In patients with pathologic tremor of almost any type, Narabayashi has recorded rhythmic burst discharges of unitary cellular activity in the nucleus intermedius ventralis of the thalamus (as well as in the medial pallidum and subthalamic nucleus) synchronous with the beat of the tremor. Neurons that exhibit the synchronous bursts are arranged somatotopically and respond to kinesthetic impulses from the muscles and joints involved in the tremor but that is not to say that there is a causal relationship between this activity and the tremor. A stereotaxic lesion in this region of the thalamus abolishes the tremor. The effectiveness of a thalamic lesion may be a result of interruption of pallidothalamic and dentatothalamic projections or, more likely, of projections from the ventrolateral thalamus to the premotor cortex, as the impulses responsible for tremor are ultimately transmitted by the lateral corticospinal tract. Some of what is known about the physiology of specific tremors is noted in the following paragraphs.
Action tremors are evident during use of the affected body part, as opposed to tremor that is apparent in a position of rest or repose. Action tremors can be roughly divided into two categories: goal directed action tremor of the ataxic type related to cerebellar disorders (discussed in Chap. 5) and postural tremors, which are either the enhanced physiologic variety or essential tremor (Fig. 4-6). A postural tremor occurs with the limbs and trunk actively maintained in certain positions (such as holding the arms outstretched) and may persist throughout active movement. More particularly, the tremor is absent when the limbs are relaxed but becomes evident when the muscles are activated. The tremor is accentuated as greater precision of movement is demanded, but it does not approach the degree of augmentation seen with cerebellar intention tremor. Most cases of action tremor are characterized by relatively rhythmic bursts of grouped motor neuron discharges that occur not quite synchronously in opposing muscle groups as shown in Fig. 4-7. Slight inequalities in the strength and timing of contraction of opposing muscle groups account for the tremor. In contrast, rest (parkinsonian) tremor, is characterized by alternating activity in agonist and antagonist muscles.
Enhanced physiologic tremor The type of action tremor that seems merely to be an exaggeration of the above-described physiologic tremor, can be brought out in most normal persons. It has the same fast frequency as physiologic tremor (about 10 Hz; see Fig. 4-7) but with greater amplitude. Such a tremor, best elicited by holding the arms outstretched with fingers spread apart, is characteristic of intense fright and anxiety (hyperadrenergic states), certain metabolic disturbances (hyperthyroidism, hypercortisolism, hypoglycemia), pheochromocytoma, intense physical exertion, withdrawal from alcohol and other sedative drugs, and the toxic effects of several drugs—lithium, nicotinic acid, xanthines (coffee, tea, aminophylline), cocaine, methylphenidate, other stimulant drugs, and corticosteroids. Young and colleagues have determined that the enhancement of physiologic tremor that occurs in metabolic and toxic states is not a function of the central nervous system but is instead a consequence of stimulation of muscular beta-adrenergic receptors by increased levels of circulating catecholamines.