Not all tremors correspond exactly with those described above and several of them may coexist. It is common for one type of tremor to show a feature ordinarily considered characteristic of another. In some parkinsonian patients, for example, the tremor is accentuated rather than dampened by active movement; in others, the tremor may be very mild or absent in repose and become obvious only with movement of the limbs. As mentioned above, a patient with a typical parkinsonian tremor may, in addition, show a fine essential tremor of the outstretched hands and occasionally even an element of ataxic tremor as well. In a similar way, essential or familial tremor may, in its advanced stages, assume the aspects of a cerebellar tremor. Further examples include patients with essential tremor or ataxic tremor who also display a rhythmic parkinsonian tremor in relation to sustained postures.
This is a rare disorder consisting of rapid, rhythmic, involuntary movements of the soft palate. For many years it was considered to be a form of uniphasic myoclonus (hence the terms palatal myoclonus and palatal nystagmus). Because of the persistent rhythmicity, it is now classified as a tremor. There are two forms of this movement, according to Deuschl and colleagues. One is essential palatal tremor that reflects the rhythmic activation of the tensor veli palatini muscles; it has no known pathologic basis. The palatal movement may impart a repetitive audible click, which ceases during sleep. The second, more common form is a symptomatic palatal tremor caused by a diverse group of brainstem lesions that interrupt the central tegmental tract(s); (Fig. 5-3). There is a latency of many months after the focal injury before the tremor becomes evident. It has been reported by Deuschl and coauthors (1990) that the experience of clicking is reported by patients with the essential, but not the symptomatic, variety. The frequency of the tremor varies greatly between patients and tends to be higher and remain fixed in the symptomatic variety.
Palatal tremor, in contrast to the essential type and all other tremors, persists during sleep and is sometimes associated with pendular nystagmus that is synchronized with the palatal movements. In some cases, the pharynx as well as the facial muscles, diaphragm, vocal cords, and even the muscles of the neck and shoulders partake of the persistent rhythmic movements. A similar phenomenon, in which contraction of the masseters occurs concurrently with pendular ocular convergence, has been observed in Whipple disease (oculomasticatory myorhythmia).
Magnetic resonance imaging (MRI) reveals no lesions to account for essential palatal tremor; in the symptomatic form, however, there are tegmental brainstem lesions accompanied by conspicuous enlargement of the inferior olivary nucleus unilaterally or bilaterally. With unilateral palatal tremor, it is the contralateral olive that becomes enlarged. It has been proposed that the lesions in the symptomatic form interrupt the circuit (dentate nucleus–brachium conjunctivum–red nucleus-central tegmental tract–olivary nucleus–dentate nucleus) that Lapresle and Ben Hamida called the triangle of Guillain-Mollaret (see Fig. 5-3). The lesions have been vascular, neoplastic, demyelinating, or traumatic, and have been found mainly in midbrain or pontine portions of the central tegmental fasciculus.
The physiologic basis of palatal tremor remains conjectural. Matsuo and Ajax postulated a denervation hypersensitivity of the inferior olivary nucleus and its dentate connections, but others have suggested that the critical event is denervation not of the olive but of the nucleus ambiguus and the dorsolateral reticular formation adjacent to it. Dubinsky and colleagues have suggested that palatal tremor may be based on the same mechanism as postural tremor—that is, presumably a disinhibition and rhythmic coupling of neurons in the olive induced by a lesion of the dentato-olivary pathway.