Almost always in Parkinson disease, the tremor is asymmetric and at the outset may be entirely unilateral. There is not a close correspondence between the degree of tremor and the degree of rigidity or akinesia. A bilateral parkinsonian type of tremor may also be seen in elderly persons without akinesia, rigidity, or mask-like facies. In some of these patients, the tremor is followed years later by the other manifestations of Parkinson disease, but in others it is not, remaining unchanged or progressing very slowly, unaffected by anti-Parkinson drugs. This entity probably equates with the earlier mentioned alternate-beat type of essential tremor. Patients with Wilson disease or an acquired form of hepatocerebral degeneration may also show a tremor of parkinsonian type, usually mixed with ataxic tremor and other extrapyramidal motor abnormalities. An alternating tremor may be seen in toxin and drug-induced parkinsonism but it is relatively symmetric and tends not to be a prominent feature. The tremor of postencephalitic parkinsonism (which is now virtually extinct) often had greater amplitude than typical parkinsonian tremor and involved proximal muscles.
Parkinsonian tremor is suppressed to some extent by the anticholinergic drugs benztropine and trihexyphenidyl; it is also suppressed less consistently but sometimes impressively by L-dopa and dopaminergic agonist drugs. Parkinsonian tremor is often associated with an additional tremor of faster frequency; the latter is of essential type and responds better to beta-blocking drugs than to anti-Parkinson medications. Stereotactic lesions or electrical stimulation in the basal ventrolateral nucleus of the thalamus diminishes or abolishes tremor contralaterally; other stimulation sites such as the internal segment of the globus pallidus and the subthalamic nucleus are also effective but possibly to a lesser degree. Chapter 38 discusses treatment of Parkinson disease in greater detail.
Pathophysiology The anatomic basis of parkinsonian tremor is not known. In Parkinson disease, the visible lesions predominate in the substantia nigra, and this was true also of the postencephalitic form of the disease. In animals, however, experimental lesions confined to the substantia nigra or striatopallidum do not result in tremor. Moreover, not all patients with lesions of the substantia nigra have tremor; in some there is only bradykinesia and rigidity. In a group of patients poisoned with the toxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a meperidine analogue that destroys the neurons of the substantia nigra pars compacta, only half developed a tremor, which had more of the characteristics of a proximal action or postural tremor than of a rest tremor as discussed by Burns and colleagues. In all likelihood, these inconsistencies reflect the complex influence of dopamine on a number of basal ganglionic structures.
Ward and others have produced a Parkinson-like tremor in monkeys by placing a lesion in the ventromedial tegmentum of the midbrain, just caudal to the red nucleus and dorsal to the substantia nigra. He postulated that interruption of the descending fibers at this site liberates an oscillating mechanism in the lower brainstem; this presumably involves limb innervation via the reticulospinal pathway. Alternative possibilities are that the lesion in the ventromedial tegmentum interrupts the brachium conjunctivum, a tegmental-thalamic projection, or the descending limb of the superior cerebellar peduncle, which functions as a link in a dentatoreticular-cerebellar feedback mechanism (see Fig. 5-3). The differential effect of drugs on tremor and bradykinesia suggest that they must have separate mechanisms.
Intention (Ataxic, Cerebellar, Goal-Directed Action) Tremor