmetry in available data across the two patients means that the full objective assessment battery is not directly comparable between cases.

Discussion of relevant literature

PPCS in working-age adults and occupational outcomes

    Persisting post-concussive symptoms affect between 24% and 43% of those who sustain a concussion (5) and constitute a significant source of occupational disability. Silverberg et al. (35) demonstrated that even among mTBI patients who achieve a formal return to work, a substantial proportion experience ongoing productivity loss, with 60% reporting affected work productivity at six to eight months post-injury, and residual symptoms, depression, anxiety, and bodily pain continuing to impair work performance. This highlights that the boundary between ‘returned to work’ and ‘fully recovered occupationally’ is not clearly defined by RTW status alone, a distinction directly illustrated by the contrasting outcomes of P1 and P2 in the present series, where P1’s full return to a skilled and physically demanding trade represents a more complete occupational recovery than the term ‘RTW’ alone would convey.

    Post-concussive symptom burden is the strongest predictor of failure to return to work at six months post-mTBI. (36) In a prospective cohort study (UPFRONT, n="1,151)," rates of complete return to work increased from 34% at two weeks to 77% at twelve months, but occupational factors influenced short-term RTW while symptom burden and psychological distress were the dominant predictors of long-term RTW.37 Both P1 and P2 in the present series presented with symptom burdens exceeding twelve months and failed to achieve RTW through prior standard management, placing them in the high-risk category described in the literature. Their subsequent successful occupational reintegration following individualised multimodal neurorehabilitation is therefore a clinically noteworthy departure from the expected trajectory.

    The vocational reorientation of P2, from spray painter to distillery proprietor, raises a question not directly addressed in the existing RTW literature: whether novel vocational self-employment constitutes a categorically different form of recovery from returning to a prior occupation, and whether conventional RTW metrics capture its significance adequately. Brandt et al. (14) reported that most employees with PPCS returned to work but only a minority worked under similar conditions to pre-injury, with employees and managers alike struggling to assess workload accurately. P2’s case suggests that for some patients with PPCS, vocational reorientation toward a different occupation better matched to the post-injury functional state may represent a more sustainable and ultimately more successful outcome than forced return to an occupation whose physical and visual demands may no longer be compatible with the residual deficit profile.

Multimodal neurorehabilitation in chronic PPCS

    The evidence base for multimodal neurorehabilitation in chronic PPCS beyond twelve months post-injury is limited but encouraging. Ross et al. (7) reported significant pre-post improvements in both subjective symptom scales and objective measures of trail making, processing speed, reaction time, and visual acuity in a retrospective chart review of patients with PPCS at a mean of approximately two years post-injury, using an intensive five-day multimodal outpatient program. The authors concluded that late-stage PPCS patients may have substantive benefits from a patient-centred, diagnostic- and problem-focused neurorehabilitation approach, and specifically hypothesised that neuroplasticity and sensory entrainment created by rigorous structured neurorehabilitation are efficacious even when patients have clinically plateaued. (7) The present two cases are consistent with this hypothesis, with both patients demonstrating objective neurophysiological improvement and meaningful functional reintegration despite presentations exceeding twelve months post-injury.

    The multi-domain objective deficit profiles of both patients, spanning autonomic dysregulation, oculomotor and saccadic circuit impairment, postural instability, and cervicogenic pathology, are consistent with the distributed neurophysiological disruption that characterises PPCS7 and explain why unimodal approaches had not produced functional recovery in either patient prior to referral.

The pathway of care described by Corwin et al. (13) emphasises that visual and vestibular rehabilitation in mTBI should be driven by individual assessment findings and delivered through coordinated multi-modal programs rather than through single-modality protocols, a principle reflected throughout both treatment courses described here.

Saccadometry as a biomarker

    Saccadometric findings in both patients were consistent with published characterisations of mTBI-related oculomotor impairment. Heitger et al. (8) demonstrated that latency distribution measurement discriminates between concussed patients and healthy controls, and that saccadometric abnormalities persist well beyond symptomatic resolution in a proportion of PPCS patients. The present cases extend this observation by documenting saccadometric improvement following targeted multimodal rehabilitation, a finding with implications for the use of saccadometry not only as a diagnostic biomarker but also as a treatment response measure. Corwin et al. (9) demonstrated correlations between saccade performance and corpus callosum white matter diffusivity, Stroop performance, and symptom burden, providing a neuroanatomical substrate for the oculomotor deficits measured at baseline in both patients.

    The persistence of some saccadometric abnormality at treatment completion in both patients, most notably trajectory scatter, is consistent with the known difficulty of fully normalising frontal-cerebellar circuit timing in established PPCS,7 and is interpreted as reflecting the structural rather than purely functional nature of the underlying circuit impairment.

Oculomotor rehabilitation

    P1 and P2’s presenting convergence insufficiency is consistent with the 20.4% prevalence of CI reported by Nordfalk et al. (18) in adults with PPCS and the 23–42% rates reported in military mTBI populations. (19) The CONCUSS clinical trial demonstrated measurable neuroplastic changes in the frontal eye fields, supplemental eye fields, parietal eye fields, cerebellar vermis, and visual cortex following office-based vergence and accommodative rehabilitation for concussion-related CI, (20) consistent with the plasticity of the vergence oculomotor system in the PPCS population and supporting the rationale for targeted vergence rehabilitation as incorporated in the treatment program.

Rhythmic entrainment and timing-based rehabilitation

    The entrainment therapy component of both treatment programs, synchronised audiovisual hand clapping with the 54 Hz, is consistent in principle with the Interactive Metronome paradigm, which operates at the same 54-beat-per-minute frequency. Nelson et al. (27) reported in a randomised controlled pilot trial that Interactive Metronome therapy added to standard rehabilitation care for soldiers with persisting cognitive complaints following blast-related TBI produced significant improvements in attention, immediate memory, and delayed memory, with effect sizes in the medium-to-large range and indicators of neuroplastic change accounting for large proportions of the variance in neuropsychological outcomes. The cognitive gains observed in both P1 and P2 across the treatment period, including the cognitive capacity that enabled P2 to undertake online vocational retraining, are consistent with the cognitive rehabilitation mechanism proposed by Nelson et al. (27)

Vestibular rehabilitation and rotational therapy

    Vestibular stimulation through the Orbital multi-axis rotational chair provided the primary peripheral vestibular rehabilitation component of both programs. The sagittal roll plane, described as an atypical movement not reproducible in activities of daily living, is consistent with the novel vestibular stimulation paradigms discussed by Sadeghi et al, (18) in the context of unidirectional rotational rebalancing of vestibular asymmetry. Multi-axis rotational therapy has been incorporated as a component of intensive multimodal PPCS programs in the published literature, (7) and audio biofeedback augmentation of vestibular rehabilitation therapy has been shown to produce larger improvements than standard vestibular rehabilitation alone in patients with chronic mTBI and persistent imbalance, with significant effects on both subjective symptom severity and objective sensory organisation testing composite scores. (39) It is the author’s opinion that full body multi axis targeted vestibular stimulation is a driver of enhanced homeostasis. (40, 41, 42, 43)

Cervicogenic management

    Cervicogenic pathology was identified and managed in both patients through spinal adjustments targeting documented segmental dysfunction. Nusholtz et al. (15) reported substantive improvement in post-concussive dizziness, headache, and related symptoms following chiropractic management of craniocervical junction dysfunction in patients with PPCS of at least six weeks duration. Bini et al. (16) confirmed in a systematic review and meta-analysis that spinal manipulative therapy produces significant short-term reductions in cervicogenic headache frequency and intensity. The cervicogenic components of both patients’ presentations, headache and restricted range of motion, are likely to have contributed to their overall symptom burden and are appropriately included as targets within the multimodal framework.

Scientific rationale for conclusions

    The neurophysiological improvements documented across both cases, and the functional and occupational outcomes that followed, are most parsimoniously explained by neuroplastic reorganisation of the sensory-cognitive-motor networks disrupted by the original mTBI, facilitated by the individualised multimodal rehabilitation program. Ross et al. (7) specifically hypothesised that neuroplasticity and sensory entrainment created by rigorous, diagnostic- and problem-focused structured neurorehabilitation are the mechanisms of efficacy in chronic PPCS, a hypothesis consistent with the findings of the present two cases.

    The saccadometric improvements in both patients are consistent with progressive rehabilitation of the frontal-cerebellar circuits mediating response inhibition and spatial remapping. (8, 9) The persistence of some trajectory scatter at treatment completion in both patients is expected given the structural rather than purely functional nature of mTBI-related white matter disruption, and is consistent with the known ceiling of neuroplastic recovery in established PPCS.

    The convergence deficit improvement is consistent with the neuroplastic changes in the vergence oculomotor network documented by Alvarez et al.²0 following targeted vergence rehabilitation, supporting a rehabilitation-driven rather than spontaneous mechanism for this component of recovery.

The occupational outcomes of both patients, full return to skilled trade employment for P1 and new vocational self-employment for P2, most likely reflect the aggregate functional recovery across all treated domains rather than improvement in any single domain, consistent with the distributed multidomain nature of the initial neurophysiological deficit profiles. The prior failure of both patients to achieve RTW through standard management argues against spontaneous recovery as the primary explanation for the occupational outcomes.

Conclusions

Primary take-away lessons

    These two cases demonstrate that working-age adults with persisting post-concussive symptoms ex- tending beyond twelve months, a population for whom standard management has proven insufficient and whose prognosis for recovery is generally considered poor, can achieve clinically meaningful neurophysiological improvement and meaningful occupational reintegration following individualised, assessment-driven, multimodal neurorehabilitation.

    The serial objective neurophysiological data from quantitative pupillometry, saccadometry, and force plate posturography provide documented evidence of measurable change across the treatment period, and the occupational outcomes demonstrate that rehabilitation impact extends to the domains of greatest practical significance for working-age patients.

    The contrast between P2’s prior inability to work and his subsequent ability to establish and staff a new commercial enterprise illustrates that in some cases of chronic PPCS the most meaningful vocational outcome is not a return to the prior occupation but an adaptive reorientation that better fits the post-recovery functional state, a nuance not well captured by standard return-to-work metrics.

    The cases collectively support the clinical case for a comprehensive, objective assessment-guided, multimodal approach in chronic PPCS, and underscore the importance of treating occupational reintegration, in whatever form it takes, as a primary outcome measure rather than a secondary observation.

Note:

Written informed consent from both patients for the publication of these case reports and the accompanying images is held by the author.

Also by this author

• Richardson D. Two case reports, M46 & M58yo, of long-term stroke recovery using a sensory motor reintegration approach. Asia-Pac Chiropr J. 2026;6.3. www.apcj.net/papers-issue-6-3/#RichardsonStrokeRecovery
• Richardson, D. A functional neurological disorder case series utilising a sensory motor integration model including Chiropractic and vestibular stimulation, Asia-Paci Chiropr J. 2025;5(3). Available at: https://www.apcj.net/papers-issue-5-3/#RichardsonFNeurox4 

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The purpose of this study is to highlight the correlation between spinal subluxations and dizziness of benign origin. There are several possible causes of dizziness and underlying pathology should always be ruled out first. That said, the potential neurological disturbance from a subluxated vertebrae as a primary cause should not be overlooked.

This case study reveals the benefits that a patient may experience when a subluxation is identified and corrected in a specific manner.

Indexing terms:  Dizziness; Chiropractic; Subluxation; Nervous system; Vestibular system; Gonstead.

Introduction

    Dizziness is a complex and potentially debilitating symptom affecting up to 30% of the global population. Annually it accounts for over three million emergency department visits. (1) It can manifest across all age groups, though it is notably more prevalent among adults aged 65 and above due to an increased likelihood of underlying health conditions. The condition is two to three times more common in females. (2) The word dizziness itself is a vague and

broad description of a condition, which is perceived and experienced very differently between individuals.

    Dizziness is commonly characterised by feelings of unsteadiness, spinning, disorientation, or perceived movement. (3) Characteristics, intensity, duration and frequency also vary greatly among patients and may guide a practitioner to a likely cause and diagnosis. There are numerous aetiologies that can result in dizziness including vestibular, neurological, cardiovascular, and musculoskeletal disorders. Among these, the role of musculoskeletal issues, particularly those involving the cervical spine, is of particular interest to chiropractic care.

    Common causes are problems or conditions that affects the ears such as Meniere´s disease and labyrinthitis, eye conditions, heart issues, stress, dehydration, low blood sugar levels, chemical or hormonal imbalances, infections or neurological disorders. (4)

    Treating a patient with dizziness normally involves identifying and addressing its underlying cause, which can be varied and sometimes multifactorial. Given the complexity of the causes, treatments can range greatly. They include: repositioning procedures such as lifestyle changes, the Epley Maneuver, physical therapy, medication and surgery. (5)

    Signs and symptoms such as confusion, difficulty speaking or understanding language, sudden severe headache or vomiting without known cause, weakness in extremities are potential red flags that should be referred out for immediate medical examination first. (6) Such possible pathological conditions are beyond the scope of this paper.

    The Gonstead chiropractic system, named after its originator Clarence S Gonstead, is a specific, detailed, and practical approach to chiropractic care that meticulously addresses biomechanical dysfunction of the spine and extremities. Examination procedures in the Gonstead method are comprehensive and the objective is to identify potential vertebral subluxations. These are biomechanical dysfunctions due to positional dyskinesia of a functional spinal unit (FSU) predominately in the spine, sacroiliac joints or temporomandibular joint (TMJ), that can create directly or indirectly neurological disturbances. (7) This can have a tremendous effect on neurological function not only at that spinal segment, but also on the entire body as altered afferent input to the central nervous system leads to abnormal somatosensory processing and therefore altered sensorimotor integration and output. (8)

    The Gonstead chiropractic adjustment aims to correct these subluxations with specificity and accuracy to restore optimal spinal function and remove any associated nerve interference. The protocol may also incorporate guidance on lifestyle modifications to support overall well-being and prevent recurrence.

    This case study examines a patient's journey through dizziness, managed via the Gonstead Chiropractic system. It aims to investigate the effectiveness of this method in addressing dizziness, of a benign aetiology believed to be due to spinal subluxations. By doing so, this study seeks to expand the relatively limited body of research on the role of specific Chiropractic techniques, like the Gonstead method, in managing common yet often mismanaged symptoms such as dizziness.

Case history

    An 81-year-old female presented with continuous dizziness and neck stiffness. The dizziness was described as a constant feeling of perceived movement and mild spinning. She reported feeling unsteady at times, but there were no tendencies of falling or fainting. Getting up or moving aggravated the symptoms. Lying down reduced the symptoms. The symptoms started suddenly two weeks prior after painting her ceiling. She had no headache, but a sensation of pressure in her head was present intermittently. No obvious spinal pain or referred neurological symptoms in extremities were present. Examination by a medical doctor and MRI of the head and cervical spine the previous week revealed no abnormalities and she was instructed to rest and give it time to pass. As this did not change her symptoms, she decided to seek a chiropractic evaluation for an opinion and alternative treatment for her ailments.

    Previously, nine months earlier, she had attended our clinic for pain in the lumbosacral area that resolved after adjustments at sacrum (S2), left sacroiliac joint (SIJ) and L2 over the course of three weeks. She did not drink coffee or consume any forms of drugs. No history of trauma, infection or use of medication was reported. She had finished treatment for anal cancer 5 year prior with no signs of recurrence. Otherwise, her medical history was unremarkable.

Clinical findings

    Observation of the patient showed an elderly lady in general good health and appearance. She did show signs of head pressure discomfort and was trying not to move to avoid aggravating the symptoms of dizziness.

    Cranial nerve screen testing was normal. Romberg’s test showed general instability withmtendency to sway forward to the left.

    Chiropractic examination revealed:

Radiographic examination

    Full spine, weight bearing radiographic images using Gonstead acquisition protocols were taken of the patient. Please refer to x-ray images at the end of this paper. The listings derived from the full spine radiographs were:

Chiropractic diagnosis

    Following full Gonstead Chiropractic history, examination and spinographic findings, the initial diagnoses made for the above cases were:

Treatment outcome

    On the first visit, both T9 and C7 were adjusted. T9 with the patient prone on the hi-lo table taking a pisiform contact on the right transverse/lamina junction. C7 taking a index finger contact on the right spinous/lamina junction with the patient seated in cervical chair. Only minor movements and cavitations were noted during these adjustments. The patient returned a week later, where she reported an increase of dizziness and neck stiffness the day after the

first adjustments, before rapid improvement in symptoms over the following days. Only minor dizziness during sudden movements was now present.

    Gonstead examination indicated a subluxation at T9 was still present and therefore this segment was adjusted again.

    The last visit was one week later where she reported feeling normal with no further signs of dizziness. T9 was adjusted with minimal force and depth on this visit, and she was instructed to contact the clinic if the symptoms returned. The primary symptoms a year later have not returned. She did report over a recent phone conversation in relation to this paper that she intermittently gets mild signs of dizziness over a short duration. She attributes this to her use of glasses, and being age appropriate. These tendencies are so mild she has not felt the need to at this point get examined by a Chiropractor or her medical doctor.

Discussion

    Understanding these four categories of dizziness provides a framework to evaluate, diagnose, and manage patients presenting with this common, yet multifaceted symptom. It also aids in determining the potential cause of the dizziness, which will ultimately guide the choice of treatment strategy. (10)

    Neurologically, the vertebral subluxation complex theory suggests that spinal misalignment or structural dyskinesia of a functional spinal unit (FSU) can lead to direct or indirect aberrant neurological function. When this occurs, various symptoms may develop, including dizziness. a biomechanical injury and inflammatory responses to the FSU, as seen in subluxations, given proximity to nerve roots, dorsal root ganglion (DRG), spinal cord and associated neurons, is

very likely to affect these delicate tissues. These are all located inside the dural sheath and are extremely sensitive to pressure from biomechanical dysfunction, chemical irritants or ischemic impacts. (11) This is especially true in the intervertebral foramen (IVF) where dorsal and ventral roots, DRG, spinal arteries and veins, the dural sheath and CSF pass through. In addition, associated disc protrusions, disc herniations and degeneration combined with arthritic changes to the facet joints can lead to further narrowing of the IVF and probable nerve root compression. (12)

    The central nervous system (CNS), including the brain and spinal cord, is the primary system for coordinating all body activities. As such, any subluxations may disrupt or distort the messages traveling along these neural pathways, potentially leading to a range of symptoms.

    In this case study, even subluxations outside the cervical area could have created neurological disturbances affecting the vestibular nuclei located in the brainstem or its connections, leading to sensations of unsteadiness.

    Biomechanically, the spine functions as a coherent unit with interdependence between its various components. For example, a lumbar or thoracic subluxation may cause compensatorychanges higher up in the spine. (13) This can affect balance and proprioception and its associated complex responses in the brain, potentially leading to sensations of dizziness.

    Spinal subluxations can contribute to the sensation of dizziness through multiple intricate neurophysiological pathways.

    One crucial concept is that the vertebral column houses the spinal cord, a significant component of the central nervous system (CNS). This communication highway facilitates the transfer of sensory and motor information between the brain and the rest of the body. Any interference in this communication, such as that potentially caused by spinal subluxations, can lead to a range of symptoms, including dizziness. (14)

    Direct or indirect mechanical pressure or chemical irritation on the spinal nerves or the spinal cord due to subluxations can cause neurological disturbances. This interference can disrupt the normal transmission of nerve impulses to the vestibular renters in the brain responsible for maintaining balance and spatial orientation. (15) Altered or distorted information received by these centres can result in a sensation of dizziness.

    Proprioception, the body's sense of position and movement in space, is also a crucial player. Particularly in the cervical spine, proprioceptive information significantly contributes to our sense of balance. Spinal subluxations can disrupt accurate proprioceptive input to the brain, creating a sensory mismatch with other systems maintaining balance, like the vestibular system and vision, leading to dizziness. (16)

    Vertebrobasilar insufficiency, a condition characterised by reduced blood flow through the vertebral arteries due to mechanical compression, often associated with cervical subluxations or as compensations for subluxations in other spinal regions, can also cause dizziness. The vertebral arteries supply the posterior brain, including the cerebellum and brainstem, crucial areas for maintaining balance. (17)

    Likely most relevant for this case study and many cases of dizziness caused by spinal subluxations is the Vestibular system.

    Our sense of balance and spatial orientation is controlled by an intricate sensory system known as the vestibular system, which resides in a part of the inner ear called the vestibular labyrinth. The vestibular system is composed of the following elements (18):

    The information from these vestibular organs is conveyed to the brainstem nuclei via the vestibular nerve. This information is then dispatched to other components of the central nervous system, including the cerebellum and cerebral cortex, where it is utilised to coordinate movement. The proper functioning of the system requires both vestibular organs, located on either side of the head, to transmit balanced signals to the brain. For the human body to maintain balance the vestibular system functions by sensing the orientation of our bodies relative to gravity. In addition, it also provides sensory input regarding equilibrium and body movement. The cerebellum can utilise this information together with sensory input from eyes as well as proprioceptive input from the musculoskeletal to coordinate balance. If thecerebellum detects insufficient balance it will communicate with appropriate muscle groups to restore balance. (19)

    The patient in this case study underwent a detailed evaluation under the Gonstead chiropractic system, which identified specific subluxations. After receiving precise Gonstead chiropractic adjustments aimed at correcting these subluxations, the patient reported a significant reduction and eventually full remission of her dizziness.

    This highlights the importance of holistic care in Chiropractic practice and suggests that subluxations in areas even outside the cervical spine can also contribute to symptoms of dizziness. Such findings expand our understanding of the interplay between spinal integrity and patient health, emphasising the potential of Gonstead chiropractic in managing dizziness. In summary, spinal subluxations can induce dizziness through direct and indirect neurological pathways and by altering cerebral blood flow. This intricate neurophysiology underscores the potential role of Chiropractic interventions in managing dizziness.

Conclusion

    This case study focuses on a patient who presented with dizziness of benign origin and responded favourably to the Gonstead Chiropractic analysis and adjustments. This is despite the absence of any upper cervical subluxation or dysfunction, which is the area of the spine one might first suspect a subluxation to be present for this condition.

    The positive outcome observed highlights the potential influence of spinal subluxations and the associated neural interferences triggering this symptom, underscoring the intricate neurological and biomechanical interconnections within the human body.

    Gonstead and many other Gonstead practitioners with him have noted the common correlation between upper cervical subluxations and dizziness. Some cases have also demonstrated involvement of the TMJ. (20) They have also reported that subluxations below the cervical spine, even to the level of the pelvic region, could result in such symptoms.

    Hence going back to the philosophy of the founding father of Chiropractic DD Palmer: he made it clear to accept the subluxation where you find it! Gonstead was also very clear to point this out, and also how important it was to leave it alone once the signs of subluxations were reduced or absent.

    When underlying pathology is ruled out, Chiropractic examination for potential nerve interference arising from a spinal subluxation should be considered in cases of dizziness. When we study the anatomy, biomechanics and neurology of the spine, it makes logical sense that nerve interference from a subluxation has the capacity to create signs and symptoms of dizziness.

Note: Image references are given in the original publication.

Abstract There may be a connection between the Qi (life force energy) and the Injury Recall Technique (IRT) developed by Dr Walter Schmitt, Jr, DC, DIBAK, DACBN. This same connection may apply to muscles that fail the autogenic inhibition (spindle cell approximation) test. It may also be relevant in cases where a Beginning or End (B&E) point of the acupuncture channels that originate or terminate on the face is used more than once during a patient visit.

Objective Develop a process based on Manual Muscle Testing (MMT) that includes this energy factor when clearing the confusion from the Central Nervous System (CNS) which may cause erroneous findings with MMT.

Method The new methodology utilises the IRT manoeuvre in combination with Therapy Localisation (TL) to the appropriate acupuncture Alarm (MU) point to address the energetic component in the procedures mentioned above. It has been used during the last one- and one-half years in an Applied Kinesiology (AK) practice to clear interference patterns from the CNS prior to treating patients’ clinical complaints.

Result Most of the patients tested demonstrated a need to have this energetic element cleared when eliminating reflexes arising from traumas and other stress-related events.

Conclusion An energetic imbalance appears to be a result of the many stresses that lead to confusion in the CNS. Use of the IRT manoeuvre in combination with the patient’s TL to the Mu Point of the appropriate acupuncture channel can eliminate this component.

Indexing terms  IRT; Alarm/Mu point; LQM; Set Point; Switching; Autogenic Inhibition.

Introduction

    Dr Wally Schmitt adapted the Injury Recall Technique (IRT) from the work of Dr Gordon Bronston, a podiatrist in Michigan. Bronston had learned his technique from its developer, Robert Croty, DPM and had used it while treating Schmitt for an ankle injury.

    IRT uses a light ankle toggle or micro flexion of the occiput on the atlas, if trauma occurs above the shoulders, to eliminate the flexor-withdrawal type of neurological reflex associated with trauma.

    Other challenges can be used to uncover hidden trauma reflexes. These include having the patient direct their eyes toward the site of the injury, turning the head and lateral spinal flexion.

    Schmitt named this more in-depth assessment Beyond IRT. (Schmitt Seminar Beyond IRT, Wilmington, NC, 1996)

    The brain can also store the memories associated with trauma. Dr. Schmitt treated these with the Location, Quality and Memory (LQM) technique. In LQM the traumatic reflex is neutralised by stimulating the appropriate B&E point when the patient recalls an aspect of the traumatic event muscle to weaken.

    B&E points are utilized for other clearing procedures as well. These include the B&E technique (Walther, Applied Kinesiology Synopsis, 2d. ED., 2000, pp. 277-278), the Nociceptive Stimulation Blocking (NSB) technique (Quintessential Applications,

    The Neurological Rationale for a Comprehensive Clinical Protocol Using Applied Kinesiology Techniques 2005 AKSP), the Cover One Eye Cerebellar Challenge (Synchronising the CNS, QA Home Study webinar, July 2020) the REM Challenge (QA Webinars – To Sleep or not to Sleep – part 1, July 2019), the

Emotional Recall technique and the Set Point technique that Schmitt developed with Michael Lebowitz, DC (1989 Selected Papers of the ICAK, pp. 25-32).

Materials and Methods

    All evaluative testing was done with MMT. The procedure involved tapping the relevant B&E point while the patient therapy localised the appropriate MU point.

Discussion

    About three years ago I observed that if a B&E point might be used more than once during a patient visit. I found that an indicator muscle would be inhibited when the patient therapy localised the Mu point for either the channel whose B&E point was used more than once or for its paired yin channel and a IRT challenge was done . Applying the IRT corrective manoeuvre while the patient maintained the TL would negate the positive challenge. I routinely perform this

procedure now as part of my IRT clearing procedure. 

    This energetic connection may also exist in the case of a hypertonic muscle. Schmitt taught that IRT could help reset muscles that are over facilitated. Such a muscle would be hypertonic to MMT and would not be inhibited by spindle cell compression. According to Schmitt’s procedure stimulating the muscle’s origin and insertion (O&I) and then performing IRT would reset the muscle to its normal resting state. Several of the patients I treated in this fashion returned with the same hypertonicity on a follow up visit. 

    I found that TL to the MU point of the acupuncture channel that ran through the muscle would recreate the muscle’s hypertonicity even after the O&I/IRT correction. I hypothesised that there might be an energetic component to the muscle’s hypertonicity that was not addressed by the O&I/IRT correction alone.

    The procedure I developed as a result of my hypothesis is to first determine if spindle cell compression inhibits a muscle. If this test fails, treat the muscle as Dr. Schmitt taught. Next have the patient therapy localise the MU point for the acupuncture channel running through themuscle and re-test the muscle. For muscles that accommodate more than one acupuncture channel several MU points may have to be tested. If the muscle fails to respond to spindle cell

compression, the patient continues to TL the MU point while the IRT manoeuvre is again performed.

    Recheck with both TL to the origin/insertion and to the MU point with the IRT challenge to determine that the muscle has been reset to normal. The procedure can be performed in the reverse order of that just described. When I have cleared the muscle using the MU point first the number of times I then have to retreat using O&I is less than vice versa.

Results

    TL to the MU point of the indicated acupuncture channel together with the IRT manoeuvre in addition to the O&I/IRT method described by Schmitt seems to restore a hypertonic muscle to a normal response pattern and prevents recidivism. In addition, an IRT challenge to the MU point of any B&E acupuncture channel used more than once during a patient visit that inhibits an indicator muscle seems to indicate a hidden IRT pattern that should be corrected.

Conclusion

    When the CNS cannot compensate for the accumulation of stresses to which it is subjected it creates confusion in the system. It may also affect the body’s QI. This effect can manifest through hypertonic muscles and through other procedures that involve the use of B&E points. It can be detected with MMT when TL to the MU point for the acupuncture channel involved combined with an IRT challenge causes the inhibition of an indicator muscle . The imbalance can be corrected by using the IRT manoeuvre while maintaining the TL to the MU point.

    More research is needed to confirm these findings.

References

5. Schmitt, Walter H. and Lebowitz, Michael: Hypothalamic Set Point Technique, Selected Papers of the ICAK, 1989 pp. 25-32

Originally published as:

Cite: Guzman IMR, Halverson J. Focal nodular hyperplasia of the liver incidentally identified in a chiropractic patient with rib pain, a case report. In: 

Objective

    To describe an adult male with focal nodular hyperplasia (FNH) of the liver mimicking right lower rib pain.

Clinical Features

    A 42-year-old male presented with right lower rib pain extending from the midsternal to the midaxillary line. The pain was sharp, aching, and radiating. He had a history of liver laceration after blunt abdominal trauma 34 years prior.

Interventions/outcomes

    Murphy’s sign was positive, and there was reduced and painful right lateral thoracic bending. Palpation of the anterior right lower ribs elicited epigastric pain. An Activator instrument-assisted adjustment was performed on rib 8, which did not relieve the pain.

    The working diagnosis was intercostal neuralgia. The patient was referred for a sonographic examination of the gall bladder to discard acute cholecystitis. The sonogram revealed an incidental large hypervascular liver mass. Multiphase contrast abdominal computed tomography was performed to further characterise the lesion, demonstrating a mildly hyperattenuating, and moderately enhancing 8.8 cm mass in the left lobe of the liver, with hypoattenuating central scar, consistent with FNH.

Conclusion

    Remote trauma may predispose patients to developing painful visceral lesions that mimic musculoskeletal pain. Diagnostic imaging plays a crucial role in securing the diagnosis and directing appropriate management.