Cortical Function




Richard Belli, D.C., D.A.C.N.B. & Randall March, D.C., D.A.C.N.B.

The human cortex is comprised of two basic divisions, the paleocortex (old), and the neocortex (new). The neocortex is what separates us humans from the beasts of the fields. The neocortex has an overall inhibiting effect on our primitive drives, exhibiting far reaching effects on the autonomic and unconscious somatic systems.

Loss of normal neocortical modulation may result in spasticity, tachycardia, gastrointestinal dysfunction, pyramidal patterns of muscle weakness, blood pressure changes, behavioral changes, changes in affect, and many other functional disorders. The associated muscle weakness patterns causing joint dyskinesia, may also result in primary musculoskeletal pain and dysfunction. The inhibitory function of the neocortex is by descending excitatory pathways to the medullary reticular formation. The medullary reticular formation then projects inhibitory activity to the spinal cord, modulating inhibitory and excitatory interneurons and the overall bias of the anterior horn. This activity results in overall control of the expression of primitive spinal cord function. Other neocortical function includes inhibition by the frontal orbital cortex on limbic centers and other primitive social drives.

The neocortex is driven by contralateral cerebellar and ipsilateral thalamic projections of which the most important are from muscle spindles, joint receptors, and Golgi tendon organs. The resulting overact input to the neocortex is from the contralateral side of the body.

Examination of the descending pathways anatomically reveals that the largest pathways are contralateral. However, this is not the functional reality; the only real significant contralateral motor function from the paleocortex is from areas 4, 4s, 6 that project to the distal flexors of the extremities (hands and feet). As a consequence of many other neurologically intertwining factors, including the inhibitory aspects of the neocortex, the overall effect is ipsilateral in many pathways, thus expressing the difference between functional neurology and textbook neuroanatomy.

Without the appropriate arsenal of tools, determining neocortical function can be frustrating, unreliable and confusing. Manual muscle testing alone, as valuable a tool as it is, can be limiting in this respect. There are too many other factors that will affect the muscle weakness patterns when there is neocortical dysfunction to make them consistently reliable. Some examples are withdrawal reflexes, spinal cord interneuron dysfunction, segmental dysfunction, and visceral involvement. With that in mind, the clinician would be wise to use non‑manual muscle testing and primary perceptual measurement to correlate with manual muscle testing of pyramidal para‑paresis to determine the location of cortical dysfunction.

Non‑manual muscle tests include deep tendon reflex, withdrawal reflex, and palatal deviation. Primary perceptual tests include color acuity from one side to another and physiological blind spot mapping. The deep tendon reflex will be increased on the side of cortical dysfunction due to the loss of descending inhibition on the gamma motor neuron which ultimately results in increased tension on the muscle spindle and hypersensitivity to stretch. The withdrawal reflex will be decreased due to neocortical loss of inhibition of spinal interneuron inhibition on the ipsilateral side, resulting in an over- all inhibition of the anterior horn. Due to decreased ipsilateral drive to the vagal motor nucleus, the soft palate, especially when one observes the palatine raphe. This mid‑line white stripe will deviate away from the dysfunctional side. (Don't use the uvula as an indicator, as it can be hanging all over the place and means nothing.) This is due to a loss of motor potentiation to the ipsilateral levator palatini muscle. The dysfunctional cortex will have a shift towards hyperpolarization, making the neurons more difficult to fire action potentials, and resulting in decreased color perception (patient fixates eyes on a central target between two sheets of colored paper [use primary colors] and determines which side seems brighter), or an increased physiological blind spot on the contralateral side.

A typical example of left cortical dysfunction might include palatal deviation to the right, increased physiological blind spot on the right, decreased color perception on the right, decreased withdrawal reflex on the left, increased deep tendon reflexes on the left, and a pyramidal pattern of muscle weakness on the left. Since the cortex is driven primarily by contralateral mechanoreceptor input, appropriate therapy might include manipulation, stretching of muscle spindles, auditory stimulation, and visual field stimulation. A more precise determination of the actual therapeutic activity would include evaluation of the thalamus and cerebellar function using sensory and motor modalities.

The neocortex is what separates us from the rest of the animal kingdom. It is very powerfully inhibitory to primitive drive. We may view the paleocortex as the "child‑brain" that is carefree and wants to romp in the fields; and the neocortex as the "adult - brain" that has social graces and behaves itself. Thus we see that the neocortex inhibits the excitatory functions of the paleocortex. If we loose this programmed inhibition, we may express many primitive drives resulting in anything from loss of social well‑being to musculoskeletal pain. It becomes apparent that there can be no tissue damage that is not related to a cortical event and that cortical events may cause tissue damage such as neurotrophic joints. In order to completely understand and treat the human condition, we must become competent in evaluation and treatment of the cortex.