2.3.4 Enhanced physiologic tremor
Symptoms
Enhanced physiologic tremor is a strengthening of physiologic tremor to more visible levels. All the mechanisms discussed in section 2.2** are believed to be involved in the genesis of physiological tremor. The contribution of each of these mechanisms depends on the body part under consideration, its position and the action in which it is involved (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Frequency range of oscillation
The frequency of oscillation for enhanced physiological tremor is reported to be 8 to 12 Hz (Deuschl, Bain, & Brin, 1998)
Prevalence and etiology
Physiologic tremor can be enhanced by stress and fatigue, by taking stimulants and other drugs, by withdrawal from drugs or alcohol, and during certain medical conditions in which elevated thyroid hormones levels or low glucose levels are present. Physiological tremor also becomes more pronounced with age (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Since these causes are very common, enhanced physiological tremor is probably experienced by everybody at some point.
Pathology and treatment
Enhanced physiologic tremor is generally not caused by a neurological disease and is usually reversible by correcting its cause (Tremor fact sheet, 2006).
2.3.5 Psychogenic tremor
Symptoms
Psychogenic tremor can present itself as a rest tremor, action tremor and posture tremor (Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Patients with psychogenic tremor have a conversion disorder, which is defined as a psychological disorder that produces physical symptoms, or suffer from another psychiatric disease (Tremor fact sheet, 2006). Psychogenic tremor cannot be attributed to any damage in the central nervous system. The characteristics of psychogenic tremor vary between patients and show fluctuations in frequency and amplitude per patient (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). The tremor greatly decreases or even disappears when the patient is distracted (Ahmed & Sweeney, 2002) (Smaga, 2003)(McAuley et al., 2004)(uit SP***). During a specific test to diagnose psychogenic tremor, the entrainment test, the patient is asked to tap his fingers on the contralateral side with a certain frequency. The clinician can then check if the frequency of the tremor affected hand shifts to the frequency that the other hand is tapping with. If the patients suffers from a psychogenic tremor the frequency will shift.
Frequency range of oscillation
The frequency of oscillation is much less stable than that of ET or PT (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Frequency of oscillation for psychogenic tremor is reported to be between 4 to 7 Hz (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) and 4 to 10 Hz (Deuschl, Bain, & Brin, 1998).
Prevalence
No information was available on the prevalence of psychogenic tremor.
Etiology, pathology and treatment
Psychogenic tremor results from a psychiatric disease of which the etiology, pathology and treatment will not be discussed.
2.3.6 Orthostatic tremor
Symptoms
Orthostatic tremor (OT) shows a postural tremor in the legs and trunk and is relieved by sitting or walking, which results in a sensation of loss of balance and causes patients to stand with their feet wide apart (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Frequency range of oscillation
The frequency of oscillation of OT is reported to be between 13 Hz and 18 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) and between 14 and 18Hz (Ahmed & Sweeney, 2002).
Prevalence
OT is a rare tremor which is probably underdiagnosed (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). OT has a prevalence lower than 64 cases per 100,000 persons in the United States according to the National Institute of Health.
Etiology
OT is believed to be a variant on essential tremor (Ahmed & Sweeney, 2002) and no other clinical signs or symptoms are present (Ahmed & Sweeney, 2002) (Tremor fact sheet, 2006).
Pathology
No lesions are found using imaging techniques on patients with orthostatic tremor (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). It is presumed that orthostatic tremor had a central origin, although it is unknown which part of the brain is responsible. The brainstem has been proposed to play an important role (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
Treatment
An anticonvulsant, clonazepam, is used in OT, as well as treatments used in essential tremor. Medications are not always effective and lose effectiveness over time (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008)(Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
2.3.7 Less common tremors
Holmes' tremor, which is also known as rubral tremor, is a combination of rest and action tremors. Causes include stroke and multiple sclerosis, where it is possible that there is a delay of weeks to years before tremor occurs (Ahmed & Sweeney, 2002) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). Lesions are most often located in the upper brain stem, thalamus and cerebellum. Holmes' tremor has a low frequency of less than 4.5 Hz (Ahmed & Sweeney, 2002) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Peripheral neuropathy, which may occur when nerves from the muscles are traumatized by injury or disease, can result in an tremor which resembles ET. The tremor may be caused by severely reduced conduction velocities in the nerves, causing a time delay on the stretch reflex (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). The frequency of tremor in neuropathy would therefore probably be dependent on the conduction velocity and the nerve length, as described in section 2.***. Other symptoms are the inability to coordinate voluntary muscle movement of the affected limbs and problems with gait and balance (Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Dystonic tremor is a postural or kinetic tremor (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007)(Tremor fact sheet, 2006) (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). Dystonic tremor occurs in patients suffering from dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions which cause painful and abnormal postures. Reciprocal inhibition and other mechanisms involved in inhibiting reflexes on several levels of the central nervous system seem to be reduced in dystonic patients (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008). When reflexes are not properly inhibited, voluntary movements become difficult due to antagonistic activity. The pathology of primary dystonia is not well understood, it is presumed that the basal ganglia are involved (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007). In secondary dystonia the disorder is brought on by another identified source of brain damage, like trauma or drugs. The frequency of oscillation for dystonic tremor is reported to be 4 to 7 Hz (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007) and 4 to 9 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008).
Task-specific tremor is mainly active while performing very specific actions. An example of task-specific tremor is primary writing tremor, which is induced by writing or similar motor activity. The frequency of the tremor ranges from 4 to 7 Hz (Grimaldi & Manto, Tremor: From Pathogenesis to Treatment, 2008) (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007).
2.4 Overview of discussed tremors
Table 1 shows all discussed forms of tremor and the conditions under which they are active. Distinction is made between characteristic activation conditions (X) and activation conditions which are not in all cases present (O).
Pathological tremor type (section 2.3)
Conditions under which the tremor is active
Table 1 Activation conditions of several tremor types (Adapted from (Rubchinsky, Kuznetsov, Wheelock, & Sigvardt, 2007))
Figure 3Figure 1 shows a speculative scheme of how different oscillators interact to produce different types of tremor.
Figure 3 TEXT*** The dashed lines and boxes indicate those mechanisms that are most uncertain.
(McAuley & Marsden, 2000)
"Peripheral mechanisms refers to those processes where the oscillatory rhythm arises peripherally, even though the primary abnormality is central. For example, a delayed antagonist burst resulting from an abnormality of cerebellar processing might act peripherally by under damping of the body part and thus increasing its mechanical oscillatory tendency."
