Although clinical phenotypic variability by itself is not an argument for separate diseases, its presence further opens that possibility. Clinically, the view of ET as a single neurologic sign no longer seems tenable. First, the tremor phenomenology itself is multifaceted. Although kinetic and postural tremors are the core features upon which diagnostic criteria are generally based (Table 1), intention tremor18and tremor at rest19may also occur in subsets of patients. The relative severity of different tremor types (kinetic more severe than postural),20the favored sites of anatomical involvement (arm more often than head, and head more often than jaw),21and the typical direction of spread over time (from arms to head rather than the converse)22are distinctive, adding a degree of subtlety and complexity to the recognition and diagnosis of a disorder that is often viewed as relatively ordinary and featureless. Indeed, perhaps owing to a lack of familiarity with these features, misdiagnosis is exceedingly common; 30% to 50% of patients diagnosed with ET do not have ET,23which may make this one of the most commonly misdiagnosed neurologic disorders. Moreover, kinetic tremor of the arms, though not the head, may be an adverse effect of many medications, further contributing to this diagnostic difficulty. The following medications may produce kinetic tremor: amiodarone, bronchodilators, cyclosporin, lithium, methylphenidate, phenylpropanolamine, procainamide, pseudoephedrine, selective serotonin reuptake inhibitors, steroids, theophylline, thyroxine, tricyclic antidepressants, and valproic acid. Second, there are motor features aside from tremor. In a large number of studies,18,24postural instability and mild to moderate gait ataxia, beyond that observed in normal aging, have been demonstrated in subgroups of patients with ET. In addition to these gait problems, eye motion abnormalities (impaired smooth pursuit initiation and pathologic suppression of the vestibulo-ocular reflex time constant) were recently described in a study of 17 ET cases.25Third, there is a growing appreciation of the existence of a variety of nonmotor features, including cognitive, psychiatric, and sensory. Cognitive features, especially mild problems with executive function and memory, were first reported in 200126and soon after by numerous other investigators.27Furthermore, a population-based study in Madrid28first demonstrated in 2006 that the odds of prevalent dementia were nearly twice as high among the subset of ET cases with older-onset disease when compared with age-matched controls. The same group later demonstrated5that the risk of developing incident dementia was nearly twice as high in the ET cases than controls. Also, a number of psychiatric correlates have been observed. The presence of specific personality traits29,30has been demonstrated. In one such study,29the observed personality profile was not related to functional disability or tremor severity, suggesting that it could be a primary disease feature rather than a response to disabling tremor.29Anxiety,31depressive symptoms,32and social phobia33have been shown to occur in patients with ET more often than in controls. Traditionally, these have been viewed as psychiatric responses to disabling tremor. Yet in a recent prospective study,4depressive symptoms preceded the onset of the tremor by several years (ie, the presence of baseline self-reported depression was associated with an increased risk of developing incident ET during follow-up). Sensory abnormalities, including olfactory deficits in some studies34and hearing loss in others,35have been reported in ET cases compared with age-matched controls, further drawing attention to the domain of nonmotor manifestations. Although a single disease may have a broad array of clinical manifestations (eg, Huntington disease), such clinical variety can also be an indication that one is dealing with a group of diseases (eg, parkinsonisms such as PD, progressive supranuclear palsy, and corticobasal ganglionic degeneration).