Abstract.
Tremor is a common symptom of both neurological and non-neurological
patients, in everyday clinical medical practice. Its correct clinical
assessment may provide important information and guide the further
investigation of the patient. In this article, there is an overview of the
most common forms of tremor that are encountered during daily practice, in
the light of the specific clinical features of each form.
1. Introduction.
The synchronous or alternating contractions of antagonist muscles generate
rhythmic, involuntary, oscillatory movement which is defined as tremor [1].
It may be related to any part or parts of the body and it is roughly
classified into rest or action tremor [2]. In the first case, the affected
area is involuntary activated while it is supported against gravity and in
the second case the terror occurs during a voluntary movement.
The etiology of tremor varies and it may involve both neurological and
non-neurological patients. In any case, taking a careful medical history and
the clinical characteristics of tremor may help to classification and
further investigation.
2. Types of tremor.
2.1 Essential tremor.
This is the most common form of a pathologic tremor. Its prevalence in the
overall population occurs with a frequency of 0.4 to 4% [3]. Its frequency
ranges from 4 to 10 Hz and for a particular patient it remains relatively
constant. It usually occurs as a monosymptomatic disorder, it is bilateral,
it involves arms, head, and less frequently the lower extremities and the
trunk are involved [4]. It is manifested as a kinetic action tremor and
rarely as a rest tremor. Its discovery signals the careful consideration of
any comorbid neurological symptoms, as it may be manifested in the contex of
a neurodegenerative disease [5].
2.2 Parkinsonian tremor.
In its classic manifestation it appears as a rest tremor (pill rolling). It
is absent in a 10-30% of the patients with Parkinson’s disease (PD) [6]
whereas in a 60-70% it may be the main manifestation of the disease for
several years without developing bradykinesia or gait disorder (benign
tremulous PD) [7].
The emergence of tremor in PD is unilateral at least in onset of the
disease. The combination of rest and postural tremor in the form of
re-emergent tremor in PD may be confused with the essential tremor. So,
whereas in a PD patient the tremor subsides when the hands are held
outstretched, it may reemerge within 8-10 seconds as a postural tremor, such
as idiopathic, only the second one occurs immediately (at a time of 0-2
seconds when the patient stretched his hands). The presence of other
clinical signs of PD such as bradykinesia or rigidity helps to identify the
parkinsonian tremor.
2.3 Cerebellar Tremor.
It is due to a lesion of the deep cerebellar nuclei or the outflow pathways
in the superior cerebellar peduncle. Injury to the cerebellar cortex does
not cause tremor [8].
It is an action tremor of both low-frequency (3-5 Hz) and large amplitude.
It is usually referred to as a terminal tremor since it exhibits an
increasing trendancy as the target is approached [1]. It is often
accompanied by other clinical signs of cerebellar lesion, such as ataxia and
dysdiadokinesis. [2].
Structural lesions (tumor, mass, sclerotic plaque, infarct, etc.) cause
unilateral tremor occurrence whereas cerebellum degeneration (alcohol,
narcotic or toxic drugs abuse), leads to bilateral tremor occurrence. The
finding of the coexistence of symptoms associated with cerebellar injury
makes a diagnosis with certainty.
2.4 Neuropathic Tremor.
It is due to peripheral nerves disorders which can cause muscle spasms. It
has been typically described in Charcot-Marie-Tooth disease [9]. It is also
observed in patients with a mild or moderate form of spinal muscular atrophy
and in Kennedy disease as well [10].
2.5 Holmes Tremor.
Lesion to structures of the midbrain near the red nucleus, because of
tumors, strokes, multiple sclerosis, etc., cause malfunction of the
cerebellar outflow tract and they cause tremor like the cerebellar one. It
is a coarse tremor, of low-frequency (3-5 Hz), postural or action tremor
[11]. Clinical signs of the oculomotor nerves or the optic tract malfunction
may coexist. Typical is the sparing of the corticospinal tracts involvement.
2.6 Post-traumatic Tremor.
It can be manifasted in any form, after head injury, within the first 18
months. It is due to central rather than peripheral lesion. After
skull-brain trauma, terror will occur in about a half of the patients over a
period that varies and it spontaneously subsides in about half the cases
[12,13].
2.7 Psychogenic Tremor.
It is the most common movement disorder of psychogenic cause. It is usually
manifested with an abrupt onset, it exhibits a cycling course of remissions
and recurrences, and it rarely affects the fingers [14]. It can appear in
any form while the range and frequency vary. It characteristicaly increases
with the intensity of attention and decreases with its distraction. It does
not respond to conventional antitremor medications but it is improved with
placebo treatment or psychotherapy [15].
2.8 Dystonic Tremor.
It is the terror that occurs in a body part that is affected by dystonia
[2]. Dystonia is manifested as twisting movements or/and abnormal posture,
due to continuous, involuntary contractions of opposing muscles. The
dystonic tremor is usually a rest tremor, exhibits a peak at 5 Hz and has a
characteristic null point. That is, if the patient moves the affected limb
in a position of maximal pull, tremor is modified and often ceases. It can
be the first clinical sign of an evolving dystonia [16].
3. Conclusion.
The tremor diagnosis is based on a careful medical history taking and the
clinical examination as well. The age of onset, the mode of occurrence, the
area of the body that is first-appeared and the progression rate, are
important factors to be taken from the medical history. Clinically, the
affected extremity should be examined in a position of full support, in a
motion state and in various positions of rotation or bent. The finger-nose
test will exhibit kinetic terminal tremors. Finally neurologic signs of a
coexistent or underlying neurological disease should be sought in any
patient with tremor.
References.
1. Deuschl G, Bain P, Brin M. Consensus statement
of the Movement Disorder Society on Tremor. Ad Hoc Scientific Committee. Mov
Disord 1998;13(Suppl 3):2-23.
2. Bain PG. Parkinsonism and related
disorders. Tremor. Parkinsonism Relat Disord 2007;13 (Suppl 3):S369-74.
3. Elble RJ. Report from a U.S. conference on essential tremor. Mov Disord
2006;21:2052-61.
4. Lou JS, Jankovic J. Essential tremor: clinical
correlates in 350 patients. Neurology 1991;41:234-8.
5. Louis ED.
Essential tremor: evolving clinicopathological concepts in an era of
intensive post-mortem enquiry. Lancet Neurol 2010;9:613-22.
6. Hughes AJ,
Daniel SE, Blankson S, et al. A clinicopathologic study of 100 cases of
Parkinson’s disease. Arch Neurol 1993;50:140-8.
7. Josephs KA, Matsumoto
JY, Ahlskog JE. Benign tremulous parkinsonism. Arch Neurol 2006;63:354-7.
8. Elble RJ. Central mechanisms of tremor. J Clin Neurophysiol
1996;13:133-44.
9. Cardoso FE, Jankovic J. Hereditary motor-sensory
neuropathy and movement disorders. Muscle Nerve 1993;16:904-10.
10.
Meriggioli MN, Rowin J, Sanders DB. Distinguishing clinical and
electrodiagnostic features of X-linked bulbospinal neuronopathy. Muscle
Nerve 1999;22:1693-7.
11. Dalvi A. Holmes tremor. In: Lyons KE, Pahwa R,
editors. Handbook of Essential Tremor and Other Tremor Disorders. Boca
Raton, FL: Taylor & Francis, 2005. p. 243-50.
12. Johnson SL, Hall DM.
Post-traumatic tremor in head injured children. Arch Dis Child
1992;67:227-8.
13. Krauss JK, Wakhloo AK, Nobbe F, et al. Lesion of
dentatothalamic pathways in severe post-traumatic tremor. Neurol Res
1995;17:409-16.
14. Deuschl G, Koster B, Lucking CH, et al. Diagnostic
and pathophysiological aspects of psychogenic tremors. Mov Disord
1998;13:294-302.
15. Koller W, Lang A, Vetere-Overfield B, et al.
Psychogenic tremors. Neurology 1989;39:1094-9.
16. Jedynak CP, Bonnet AM,
Agid Y. Tremor and idiopathic dystonia. Mov Disord 1991;6:230-6.