Tremors exist in many conditions. This article describes, the diagnosis,
treatment and care of those with tremors. It is presented here for education and
research.
 
Tremor
 
Marjorie M. Gillespie
 
ABSTRACT:       Tremor is a rhythmic, involuntary muscular contraction
with consistency of rate, amplitude and pattern. It is the most
common of all involuntary movements. Several systems for
classifying tremor exist with the most frequent system classed
according to behavioral context, ie, resting, postural and
action. Clinical recognition of tremor type is extremely
important as type determines prognosis, treatment, and need for
genetic counseling. The most common forms are parkinsonian,
physiological, cerebellar intention and essential tremor.
Essential or hereditary tremor is the most common of all
neurologic conditions with 3-4 million Americans affected.
Nursing implications of caring for essential tremor patients are
presented.
J Neuroscience Nursing 1991;23(3):170-174.
Questions or comments about this article may be directed to
Marjorie M. Gillespie, RNC,BS,FNP at the National Institute of
Health, 9000 Rockville Pike, Bldg. 10, Room 5c103, Bethesda,
Maryland 20892. She is a research nurse.
 
Copyright American Association of Neuroscience Nurses
0047-2603/91/2303-0170$1.25
 
Introduction
 
 Almost everyone experiences tremor at some point in life. It is
a symptom which occurs as an exaggeration of normal physiologic
mechanisms, in isolated monosymptomatic syndromes (essential
tremor) or as a manifestation of a variety of neurologic
diseases (the most common being Parkinson's disease).[1] This
article describes and differentiates the major forms of tremor
while focusing on the movement disorder known as essential or
hereditary tremor.
 
Tremor Characteristics
 
 Tremor is described as a rhythmic, involuntary muscle
contraction with consistency of rate, amplitude and pattern.
Most tremors result from regular, oscillatory contractions of
agonistic and antagonistic muscles.[2] The involuntary
oscillation is often continuous, but as with other movement
disorders disappears with sleep. Two important characteristics
of tremor are amplitude or size of tremor and frequency or rate
of oscillation. Frequency is described in units called Hertz
(Hz) with one Hertz equal to one cycle per second. With the use
of computerized accelerometers, the physiologic characteristics
of tremor can be precisely measured. This becomes important in a
research setting, but in the average clinical setting they are
generally estimated by observing the patient. Tremor
characteristics can also be categorized by electromyographic
(EMG) activity.
 
 Tremor can affect various body parts such as the hands, head,
facial structures (chin, tongue, lips and ears), vocal cords,
trunk and legs. Ninety-four percent of all tremors occur in the
hands and may be unilateral or bilateral. Tremor has been
classified in various ways, most commonly by behavioral context
or position. Resting or static tremor occurs when the muscle is
at rest such as when the hands are on the lap. Postural tremor
occurs with attempting to maintain a posture, for example, with
hands extended. Action or intention tremor occurs during
purposeful movement.
 
 Tremor is a clinical sign which may be caused by numerous
conditions (Table 1). Since postural end action tremors often
occur together, they are combined here. There can be overlap
with some conditions having tremor in more than one behavioral
context. The tremor of Parkinson's disease is the most common
resting tremor, while physiologic, exaggerated physiologic and
essential are the most common postural action tremors.
Cerebellar dysfunction is the primary cause of intention tremor.
Occasionally essential tremor can occur at rest and parkinsonian
tremor can be present during posture and intention, but this is
usually seen in the more severe cases. Listed under exaggerated
physiological tremor are various causal factors, all of which
may increase other tremors as well. Variants of essential tremor
include primary writing tremor (occurs only when writing) and
orthostatic tremor (occurs in legs and trunk when standing, but
not walking).
 
 In addition to distinguishing one tremor type from another,
there are other abnormal involuntary movements which can
sometimes resemble tremor. These include psychogenic or
hysterical tremor, myoclonus, asterixis, spasms of dystonia,
tics or chorea. Hysterical tremor is suspected when tremor is
not rhythmic and changes or stops when the patient is distracted
or asked to perform mental calculations. Myoclonus and asterixis
are brief irregular jerky movements often caused by metabolic
encephalopathies or a structural central nervous system lesion.
Dystonic spasms, tics and chorea are other involuntary movements
which can appear as tremors when they have a regular pattern.
 
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Table 1
 
             Classification of Tremor
 
Rest tremors
 
  Parkinson's disease
  Other parkinsonian syndromes (less commonly)
  Wilson's disease
  Essential tremor-only if severe
 
Postural action tremors
 
  Physiological tremor
  Exaggerated physiological tremor (the following factors
  can also aggravate other forms of tremor)
    Stress, fatigue, anxiety, emotion
 
    Endocrine: hypoglycemia. thyrotoxicosis,
         pheochromocytoma, adrenocorticosteroids
    Drugs and toxins: beta agonists, dopamine agonists.
      amphetamines, lithium, tricyclic antidepressants,
      neuroleptics, theophylline, caffeine, valproic acid,
      alcohol withdrawal, mercury, lead arsenic and others
   Essential tremor (hereditary or sporadic)
   Other neurologic disorders
    Parkinson's disease (occasionally)
    Dystonia
   Peripheral neuropathy
   Cerebellar tremor
 
Intention tremors
   Disease of cerebellum
   Multiple sclerosis, trauma, tumor, vascular, acquired
    hepatocerebral degeneration, drugs, toxins (eg, mercury)
   and others
 
Adapted from Weiner WJ, Lang AE: Tremor. Page 245 in: Movement
Disorders: A Comprehensive Survey. Futura  Publishing. 1989.
 
-----------------------------------------------------------
 
Tremor Types
 
 Tremor in Parkinson's disease is predominantly of a
resting type although postural and intentional tremors can be
present as well. Stressful situations may enhance the tremor.
Resting tremor is somewhat of a misnomer because when patients
are lying entirely relaxed, there is often no tremor. On the
other hand, when they are relaxing with some tone (ie, holding
hands on lap), an involuntary tremor of the hands and sometimes
a similar tremor of the face, jaw, neck and legs appears. When
the patient voluntarily uses the limb or changes its position,
the tremor either entirely disappears or is markedly reduced.[3]
After a while, sometimes only seconds, tremor returns when the
limb is held in a new position. This tremor is often described
as "pill rolling" because the thumb and finger movements give
the appearance of rolling a small object. Parkinsonian tremor is
present when walking, disappears with sleep, increases with
stress and does not improve with alcohol. The frequency is
characteristically 4-5 Hz but can be between 3 and 7Hz on
occasions. In addition to tremor, parkinsonian patients usually
have other basal ganglia symptoms of bradykinesia, rigidity and
abnormalities of postural reflexes. The etiology of Parkinson's
disease is unknown but many theories exist, including
environmental and genetic causes. The pathophysiology of the
parkinsonian tremor is thought to be substantia nigral
degeneration with striatal dopamine deficiency.[3]
 
 Tremor at rest is more of an embarrassment than
a handicap because it tends to disappear during purposeful
action. However, some patients find tremor the most annoying
symptom. Occasionally, resting tremor can produce functional
disability such as difficulty dressing or eating. The tremor
usually responds to dopaminergic or anticholinergic therapy, but
can be the most difficult of the parkinsonian symptoms to treat.
 
Physiological Tremor
 
 Everyone has a very low amplitude tremor that can occasionally
be observed when the arms are extended and made even more
obvious by placing a paper over the hands. This is a normal
physiological phenomenon. During times of stress or for various
other reasons, the tremor amplitude becomes enlarged and it is
called exaggerated physiological tremor. The frequency is
usually 8-12 Hz. The pathophysiology is thought to involve the
sympathetic nervous system and in particular the noradrenergic
system. Experiments have shown physiologic tremor can be
increased by intravenous or intraarterial infusions of adrenalin
and can he blocked by beta blockers.
 
 The best treatment for enhanced physiological tremor is to
withdraw the precipitating cause if possible. If this is not
possible, such as with a musician or actor with stage fright,
treatment with low dose beta-adrenoreceptor antagonists may be
useful. If this is a very rare event, an occasional dose of
diazepam may be effective. Reassuring patients this is a normal
response may help to set their minds, at ease.
 
Cerebellar Intention Tremor
 
 Cerebellar intention tremor is an action tremor which occurs
during goal-directed movement such as touching finger to nose.
Tremor intensity increases as the target is approached.
Intention tremor without postural tremor most frequently results
from cerebellar dysfunction. It can be flapping or wing beating
in character, resembling a bird flapping its wings. Cerebellar
intention tremor can be extremely disabling with some patients
unable to perform any purposeful actions. It is believed to be
caused by a loss of modulatory control and feedback mechanisms
in the cerebellar connections. Most cerebellar intention tremors
are difficult to treat, such as those seen in patients with
multiple sclerosis. There is no drug which significantly
improves cerebellar intention tremor and although stereotactic
thalamotomy may improve the tremor it does not improve
function.[4] It is believed thalamotomy works by eliminating
tremor from the contralateral side by interruption of circuits
mediating input to the motor system from both basal ganglia and
cerebellum.[3]
 
Essential Tremor
 
 Essential tremor is the most common of all neurologic
conditions. An estimated 2-4 million people in the United States
have such tremor In approximately  one-half of the cases the
disease is familial. The disease is an autosomal dominant trait
which means children of an affected individual will have a 50%
chance of developing tremor.
 
 Essential tremor is characterized by the presence of a postural
action tremor seen especially in the upper extremities without
parkinsonian, cerebellar or other neurologic signs. When there
is a family history, it is called familial tremor. When it is
sporadic, it is called essential or benign, although it is often
not benign for the patient. When it is sporadic without family
history and onset over age 65 it is sometimes called senile
tremor. For the purposes of this discussion it will be called
essential tremor.
 
 Age of onset varies widely from childhood through adulthood
with a mean age of 45 years. Onset is usually insidious
beginning unilaterally with progressive involvement of upper
extremities over 2-3 years, and sometimes lower extremities.
Head and voice involvement are very common. The head tremor may
be either affirmative (up and down in direction) or negative
(side to side) and is often the least responsive to treatment.
Speech has a characteristic quivering intonation which results
in a fluctuating and rhythmical sound. The tremor time
progression is variable.
 
 The tremor frequency is characteristically 4-9 Hz. The amplitude
varies greatly and is influenced by the same factors as
physiological tremor. Usually essential tremor is most evident
with hands held in posture and during voluntary movement. When
it is severe, it may persist even at rest making distinction
from parkinsonian tremor difficult. It is estimated 10% of
patients diagnosed with Parkinson's disease really have
essential tremor[3] Other factors distinguishing essential
tremor from parkinsonian tremor are the lack of accompanying
symptoms of bradykinesia, rigidity and impaired reflexes,
absence during walking, lack of response to conventional
parkinsonian medication, response to alcohol and beta
adrenoreceptor antagonists and positive family history.
 
 The etiology and pathophysiology of essential tremor are not
known, but research has led to many theories implicating both
the central and peripheral nervous systems. These include
central oscillator defects, altered mechanical properties of the
limb and alteration in motor neuron firing patterns. It is
generally felt combination of both central and peripheral
mechanisms are responsible for producing the tremor.[1]
 
 Neuropathologic studies of autopsy cases have found no
significant pathology. No abnormalities in muscle spindle
feedback or sensitivity of peripheral beta receptors has been
detected. Yet unpublished preliminary results using positron
emission tomography (PET) scanning show alteration of glucose
metabolism) in the thalamus and inferior olives of essential
tremor patients. The inferior olives are in the medulla and
serve as input pathways to the cerebellum. The thalamus has long
been suspected because stereotactic thalamotomy has been shown to
stop tremor in severe refractive cases. The thalamus relays muscle
control signals from the cerebellum and brainstem to the motor
cortex and basal ganglia.
 
 The treatment of essential tremor depends upon degree of
functional disability. This tremor is more disabling than
parkinsonian tremor because it occurs with action. An estimated
15% of patients are forced to retire from their jobs and 3% are
totally disabled.[1] When essential tremor is mild and causes no
disability, medication may not be necessary and simply
reassuring patients the tremor is not indicative of a serious
neurologic disease may be sufficient. Drug treatments currently
in use are unpredictable, often do not completely relieve the
tremor and have unpleasant side effects. Some patients may
require only periodic treatment and others continuous drug
therapy. As a last resort, a few patients with very severe and
disabling tremor (who do not respond to medical treatment) may
be helped by thalamotomy.
 
 Sedatives and minor tranquilizers (such as diazepam) were the
first drugs used to treat essential tremor. Many patients still
rely on this treatment to quiet the tremor in specific
situations. Alcohol in small quantities (a single cocktail or
beer) will often suppress the tremor for 30-60 minutes. This
response is sometimes used as a diagnostic measure.[1]
 
 Beta adrenoreceptor antagonists (beta blockers) provide the
most effective treatment of essential tremor. This was
discovered serendipitously when a physician noticed the effect
of propranolol (Inderal) on a patient's tremor while treating
him for atrial tachycardia. Propranolol is the most commonly
used drug with an optimal dose of 120 mg producing improvement
in 75% of patients with essential tremor.[3] Other beta blockers
have also been shown to be effective in reducing tremor. Table 2
shows frequently used medications, contraindications, and
adverse effects.
 
 In addition, primidone (Mysoline) has also been found effective
in reducing amplitude of tremor in doses of 50-250 mg/day.
Primidone is an antiepileptic drug with two active metabolites,
phenyl-ethyl  malonamide (PEMA) and phenobarbital. Its method of
action is not known.
 
------------------------------------------------------------------------
 
                               Table 2
 
                    Essential Tremor Medications
 
Medication           Initial/Max Dose Contraindications Adverse effects
 
1. Beta adrenorecptor                 Heart block            Bradycardia
   antagonists                        Sinus Bradycardia      Hypotension
 
propranolol (Inderal) 10/480 mg tid  Bronchial asthma(except Depression
nadolol (Corgard)     40/240 mg qd   metoprolol)           General slowing
timolol (Blocadren)   10/60 mg bid   Congestive Heart Fail Hallucinations
metoprolol (Lopressor)50/200 mg bid  Diabetes mellitus     Insomnia
atenolol (Tenormin)   50/200 mg qd                         Weight gain
                                                           Impotency
                                                       Nausea and vomiting
 
2. Primidone (Mysoline)25/250 mg qd  Porphyria              Ataxia
                                     Phenobarbital          Vertigo
                                    hypersensitivity   Nausea and vomiting
                                                        Hyperirritability
                                                            Impotency
                                                            Anemia
                                                            Depression
                                                            Sedation
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Nursing Implications
 
 The nursing care of patients with essential tremor varies with
severity of the tremor and disability. Some patients (especially
mild or familial cases) accept the tremor, learn to live with it
and may never seek medical attention. Other more severely
affected individuals may require extensive treatment and nursing
care. In assessing and caring for tremor patients, there are
several important factors specific to this illness the
neuroscience nurse should keep in mind.
 
 When eliciting a tremor history it is important to know the age
at onset, pattern of onset and progression, factors improving or
exacerbating tremor, any medications tried and the response, any
history of other medications which may cause tremor, caffeine
and alcohol intake, effect of alcohol on the tremor and family
history. It is also important to question the patient about any
history of bronchial asthma which be exacerbated by beta
adrenoreceptor antagonists or any history of heart block, sinus
bradycardia, congestive heart failure or diabetes which would be
contraindications to beta adrenoreceptor antagonist therapy. In
addition, the pulse rate should be greater than 50 with no lying
or standing hypotension if beta adrenoreceptor antagonists are
to be used.
 
 The physical assessment begins by carefully observing for
resting tremor in the head, face, arms, hands, trunk, legs and
feet while the patient is sitting quietly. Listen to voice
quality for any vocal tremor. If present, the voice will have a
quivering intonation. Then ask the patient to sit with hands on
lap, arms outstretched and touch finger to nose. These positions
will allow you to assess resting, postural and action tremors in
arms. If resting tremor is present, you should also check for
rigidity and have the patient touch each finger to thumb to
assess rapid alternating movements. Writing is also important in
assessing upper extremity tremor It is useful to have the
patient draw a spiral and write his name. Unlike the
micrographia of Parkinson's disease, the essential tremor
patients writing is very large and shaky. Observe the lower
extremities at rest, hold legs out, tap toes and run the heel
down the shin. As the patient walks, observe the gait as well as
tremor in hands and arm swing. Check balance by asking the
patient to stand with feet together and gently pulling toward
you. Unlike parkinsonian patients, essential tremor should not
cause loss of balance, decreased arm swing or gait abnormalities.
 
 It is important in reporting the tremor to note the body part
or parts involved, the positional context in which the tremor
occurs, any additional neurologic findings and the approximate
frequency and amplitude of the tremor (can be described as
coarse, fine, rapid, slow, etc). If there is a family history, a
family genogram would provide useful information.
 
 When planning nursing interventions or teaching the patient or
caregiver, the nurse needs to assess ability to perform
functions of daily living and provide assistance where needed.
Many of these patients have difficulty with personal hygiene,
dressing, writing and feeding. Ambulation, especially on stairs
may also be a problem if the patient has head or lower extremity
tremor or even upper extremity involvement making holding onto
hand railings impossible. Nutritional status may be compromised
due to difficulties eating. drinking and preparing food. These
patients may have inadequate caloric intake and should have
their weight monitored regularly. They may require food
supplements.
 
 In addition to functional disabilities, the social and
psychological impact of the disease must also be assessed. Many
of these patients tend to withdraw from social situations,
especially those requiring eating and drinking. Depression is
common due to the altered physical appearance and loss of
function. Family relationships may be affected because of the
functional disabilities which may cause role reversals or the
need to relinquish duties previously performed.
 
 Teaching is a very important part of the nursing care. It
should include education about the illness, practical solutions
to annoying disabilities and medication information. Some
practical suggestions include velcro closure on clothes instead
of buttons and zippers, use of special eating utensils,
increased use of finger foods and straws. Many banks will now
approve the use of signature stamps for patients who cannot
write their names, a very common problem. Caregivers should also
be taught to let patients care for themselves as much as
possible without becoming frustrated. This is often very
difficult. Medication teaching should be frequently reinforced.
Patients receiving any of the beta adrenoreceptor antagonists
should be aware of adverse effects and taught to take their
pulse daily (at least in the beginning stages of treatment).
They should also have frequent lying and standing blood pressure
checks. These drugs should not be stopped abruptly, because of
possible rebound cardiac effects. When primidone is used,
patients should be instructed about possible adverse effects and
the fact this drug should also be tapered to avoid rebound
tremor phenomenon. It should be started at very low doses and
gradually increased since there is a high initial incidence of
adverse effects. Patients should be warned of the potential for
alcohol or sedative addiction if they frequently use these
methods to control the tremor.
 
 The patient and family should be educated about the disease
itself. One good source of information is the International
Tremor Foundation in Chicago.* The foundation supplies printed
information, patient and family services, newsletters and
educational symposia for patients and families.
 
 Depending upon the individual's life situation, some patients
may benefit from referrals to occupational therapy as well as
genetic and vocational counseling. Occupational therapy can
often provide useful advice and tools to help with activities of
daily living. Genetic counseling is especially important for
young patients who may worry about passing the tremor to future
generations. patients with a positive family history should know
their children will have a 50% chance of inheriting the tremor.
 
* International Tremor Foundation, 360 West Superior Street,
Chicago, Illinois 60610, 312-664-2344.
 
 Vocational and educational counseling may include direction of
young patients or children with strong family histories to
careers which do not require fine motor skills or public
appearances. Career changes may be necessary for those who
cannot function in their current occupation.
 
Summary
 
 Essential tremor, although not life threatening as many
neurologic disorders are, can none the less be very disabling
for affected individuals. It is by no means a benign tremor as
it is often termed. However, effective treatment is available
for most tremor patients. Neuroscience nurses can make
significant contributions to the assessment, treatment and day
to day living of tremor patients.
 
Acknowledgment
 
 The author wishes to thank Mark Hallett, MD and Thomas Chase,
MD for their assistance and ongoing support and to express deep
gratitude to Donna Thomas for her assistance.
 
References
 
1. Weiner WJ. Lang AE: Tremor. Pages 221-249 in: Movement
Disorders: A comprehensive Survey, Futura Publishing,1989
2. Malasanos LJ: Tremors; Associations and assessment. J
Neurosurg Nurs 1982; 14(6):290-294.
3. Young RR: Tremor. Pages 435-451 in: Diseases of the Nervous
System: Clinical Neurobiology, Asbury AK. McKhann GM, McDonald
WI (editors). WB Sanders, 1986.
4. Hallett M; Differential diagnosis of tremor. Pages 553-595
in: Handbook of Clinical Neurology, Vikin PJ, Bruyn GW. KIawans
HL (editors). Elsevier Science Publishers, 1989. 5. Findlay LJ,
Koller WC; Essential tremor: A review, Neurology 1987;
37:1194-1197.
 
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