Functional Neurology


Functional Neurological Examination of the Pupils
Functional Neurology
Written by Randy Beck, B.Sc., D.C., Ph.D.   
Tuesday, 05 June 2007 10:33

Welcome back to the continuing series investigating the functional neurological approach to patient management. We are continuing from last month’s article, where a variety of definitions and explanations concerning examination techniques were outlined. We will start our examination process of the neuraxis with the pupils.

Examination of the pupils

Pupil size reflects a balance in tone between the sympathetic and parasympathetic nervous systems. You can get a reasonable measure of the actual sympathetic tone in the patient by measuring the resting pupil size in darkness. The sympathetic tone is represented by the degree of dilation of the pupil and demonstrates the degree of resting constriction in vascular smooth muscle in most parts of the body. Vestibular, cerebellar and cortical influences on both sympathetic and parasympathetic tone should also be considered.

Various components of the pupil light reflex are subserved by each component of the autonomic nervous system. The time to activation (TTA), amplitude of constriction, smoothness and maintenance of constriction, time to fatigue (TTF) and time to redilation of the pupil response need to be measured and recorded in each pupil. These are all aspects of the pupil light reflex that have been researched and correlated with the central integrative state of the various contributing components of the nervous system.

Pupil constriction pathways

Accommodation is the constriction of the pupil that occurs during convergence of the eyes for close focusing.

The Edinger-Westphal nucleus is activated by the adjacent oculomotor nucleus, which activates the medial rectus muscle more powerfully than the light reflex. There is also contraction of the ciliary muscle to aid close focusing, which is referred to as the near response.

Parasympathetic fibres lie superficially on the oculomotor nerve and they relay in the ciliary ganglion of the orbit, which lies on the branch to the inferior oblique muscle. They begin in dorsal position and rotate to a medial and then inferior position as they enter the orbit. Blood supply to the pupil fibres is different to the main trunk of the nerve. The pupil fibres receive their blood supply from the overlying pia mater, therefore the pupil fibres are usually spared in an oculomotor nerve trunk infarction.

An afferent pathway lesion results in a Marcus-Gunn pupil. The swinging light test will reveal that the affected pupil will not react to light as well as the other pupil, but it may constrict normally in response to stimulation of the opposite pupil during testing of the consensual light reflex. This occurs in multiple sclerosis, and diabetes conditions that affect the optic nerve due to demyelination or vascular lesions. You might also expect this to occur when there is an increase in sympathetic tone to the pupil on the side of relative afferent defect. This could distinguish a high firing intermediolateral (IML) cell column from transneural degeneration (TND) in the mesencephalon.

The Wernicke pupil reaction refers to differential summation, depending on whether you are shining the light into the nasal or temporal aspects of the retina (i.e., intact or ablated fields). This may be observed in an optic tract lesion. Supposedly, the resting size of the pupil is uninterrupted, due to the consensual light reflex.

The nasal half of the retina is significantly more sensitive to light than the temporal half of the retina, and the direct responses are significantly larger than the consensual response. With temporal retina stimulation, the direct and consensual reflexes are nearly the same. Direct and consensual pupil reactions, when stimulating the temporal retina, are nearly equal. This may suggest an input of temporal retina to both sides of the pretectum. Such a crossing of temporal fibres may take place in the chiasm.

The net effect of the pupillary light reaction, which involves shining light into the monocular zone from the temporal hemi-field of one eye, leads to greater constriction of the pupil on that side.

Parinaud Syndrome results when damage to decussating fibres of the light reflex at the level of the superior colliculus is present. This results in semi-dilated pupils fixed to light, plus loss of upward gaze.

The Argyll Robertson pupil is most commonly seen in neurosyphilis. Common signs are bilateral ptosis, an increased frontalis tone, as well as a pupil that is irregular, small, and fixed to light, but constricts with accommodation. This type of pupil can not be dilated by atropine.

Differential diagnosis of this particular pupillary dysfunction includes senile miosis, pilocarpine or β-blocker drops for glaucoma. This pattern of findings is reversed in encephalitis lethargica.

Holmes-Adie pupil or tonic pupil occurs due to degeneration of the nerve fibres in the ciliary ganglion and is thought to be produced by a combination of slow inhibition of the sympathetic and partial reinnervation by parasympathetic fibres.

This condition can also be associated with loss of patella reflex, decreased sweating, blurred vision for near work and eye pain in bright light.

Horner’s Syndrome.

Disruption of the sympathetic chain at any point from the hypothalamic or supraspinal projections to the oculomotor nerve can result in a spectrum of symptoms referred to as Horner’s syndrome. The classic findings in this syndrome include ptosis, miosis and anhidrosis, but a number of other abnormalities may also be present. Ptosis or drooping of the upper eyelid is caused by the interruption of the sympathetic nerve supply to the muscles of the upper eyelid. Miosis or decreased pupil size is a result of the decreased action of the dilator muscles of the iris due to decreased sympathetic input. This results in the constrictor muscles acting in a relatively unopposed fashion, resulting in pupil constriction. A Horner’s pupil will still constrict when light is shined on the pupil, although careful observation is sometimes required to detect the reduced amount of constriction that occurs. Innervation to superior and inferior tarsus muscles is carried in CN III. Vasomotor fibres are carried in the nasociliary branch of CN V and make no synapses in the ciliary ganglion after branching off from the carotid tree.

Pupillodilator fibres are carried in the long ciliary branches of the nasociliary nerve. This syndrome is characterised by the following signs and symptoms:

• Ptosis / apparent enophthalmos

• Small pupil

• Anhydrosis (forehead or forequarter of body)

• Blood shot eye (loss of vasoconstrictor activity)

• Heterochromia

Horner’s syndrome can occur due to lesions at various peripheral and central sites. Some of these sites may be in the spinal cord, hemispheric lesions of the brain, in the brain stem, nerve root lesions, the carotid artery, the jugular foramen, the orbit or the cavernous sinus.

Depending on the location of the lesion, other cranial nerves may be involved, such as III, IV, VI and VI when it is near the cavernous sinus or superior orbital fissure, and IX, X and XII when the lesion is at the base of the skull.

In the spinal cord, the mixed signs associated with syringomyelia may be present because of the widening of the central canal. This widening of the central canal would cause a loss of segmental reflexes.

When T1 nerve root involvement exists, Horner’s Syndrome may be present with weakness of finger abduction and adduction, wasting of the intrinsic hand muscles, loss of pain sensation in the medial aspect of the arm and armpit and deep pain in the armpit. This is rarely due to spinal degeneration and serious causes such as Pancoast’s tumor should be considered. Referral for MRI, chest X-rays and / or CT scan should then be considered.

Different lesion levels affect sweating differently. Central lesions may affect sweating over the entire forequarter, due to involvement of the descending pathways from the hypothalamus. Lower neck lesions may affect sweating over the face only, due to involvement of sympathetic efferents in the arterial plexus (carotid / vertebral).

Lesions above the superior cervical ganglion may not affect sweating at all, or it may be restricted to the forehead.


Randy Beck, B.Sc., D.C., Ph.D., is a graduate of Canadian Memorial Chiropractic College. He has completed postgraduate studies in Psychology, Immunology and Neurology. He is presently involved in a number of international research projects and is co-authoring a textbook on Functional Neurology. He was formerly the Dean of Chiropractic and Basic Sciences and Director of Research at the New Zealand College of Chiropractic. Presently, he practices Chiropractic Functional Neurology at the Papakura Neurology Center and The Maungakiekie Clinic located in Auckland, New Zealand.

 

References

Beck, R. W. Functional Neurology for Manual Therapists. Elsevier, UK. 2007 (in Press).

 
The Functional Neurological Approach to Physical Examination of the Neuraxis
Functional Neurology
Written by Randy Beck, B.Sc., D.C., Ph.D.   
Friday, 04 May 2007 14:11

Welcome back to the continuing series exploring functional neurology. In the next several articles I will be introducing some examination techniques and how they can be used to evaluate the level of function in various areas of the neuraxis. Let’s get started!

Steven Rose, the award winning neuroscientist from Cambridge, has stated that all scientific knowledge about the world comes from two types of study: the search for underlying regularities in seemingly dissimilar phenomena; and the analysis of the causes of variation or, in other words, looking for the small differences in seemingly similar phenomenon. We apply these axioms in the functional neurological examination.

The neurological examination is traditionally taught using a disease or ablative lesion orientated model. While this approach may help to detect the presence of both serious and benign disorders, it is less helpful for the practitioner who wishes to investigate and estimate the physiological functional integrity of the nervous system. A more functional approach to the neurological examination heightens the examiner’s sensitivity to physiological aberrations that are responsible for the vast majority of neurological symptoms. At the same time, a practitioner using this approach is more likely to detect subtle signs of pathology.

The practitioner who intends to utilize the functional approach of examination must be concerned with the identification of ablative lesions and the presence of disease processes, but must also attempt to identify any physiological lesions that are manifesting themselves as physical symptoms. For example, a common presentation in my office is an athlete with a shoulder or wrist dislocation or sprain for which they have been strapped or casted for a period of time. Now the cast or strapping has been removed and they have started a rehabilitation program. They present to me with headaches, lack of concentration, balance problems, incoordination and decreased drive to return to their previous activity level. The decreased movement in the joints involved during the casting period has resulted in a functional change in some of the neuronal circuits in their spinal cord, brainstem, cerebellum and cortex that receive input from the area. The rehabilitation program did not allow for this but focused on the joints and soft tissues, resulting in over stimulation to areas of the neuraxis that had down regulated their activity capability during the period of inactivity. This over stimulation has resulted in transneural degeneration and injury to certain neuronal circuits that have resulted in the symptoms that the patient has presented with. In these cases, a thorough neurological examination must be performed to both identify any physiological lesions and to rule out any ablative lesions that may also present with similar symptoms.

So how can we evaluate this patient to determine if he has a physiological dysfunction and, if so, what areas are involved? We need to have a system that will allow us to measure small changes in the state of function at various levels of his neuraxis.

The Five Parameters of Effector Response Are Important Clues in Gauging the Central Integrative State (CIS) of Upstream Neuron Systems

The response of an effector (e.g., muscle) to a stimulus or command is largely dependent on the central integrative state of the presynaptic neuronal pool projecting to the motor neuron of the effector. Therefore, the CIS of a neuronal pool can be predicted or estimated by observing the characteristics of the motor response of the downstream motor neuron to a unit stimulus. The parameters of the effector response observed can be summarized under the following observational findings:

1. Latency and velocity of the response,

2. Amplitude of the response,

3. Smoothness of movement of the response,

4. Fatigability of the response,

5. Direction of the response.

All of the responses observed during the functional examinations performed on a patient should be evaluated with the above parameters in mind. It is also important to visualize the pathways that are actively involved in producing the actions that you are examining. This allows the practitioner the advantage of performing additional or more detailed tests directed at the same pathways throughout the examination, should disparities in the patient’s responses become apparent.

Latency and Velocity of a Response

The latency refers to the time between the presentation of a stimulus and the motor, sensory, autonomic or behavioural response of the patient. This provides information concerning conduction time along nerve axons and spatial and temporal summation occurring in the neurons involved in the functional action chain of the response. The velocity of the response is another window of spatial and temporal summation and conduction time.

The time to summation (TTS) and time to peak summation (TTSp) are abbreviations that describe, respectively, the latency and average velocity of effector responses. The pupillary action observed in response to a light stimulus offers a good illustration of these concepts. Under normal conditions, the pupils will respond with a relatively equal TTS and TTSp in both eyes when stimulated with an equal light stimulus. However, in the situation were the central integrative state of the neurons in the right Edinger-Westphal nucleus or mesencephalic reticular formation is further away from threshold, the TTS of the right eye would be expected to be increased from that of the left. The same result may be expected when measuring the velocity of the response, or an increased time to maximal pupil constriction (increased TTSp). The same result, that is increased TTS and TTSp in the right eye, may be found with an afferent pupil defect such as would occur if the right eye end organ were impeded by a photoreceptor or axonal conduction deficit, such as in retinal or optic nerve dysfunction. Thus, the need for a complete fundoscopic and visual acuity exam when unequal pupil responses are present.

Amplitude of a Response

The amplitude of the response refers to the maximum change in the parameters being assessed. This can be a useful indicator of the relative frequency of firing in a neuronal pool—for example, the degree of excursion of the eye during the smooth phase of pursuit movement during opticokinetic testing of eye movements or, in keeping with our first example, the maximum change in pupil size when testing the pupil light reflex.

Smoothness of a Response

Smoothness of any movement is dependent on complex interactions between multiple neuronal pools. An example is the smoothness of visual tracking in the horizontal plane. This requires complex interactions between the cerebellum, vestibular system, neural integrator, and occipital, parietal and frontal lobes. A poor central integrative state in any of these areas may affect the quality of visual tracking in one or more directions. Specific features of the visual tracking deficit may alert to greater involvement of one area over another. Uncoordinated or jerky movements are referred to as dysmetric in nature.

Fatigability of a Response

This refers to the ability to maintain a response during continued or repeated presentation of a stimulus. A progressive reduction in the amplitude and speed of a tendon jerk reflex over several repeated taps with the reflex hammer is a good example of this response. For instance, most normal systems should be able to sustain the reflex response for five to six taps before fatigue sets in. Poor maintenance of a response reflects increased fatigability. The fatigability coefficient is an arbitrary descriptor of the fatigability of a neuronal pool.

Direction of a Response

The direction of response elicited is compared to the expected normal response, to provide further information about the integrity of a neuronal pool. For example, the direction of change of pupil size when shining a light in the eye, the direction of nystagmus during caloric irrigation of the ear, and the direction of change of skin temperature in response to a cognitive task or vestibular stimulation, all have an expected normal response direction. If the direction of response is different to the expected outcome, this may indicate the presence of pathology, fatigue or plastic alterations in neural circuitry.

Try evaluating these five response characteristics in the different tests you include in your physical examinations over the next month.

In the next article we will look at specific examination techniques for various levels of the neuraxis.

Randy Beck, B.Sc., D.C., Ph.D., is a graduate of Canadian Memorial Chiropractic College. He has completed postgraduate studies in Psychology, Immunology and Neurology. He is presently involved in a number of international research projects and is co-authoring a textbook on Functional Neurology. He was formerly the Dean of Chiropractic and Basic Sciences and Director of Research at the New Zealand College of Chiropractic. Presently, he practices Chiropractic Functional Neurology at the Papakura Neurology Center and The Maungakiekie Clinic located in Auckland, New Zealand.

 

References:

1. Beck, R. W. Functional Neurology for Manual Therapists. Elsevier, In press. 2007.

2. Rose, S. The making of memory: From molecules to mind. ISBN 0099449986, Random House, 2003.

 
Anatomy and Physiology of the Autonomic Nervous System
Functional Neurology
Written by Randy Beck, B.Sc., D.C., Ph.D.   
Wednesday, 04 April 2007 12:52

One of the most important concepts in functional neurology is that we can utilize the motoric output of the nervous system end organs as a guide to the level of activation in the central nervous system. The first examination techniques we will explore will utilize this concept as it applies to the autonomic nervous system. First, a brief review of anatomy and physiology of the autonomic nervous system may be useful.

Organization of the Autonomic Nervous System

The autonomic nervous system comprises the major autonomous or non-volitional efferent outflow to all organs and tissues of the body, with the exception of skeletal muscle. Anatomically, the autonomic outflow from the spinal cord to the end organ occurs through a chain of two neurons consisting of a pre- and postganglionic component. The preganglionic component neurons live in a lateral area of grey matter of the spinal cord called the intermediolateral cell column or IML. The postganglionic component neurons vary in the locations with some living in the paraspinal or sympathetic ganglia, and others in ganglia distant from the cord, known as stellate ganglia. Although, historically, only the efferent connections were considered to be of functional importance, all of the projections of the autonomic nervous system are reciprocal in nature and involve both afferent and efferent components.

The autonomic system can be divided into three functionally and histologically distinct systems: the parasympathetic, sympathetic and enteric systems. All three systems are modulated by projections from the hypothalamus. Hypothalamic projections that originate mainly from the paraventricular and dorsal medial nuclei influence the parasympathetic and sympathetic divisions as well as the enteric division of the autonomic nervous system. These descending fibres initially travel in the medial forebrain bundle and then divide to travel in both the periaquaductal grey areas and the dorsal lateral areas of the brainstem and spinal cord. They finally terminate on the neurons of the parasympathetic preganglionic nuclei of the brainstem, the neurons in the intermediate grey areas of the sacral spinal cord and the neurons in the intermediolateral cell column of the thoracolumbar spinal cord. Descending autonomic modulatory pathways also arise from the nucleus solitarius, noradrenergic nuclei of the locus ceruleus, raphe nuclei, and the pontomedullary reticular formation.

The parasympathetic system communicates via both efferent and afferent projections within several cranial nerves, including the oculomotor (CN III) nerve, the trigeminal (CNV) nerve, the facial (CNVII) nerve, the glossopharyngeal nerve, the vagus (CNX) and accessory (CNXI) nerves. The vagus nerve and sacral nerve roots compose the major output route of parasympathetic enteric system control.1

Axons of the preganglionic nerves of the parasympathetic system tend to be long, myelinated type II fibres. The postganglionic axons tend to be somewhat shorter, unmyelinated C fibres, which means they conduct information at a much slower rate of speed. The cell bodies of parasympathetic preganglionic neurons are located in discrete nuclei at various levels of the brainstem and in the intermediolateral cell column of sacral 2-4 levels in the spinal cord or lumbar 1-2 vertebral level. In contrast to the sympathetic system, the preganglionic parasympathetic axons are generally longer than the postganglionic axons as they synapse in ganglia that are further from their origin and closer to the effector organ.

The neurotransmitter released both pre- and postsynaptically in the parasympathetic system is acetylcholine. Functionally, the neurological output from the parasympathetic system is the integrated end product of a complex interactive network of neurons spread throughout the mesencephalon, pons and medulla. The outputs of the cranial nerve nuclei, including the Edinger-Westphal nucleus, the nucleus tractus solitarius, the dorsal motor nucleus, and nucleus ambiguus are modulated via the mesencephalic and ponto-medullary reticular formation. This complex interactive network receives modulatory input from wide areas of the neuraxis including all areas of cortex, limbic system, hypothalamus, cerebellum, thalamus, vestibular nuclei, basal ganglia and spinal cord.2,3,4,5,6

The sympathetic system enjoys a wide-ranging distribution to virtually every tissue of the body. The presynaptic neurons live in a region of the grey matter of the spinal cord called the intermediomedial and intermediolateral cell columns located in laminae VII. Axons of these neurons exit the spinal cord via the ventral rami, where they further divide to form the white rami communicantes. The fibres then follow one of several pathways, including:

1) synapse in the paravertebral or prevertebral ganglia segmentally.

2) synapse in segmental regions of the paravertebral or prevertebral ganglion other than those at which they exited.

3) continue as presynaptic myelinated fibres into the periphery and do not synapse in the prevertebral or paravertebral ganglia.

The output of the preganglionic neurons of the sympathetic system is the summation of a complex interactive process involving segmental afferent input from dorsal root ganglion and supra-segmental input from the hypothalamus, limbic system, and all areas of cortex via the mesencephalic and ponto-medullary reticular formations.6,7,8

Most post ganglionic fibres of the sympathetic nervous system release norepinephrine as their neurotransmitter. The chromaffin cells of the adrenal medulla, which are embryological homologues of the paravertebral ganglion cells, are also innervated by preganglionic sympathetic fibres which fail to synapse in the paravertebral ganglia as described above. When stimulated, these cells release a neurotransmitter/neurohormone that is a mixture of epinephrine and norepinephrine with a 4:1 predominance of epinephrine.9

Both epinephrine and norepinephrine are manufactured via the tyrosine- dihydroxyphenylalanine (DOPA)-dopamine pathway and are called catecholamines.When the body is in a neutral environment, catecholamines contribute to the maintenance of homeostasis by regulating a variety of functions such as cellular fuel metabolism, heart rate, blood vessel tone, blood pressure and flow dynamics, thermogenesis and, as explained below, certain aspects of immune function.

When a disturbance in the homeostatic state is detected, both the sympathetic nervous system and the hypothalamus-pituitary-adrenal axial system become activated in the attempt to restore homeostasis via the resulting increase in both systemic (adrenal) and peripheral (post ganglionic activation) levels of catecholamines and glucocorticoids. In the1930’s, Hans Selye described this series of events or reactions as the general adaptation syndrome or generalized stress response.10 Centrally, two principal mechanisms are involved in this general stress response; these are the production and release of corticotrophin releasing hormone produced in the paraventricular nucleus of the hypothalamus and increased norepinephrine release from the locus ceruleus norepinephrine releasing system in the brain stem. Functionally, these two systems cause mutual activation of each other through reciprocal innervation pathways.11 Activation of the locus ceruleus results in an increased release of catecholamines, of which the majority is norepinephrine, to wide areas of cerebral cortex, subthalamic and hypothalamic areas. The activation of these areas results in an increased release of catecholamines from the postganglionic sympathetic fibres as well as from the adrenal medulla.

Most Areas Modulating the Autonomic Systems Are Bilateral Structures

It is worth noting at this point that, with the exception of a few midline structures in the brainstem, the locus ceruleus and the raphe nuclei, all other structures that modulate the autonomic output are bilateral structures. This presents the possibility that asymmetric activation or inhibition lateralised to one side or the other may translate to the activity of the end organs and produce asymmetries of function from one side of the body to the other.12 Accurately assessing the asymmetric functional output of the autonomic nervous system is a valuable clinical tool in evaluating asymmetrical activity levels of cortical or supraspinal structures that project to the output neurons of the autonomic system.

Randy Beck, B.Sc., D.C., Ph.D., is a graduate of Canadian Memorial Chiropractic College. He has completed postgraduate studies in Psychology, Immunology and Neurology. He is presently involved in a number of international research projects and is co-authoring a textbook on Functional Neurology. He was formerly the Dean of Chiropractic and Basic Sciences and Director of Research at the New Zealand College of Chiropractic. Presently, he practices Chiropractic Functional Neurology at the Papakura Neurology Center and The Maungakiekie Clinic located in Auckland, New Zealand.

References:

1. Furness, J. B. and M. Costa. Types of nerves in the enteric nervous system. Neuroscience 5: 1-20, 1980.

2. Walberg, F. Further studies on the descending connections to the inferior olive. Reticulo-olivary fibers: an experimental study in the cat. Journal of Comparative Neurology 114: 79-87, 1960.

3. Angaut, P. and A. Brodal. The projection of the vestibulocerebellum onto the vestibular nuclei of the cat. Archs ital Biology 105: 441-79, 1967.

4. Brodal, A. Neurological Anatomy. London, Oxford University Press, 1969.

5. Brown, L. T. Corticorubral projections in the rat. Journal of Comparative Neurology 154: 149-68, 1974.

6. Webster, K. E. The brainstem reticular formation. The biological basis of Schizophrenia. G. Hennings and W. A. Hemmings. Lancaster, M.T.P. Press.1978.

7. Donovan, B. T. Mammillian Neuroendocrinology. New York, McGraw-Hill.1970.

8. Williams, P., L. and R. Warwick. Grey’s Ananatomy. Edinburgh, Churchill Livingston.1984.

9. Elenkov, I., J., R. Wilder, L., et al. The Sympathetic Nerve-An integrative interface between two supersystems: The brain and the immune system. Pharmacological Reviews 52(4): 595-675. 2004.

10.Selye, H. Thymus and the adrenals in the response of the organism to injuries and intoxications. Br. J. Experimental Pathology 17: 234-38, 1936.

11.Chrousos, G., P. and P. W. Gold. The concepts of stress and stress system disorders: Overview of physical and behavioral homeostasis. J. Amer. Med. Assoc. 267: 1244-52. 1992.

12.Lane, R.D. and Jennings J.R. Hemispheric asymmetry, autonomic asymmetry, and the problem of sudden cardiac death. In Brain Asymmetry. Davidson, R. J. and Hugdahl, K. eds. The MIT press, Cambridge, Massachusetts.1995.

 

 
Diagnosis through Functional Neurology
Functional Neurology
Written by Randy Beck, B.Sc., D.C., Ph.D.   
Sunday, 04 March 2007 11:33

Welcome back to the continuing Functional Neurology series. I would like to thank everyone for the wonderful emails that I have been receiving and I will try to address all of your questions as the series of articles progresses.

I will take the opportunity to answer the most commonly asked question to date "Where can we learn more about Functional Neurology?" The best place to investigate the recognized programs that are available is to visit the American Chiropractic Neurology Board website at www.acnb.org. My own personal experience has been with the Carrick Institute of Graduate Studies (www.carrickinstitute.org), which I have found to be an excellent institution. Elsevier is also publishing a textbook on the subject in the coming year, which will offer much more detailed explanations of all the topics that we will cover in this series.

In the next few segments, we will explore the various examination techniques that can be utilized in Functional Neurology to gain an understanding of the longitudinal level of the lesion and to monitor the effects of any treatment. First, we need to define a few terms such as the longitudinal level of the lesion and ablative and physiological lesions.

Longitudinal Level of a Lesion in the Neuraxis

Lesions in a nerve pathway may occur at one or more points along the pathway. Identifying the level at which the lesion has occurred is usually accomplished by taking a thorough history and performing a thorough physical examination on the patient. A nerve pathway may become dysfunctional at one or more of the following:

• the receptor level,

• the effector organ level,

• in the efferent and afferent nerve axons of the peripheral nerve,

• the spinal cord level,

• the brainstem and cerebellar level,

• the thalamus/basal ganglionic level,

• the level of the cortex.

Lesions at the receptor level may be ablative, may be caused by states of habituation, or may be due to a decreased environmental stimulus. Often, the sensitivity of a receptor is cortically mediated and cortical hyper- or hyposensitivity states may be confused with a receptor lesion. The level of response of a receptor is often measured through the response of an effector organ and this may also result in confusion between a receptor lesion and an effector dysfunction.

Effector or end organ lesions may be hyper or hypo functional in nature. In skeletal muscle, hypo-functional disorders can be caused by myopathies, neurotransmitter or neuro-receptor dysfunction, oxidative phosphorylation disorders and lack of use. Hyper-functional disorders can be caused by metabolic and ionic imbalances. Often, disinhibition of ventral horn cells can result in a hyper-functional state, such as rigidity and spasms of the end organ. This is actually a spinal cord (corticospinal tract lesion) or supraspinal (upper motor neuron) level of involvement, which could be confused with an end organ dysfunction.

Peripheral nerve lesions usually involve both motor and sensory functional disturbances. The distributions of the peripheral nerves have been anatomically and functionally mapped fairly accurately and these distributions can be used to identify the location of a specific peripheral nerve dysfunction. Often the end organs of such a muscle will show specific forms of activity (flaccid paralysis) or neurologically induced atrophy (muscle wasting) when a peripheral nerve is involved.

Spinal cord lesions may exhibit disassociation of sensory and motor symptoms, depending on the specific areas of involvement of the spinal cord. Specific tract lesions may demonstrate classical symptoms, as in dorsal column lesions and loss of proprioception. When specific areas of the cord are involved, the patient may exhibit classical symptoms of a well-defined syndrome, such as posterior lateral medullary infarcts and symptoms of Wallenberg’s syndrome.

Lesions of the brainstem and cerebellum often result in widespread seemingly unrelated symptoms, which can include cerebellar degeneration and changes in cognitive function, or dysautonomia, with brainstem dysfunction. These can be one of the most challenging levels of lesion to treat, due to the involvement of both upstream and downstream neuronal systems, which experience altered function concomitantly.

Basal ganglionic and thalamic levels usually result in movement disorders and disorders of sensory reception including pain disorders. Basal ganglionic disorders have also been implicated in a variety of cognitive function disorders as well.

Lesions at the cortical level can manifest as dysfunction at any other level in the neuraxis and, as such, are often very difficult to pinpoint. Many of the cortical functions, if not all cortical functions, are highly integrated over diffuse areas of cortex which, once again, makes targeting specific neuron circuits difficult.

Ablative and Physiological Dysfunctional Lesions

Ablative lesions are lesions that result in the death or destruction of neural tissues. This type of lesion commonly occurs as the result of a vascular stroke, where tissues experience critical levels of hypoxia or anoxia and die as a result. Direct or indirect trauma, as in the "coup counter coup" injuries in whiplash or head trauma, can also result in ablution of tissues or function. Replacement of the damaged tissue is usually very slow, if it occurs at all, and restoration of function depends on rerouting of nerve pathways or regrowth of new synaptic connections.

Physiological lesions are functional lesions that result from over stimulation, excessive inhibition, excessive disinhibition, or under stimulation of a neuronal system. Correction of these functional lesions is dependant on restoring normal levels of activation to the involved systems. The results are usually apparent relatively quickly and can occur almost immediately in some cases.

Often the symptom presentation of these two types of lesions can be very similar, so the possibility of an ablative lesion must be ruled out before the diagnosis of a physiological lesion is made.

For example, in Huntington’s Disease (HD) the neurons in the neostriatum degenerate. The neural circuits of the basal ganglia involve a direct and an indirect pathway. The degeneration in Huntington’s Disease appears to be more pronounced in the output neostriatal neurons of the indirect pathway. This results in the disinhibition of the globus pallidus pars externa (GPe) which, in turn, results in an over-inhibition of the subthalamic nucleus. The functional over inhibition of the subthalamic nucleus results in a situation that resembles an ablative lesion to the subthalamic nucleus and results in a hyperkinetic movement disorder. In this case, the lesion is not purely physiological in nature because the neostriatal neurons have actually degenerated, but the result is the physiological functional state of over-inhibition of a neuron system.

Randy Beck, B.Sc., D.C., Ph.D., is a graduate of Canadian Memorial Chiropractic College. He has completed postgraduate studies in Psychology, Immunology and Neurology. He is presently involved in a number of international research projects and is co-authoring a textbook on Functional Neurology. He was formerly the Dean of Chiropractic and Basic Sciences and Director of Research at the New Zealand College of Chiropractic. Presently, he practices Chiropractic Functional Neurology at the Papakura Neurology Center and The Maungakiekie Clinic located in Auckland, New Zealand.

 

 


 

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