Diagnosis through Functional Neurology

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.


Leave a Reply