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TREMOR

Nadya Zaragita (= = ) ~| 130110110184 | Tutor B1 NBSS

Definition: a more or less involuntary and rhythmic oscillatory movement produced by


alternating or irregularly synchronous contractions of reciprocally innervated muscles.

General categories:

Normal (or physiologic)


o Present in all contracting muscle groups, throughout the waking state and
in certain phases of sleep
o Very fine movement, can barely be seen by naked eye
o Frequency: 8-13 Hz (usually 10 Hz in adulthood)
o Cause: mechanical activity of cardiac origin, spindle input, unfused grouped
firing rates of motor neurons, natural resonating frequencies and inertia of
the muscles and other structures (hypothesis)

Abnormal (or pathologic)


o Affects certain muscle groupsthe distal parts of the limbs (especially the
fingers and hands); less often, the proximal parts; the head, tongue, jaw, or
vocal cords; and rarely the trunkand is present only in the waking state.
o Frequency: 4 to 7 Hz
o In clinical analysis, they are usually distinguishable on the basis of (1)
rhythmicity, (2) amplitude, (3) frequency, and (4) relation to movement,
postural set, and relaxation.
POSTURAL AND ACTION TREMORS

Present when the limbs and trunk are actively maintained in certain positions (such as
holding the arms outstretched) and that may persist throughout active movement.

The tremor is absent when the limbs are relaxed but becomes evident when the
muscles are activated.

Characterized by relatively rhythmic bursts of grouped motor neuron discharges that


occur not quite synchronously and simultaneously in opposing muscle groups.

Types of action tremors:


o Enhanced Physiologic Tremor

An exaggeration of normal or physiologic tremor.

Frequency: 10 Hz, but a greater amplitude.

Best elicited by holding the arms outstretched with fingers spread apart

Characteristic of intense fright and anxiety, certain metabolic


disturbances (hyperthyroidism, hypercortisolism, hypoglycemia),
pheochromocytoma, intense physical exertion, withdrawal from alcohol
and other sedative drugs, and the toxic effects of several drugs
lithium, nicotinic acid, xanthines (coffee, tea, aminophylline, colas), and
corticosteroids.
o Alcohol Withdrawal Tremor

Frequency:

>8 Hz and continuous activity in antagonistic muscles, thus


resembling physiologic tremor but of greater amplitude and
responsive to propranolol (Koller et al).

<8 Hz, is characterized by discrete bursts of EMG activity


occurring synchronously in antagonistic muscles, like that
observed in one type of familial tremor.
o Essential (Familial) Tremor

Most Common.

Frequency: 4 to 8 Hz

Very often occurs as the only neurologic abnormality in several


members of a family.

Inheritance is as an autosomal dominant trait with virtually complete


penetrance.

Appears late in the second decade, but it may begin in childhood and
then persist.

The frequency diminishes slightly with age while its amplitude


increases.

The identifying feature is its appearance or marked enhancement with

attempts to maintain a static limb posture.


Worsened by emotion, exercise, and fatigue.
Generated by more or less rhythmic and almost simultaneous bursts of
activity in pairs of agonist and antagonist muscles.

Treatment: reduce alcohol consumption, beta-adrenergic antagonist


propranolol or metoprolol or nadolol, anticonvulsant primidone
(Mysoline, in low doses of 25 to 50 mg initially and raised slowly) of
time, gabapentin, topiramate, amantadine,
o Tremor of Polyneuropathy

In patients with chronic demyelinating and paraproteinemic


polyneuropathies

Caused by IgM antibodies to myelin-associated glycoprotein (MAG)

Vary greatly in amplitude with considerable side-to-side oscillation

It is hypothesized that there is a disturbance of muscle spindle


afferents.
o Other Forms of Action Tremor

Anatomy and mechanism are obscure.


PARKINSONIAN (REST) TREMOR

A coarse, rhythmic tremor.

Frequency: 3-5 Hz, variable amplitude.

Electromyographically, characterized by bursts of activity that alternate between


opposing muscle groups.

Location: in one or both hands and forearms and less frequently in the feet, jaw, lips,
or tongue.

Takes the form of flexion-extension or abduction-adduction of the fingers or the hand;


pronation-supination of the hand and forearm is also a common presentation (pillrolling tremor).

Occurs when the limb is in an attitude of repose and is suppressed or


diminished by willed movement, at least momentarily, only to reassert itself
once the limb assumes a new position.

Under conditions of complete rest (in all except the lightest phases of sleep) the tremor
disappears.

It continues while the patient walks; it may become apparent or be exaggerated during
walking.

The eyelids, if they are closed lightly, tend to flutter rhythmically (blepharoclonus), and
the tongue, when protruded, may move in and out of the mouth at about the same
tempo as the tremor elsewhere.

Resting tremor is most often a manifestation of the Parkinson syndrome.

In some of these patients, the tremor is followed years later by the other
manifestations of Parkinson disease, but in many others it is not, the tremor remaining
unchanged for many years or progressing very slowly, unaffected by anti-Parkinson
drugs.

Suppressed by: phenothiazine derivative ethopropazine (Parsidol), trihexyphenidyl


(Artane), and other anticholinergic drugs; less consistently L-dopa and dopaminergic
agonist drugs.
INTENTION (ATAXIC) TREMOR

Its salient feature is that it requires for its full expression the performance of an
exacting, precise, projected movement.

The tremor is absent when the limbs are inactive and during the first part of a
voluntary movement, but as the action continues and fine adjustments of the
movement are demanded (e.g., in touching the tip of the nose or the examiners
finger), an irregular, more or less rhythmic (2- to 4-Hz) interruption of forward
progression with side-to-side oscillation appears and may continue for several beats
after the target has been reached.

This type of tremor points to disease of the cerebellum or its connections, particularly
via the superior cerebellar peduncle, but certain peripheral nerve diseases may
occasionally simulate it.

More violent type of tremor associated with cerebellar ataxia (lifting the arm slightly or
maintaining a static posture with the arms held out to the side) lesion is usually in
the midbrain, involving the upward projections of the dentatorubrothalamic fibers and
the medial part of the ventral tegmental reticular nucleus.

Betaadrenergic blocking agents, anticholinergic drugs, and L-dopa have little


therapeutic effect.

Geniospasm: strongly familial episodic tremor disorder of the chin and lower lip that
begins in childhood and may worsen with age.

Primary Orthostatic Tremor: A rare tremor isolated to the legs that is remarkable by
its occurrence only during quiet standing and its cessation almost immediately on
walking. Frequency:14 to 16 Hz, making it difficult to observe and more easily palpable.
Causes the sensation of imbalance. Many of these cases have responded to the
administration of clonazepam, gabapentin, mysoline, or sodium valproate.

Dystonic Tremor: Tend to be focal in the neck, which is typically rotated slightly to
one side, or they may be evident in one dystonic hand. The tremor is not entirely
rhythmic, sometimes jerky, and often intermittent.
HYSTERICAL TREMOR

Tremor is a relatively rare but quite dramatic manifestation of hysteria.

Hysterical tremors are usually restricted to a single limb; they are gross in nature, are
less regular than the common static or action tremors, and diminish in amplitude or
disappear if the patient is distracted, as, for example, when asked to make a complex
movement with the opposite hand.

If the affected hand and arm are restrained by the examiner, the tremor maymove to a
more proximal part of the limb or to another part of the body (chasing the tremor).

Hysterical tremor persists in repose and during movement and is less subject than
nonhysterical tremors to the modifying influences of posture and willed movement.

Tremors of Mixed or Complex Type

Not all tremors correspond exactly with those described above.


The features of one type of tremor may be so mixed with those of another that
satisfactory classification is not possible.

Pathophysiology of Tremor

In patients with tremor of either the parkinsonian, postural, or intention type,


Narabayashi has recorded rhythmic burst discharges of unitary cellular activity in the
nucleus intermedius ventralis of the thalamus (as well as in the medial pallidum and
subthalamic nucleus) synchronous with the beat of the tremor.
Neurons that exhibit the synchronous bursts are arranged somatotopically and respond
to kinesthetic impulses from the muscles and joints involved in the tremor.
A stereotaxic lesion in any of these sites abolishes the tremor.
Essential Tremor
o Action tremors of essential and familial type can be abolished or diminished
(contralaterally) by small stereotactic lesions of the basal ventrolateral nucleus
of the thalamus by strokes that interrupt the corticospinal system, and by gross
unilateral cerebellar lesions.
o The locus of the generator for essential tremor is still unknown.
o Based on electrophysiologic recordings in patients, two likely origins of
oscillatory activity are the olivocerebellar circuits and the thalamus.
o Whether a particular structure possesses an intrinsic rhythmicity or, as
currently favored, the tremor is released by disease as an expression of
reciprocal oscillations in circuits of the dentato-brainstemcerebellar or
thalamic-tegmental systems is not at all clear.
o Studies of blood flow in patients with essential tremor affirmed that the
cerebellum is selectively activated.
o Dubinsky and Hallett have demonstrated that the inferior olives become
hypermetabolic when essential tremor is activated, but this has been
questioned by Wills and colleagues, who recorded increased blood flow in the
cerebellum and red nuclei but not in the olive.
Parkinsonian Tremor
o The exact anatomic basis of parkinsonian tremor is not known.
o In Parkinson disease, the visible lesions predominate in the substantia
nigra, and this was true also of the postencephalitic form of the disease.
o In animals, however, experimental lesions confined to the substantia nigra do
not result in tremor; neither do lesions in the striatopallidal parts of the basal
ganglia.
o Ward and others have produced a Parkinson-like tremor in monkeys by placing
a lesion in the ventromedial tegmentum of the midbrain, just caudal to the red
nucleus and dorsal to the substantia nigra.
o Ward postulated that interruption of the descending fibers at this site liberates
an oscillating mechanism in the lower brainstem; this presumably involves the
limb innervation via the reticulospinal pathway.

Alternative possibilities are that the lesion in the ventromedial tegmentum


interrupts the brachium conjunctivum, or a tegmental- thalamic projection, or
the descending limb of the superior cerebellar peduncle, which functions as a
link in a dentatoreticularcerebellar feedback mechanism, a hypothesis similar
to the one proposed for essential tremor.

Ataxic tremor
o This has been produced in monkeys by inactivating the deep cerebellar nuclei
or by sectioning the superior cerebellar peduncle or the brachium conjunctivum
below its decussation.
o A lesion of the nucleus interpositus or dentate nucleus causes an ipsilateral
tremor of ataxic type, as one might expect, associated with other
manifestations of cerebellar ataxia.
PALATAL TREMOR (PALATAL MYOCLONUS)

A rare and unique disorder consisting of rapid, rhythmic, involuntary movements of the
soft palate.
There are two forms:
o Essential palatal tremor and reflects the rhythmic activation of the tensor veli
palatini muscles; it has no known pathologic basis. The palatal movement
imparts a repetitive audible click, which ceases during sleep.
o Symptomatic palatal tremor; it involves the levator veli palatini muscles and is
due to a diverse group of brainstem lesions that interrupt the central tegmental
tract(s), which contain descending fibers from midbrain nuclei to the inferior
olivary complex. Its sometimes associated with oscillopsia and uilateral or
bilateral cerebellar signs.

Magnetic resonance imaging reveals no lesions to account for essential palatal tremor;
in the symptomatic form, however, one can see the tegmental brainstem lesions and
conspicuous enlargement of the inferior olivary nucleus unilaterally or bilaterally.

It has been proposed that the lesions in the symptomatic form interrupt the circuit
(dentate nucleusbrachium conjunctivum central tegmental tractolivary nucleus
dentate nucleus) that Lapresle and Ben Hamida have called the triangle of Guillain and
Mollaret.

Clonazepam, sodium valproate, and gabapentin have suppressed the movement in


some cases. Tetrabenazine and haloperidol have been helpful on occasion.
REFERENCE:
Ropper, AH. Brown, RH. Adams and Victors Principles of Neurology. 8 th edition. McGraw-Hill;
2005.
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