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Essential tremor is a monosymptomatic disorder

Classic essential tremor (ET) is widely regarded as a monosymptomatic disorder with no neurological signs or symptoms other than tremor. Muscle tone is normal, and there is no clinical evidence of another neurological disorder. Tremor may be palpable during the manual testing of muscle tone, particularly when muscle tone is enhanced by voluntary action of another body part (Froment’s sign). This “cog-wheeling” is merely palpable action tremor and is not a sign of coexistent Parkinson’s disease. The Consensus Statement of the Movement Disorder Society on Tremor regarded as indeterminate the classification of action tremor in the head or upper limbs in a patient with other neurological signs, such as subtle bradykinesia, reduced arm swing, and questionable dystonic posturing. This classification scheme for action tremor with other neurological signs is admittedly somewhat arbitrary because there is still no definitive test or biological marker to confirm the diagnosis of ET. Genetic markers will soon be available, but it is now certain that genetic defects on at least three different chromosomes can produce classic ET. It remains to be seen whether the genetic heterogeneity of ET is associated with clinical heterogeneity and other neurological signs. Currently, one can only examine the published clinical studies that looked for clinical relationships between ET and other disorders, and in this review, I explain why I believe the results of these studies support the definition of ET as a monosymptomatic disorder. The definition of classic ET as a monosymptomatic disorder must be accompanied by the caveat that some patients exhibit subtle signs of ataxia. Patients with advanced ET often exhibit a crescendo increase in tremor as the upper limb approaches its target. This intention tremor is indistinguishable from the intention tremor that occurs in patients with lesions in the brachium conjunctivum, in the vicinity of the ventrolateral thalamus. ET patients with intention tremor exhibit a delayed activation of the antagonistic muscles during rapid movements such as reaching, and this antagonistic muscle delay is similar to that produced by cerebellar disease. In addition, some patients with ET exhibit impaired tandem walking, even though there is no other evidence of gait or postural disturbance. Neuroimaging studies have shown that the cerebellum is involved in the pathophysiology of ET and that the cerebellar relay nucleus of the ventrolateral thalamus is also involved. Therefore, subtle signs of ataxia other than tremor are not surprising. Subclinical deficits in cognitive function, consistent with frontocerebellar pathway dysfunction, have been found in two small studies of elderly patients with advanced ET. One study involved patients referred for stereotactic surgery, and the other recruited patients from a movement disorder clinic. Therefore, the patients were not representative of the general population of ET patients, and larger studies with better controls and less recruitment bias are needed. Interestingly, an 80-year-old ET patient with bilateral, ventrolateral, thalamic deep brain stimulators reported increased confusion, anger, tension, anxiety, and fatigue when the stimulators were off, and he exhibited improved verbal fluency and verbal recall when the stimulators were on. Thus, the anxiety and depression produced by advanced tremor could reduce memory and cognitive function, independently of the underlying pathophysiology of ET. Some but not all retrospective studies of clinic populations have revealed an association between Correspondence to: Rodger J. Elble, MD,.Department of Neurology, Southern Illinois University School of Medicine, P.O. Box 19643, Springfield, IL 62794-9643. E-mail: relble@siumed.edu Received 14 December 2001; Accepted 22 February 2002 Published online 16 April 2002 in Wiley InterScience (www. interscience.wiley.com). DOI 10.1002/mds.10222 Movement Disorders Vol. 17, No. 4, 2002, pp. 633–637 © 2002 Movement Disorder Society