Figure 3-3. Lateral (A) and medial (B) surfaces of the human cerebral hemispheres, showing the areas of excitable cortex, numbered according to the scheme of Brodmann. (Reprinted with permission from House EL, Pansky B: A Functional Approach to Neuroanatomy, 2nd ed. New York, McGraw-Hill, 1967.) See also Fig. 22-1.
Figure 3-4. The representation of body parts in the motor cortex, commonly called the motor homunculus. The large area of cortex devoted to motor control of the hand, lips, and face is evident. A in the smaller diagram represents the motor cortex; B is the sensory cortex.
Figure 3-5. A. Supranuclear facial palsy. There is lower facial weakness contralateral to the lesion, but the upper face is spared due to its bilateral cortical innervation. B. Nuclear and infranuclear facial palsy. Both upper and lower portions of the face are weak.
Figure 3-6. A. The plantar response is elicited by stroking from the heel to the ball of the foot. B. The normal plantar response consists of flexion of the toes. C. The extensor plantar response (Babinski sign) consists of extension of the great toe coupled with fanning of the remaining digits.
Disorders of Movement and Posture
In this chapter, disorders of the automatic, static, postural, and other less-modifiable motor activities of the nervous system are discussed. Many of them are an expression of what has come to be called the extrapyramidal motor system, meaning—according to S.A.K. Wilson, who introduced this term—the motor structures of the basal ganglia and certain related thalamic and brainstem nuclei. However, others such as myoclonus and various tremors have obscure or multiple causes. These are discussed together because they are often combined and because of their inclusion in the clinical specialty of movement disorders.
The activities of the basal ganglia and the cerebellum are blended with and modulate the corticospinal system and the postural influence of the extrapyramidal system is indispensable to voluntary corticospinal movements. This close association of the basal ganglia and corticospinal systems becomes evident in the course of many forms of neurologic disease. In many aberrant motor patterns, one sees evidence not only of the activity of the basal ganglia but also of labyrinthine, tonic neck, and other postural reflexes that are mediated through nonpyramidal brainstem motor systems, including the vestibulospinal, rubrospinal, and reticulospinal tracts. Observations such as these have blurred the original distinctions between pyramidal and extrapyramidal motor systems. Nevertheless, this division remains a useful concept in clinical work because it informs a distinction among several motor syndromes—one that is characterized by a loss of volitional movement accompanied by spasticity—the corticospinal syndrome; a second by bradykinesia, rigidity, and tremor without loss of voluntary movement—the hypokinetic basal ganglionic syndrome; a third by involuntary movements (choreoathetosis and dystonia)—the hyperkinetic basal ganglionic syndrome; and yet another by incoordination (ataxia)—the cerebellar syndrome. Table 4-1 summarizes the main clinical differences between corticospinal and extrapyramidal syndromes.