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461
sion, muscle twitching, seizures, nausea, vomiting, and oliguria.
◆ Fracture. Localized spasms and pain are
mild if the fracture is nondisplaced, intense if
it’s severely displaced. Other findings include
swelling, limited mobility and, possibly, bony
crepitation.
◆ Hypocalcemia. The classic feature is
tetany—a syndrome of muscle cramps and
twitching, carpopedal and facial muscle
spasms, and seizures, possibly with stridor.
Both Chvostek’s and Trousseau’s signs may be
elicited. Related findings include paresthesia of
the lips, fingers, and toes; choreiform movements; hyperactive deep tendon reflexes; fatigue; palpitations; and cardiac arrhythmias.
◆ Hypothyroidism. Muscle involvement may
produce spasms and stiffness, along with leg
muscle hypertrophy or proximal limb weakness
and atrophy. Other findings include forgetfulness and mental instability; fatigue; cold intolerance; dry, pale, cool, doughy skin; puffy face,
hands, and feet; periorbital edema; dry, sparse,
brittle hair; bradycardia; and weight gain despite anorexia.
◆ Muscle trauma. Excessive muscle strain
may cause mild to severe spasms. The injured
area may be painful, swollen, reddened, or
warm.
◆ Respiratory alkalosis. Acute onset of mus-
cle spasms may be accompanied by twitching
and weakness, carpopedal spasms, circumoral
and peripheral paresthesia, vertigo, syncope,
pallor, and extreme anxiety. With severe alkalosis, cardiac arrhythmias may occur.
◆ Spinal injury or disease. Muscle spasms
can result from spinal injury, such as cervical
extension injury or spinous process fracture, or
from spinal disease such as infection.
O
THER CAUSES
◆ Drugs. Common spasm-producing drugs in-
clude diuretics, corticosteroids, and estrogens.
P
EDIATRIC POINTERS
Muscle spasms rarely occur in children. However, their presence may indicate hypoparathyroidism, osteomalacia, rickets or, rarely, congenital torticollis.
Muscle spasticity
[Muscle hypertonicity]
Spasticity is a state of excessive muscle tone
manifested by increased resistance to stretching
and heightened reflexes. It’s commonly detected
by evaluating a muscle’s response to passive
movement; a spastic muscle offers more resistance when the passive movement is performed
quickly. Caused by an upper-motor-neuron lesion, spasticity usually occurs in the arm and
leg muscles. Long-term spasticity results in
muscle fibrosis and contractures. (See How
spasticity develops, page 462.)
H
ISTORY AND PHYSICAL
EXAMINATION
Once you detect spasticity, ask the patient about
its onset, duration, and progression. What, if
any, events precipitate onset? Has he experienced other muscular changes or related symptoms? Does his medical history reveal any incidence of trauma or degenerative or vascular
disease?
Take the patient’s vital signs, and perform a
complete neurologic examination. Test reflexes
and evaluate motor and sensory function in all
limbs. Evaluate muscles for wasting and contractures.
During your examination, keep in mind that
generalized spasticity and trismus in a patient
with a recent skin puncture or laceration indicates tetanus. If you suspect this rare disorder,
look for signs of respiratory distress. Provide
ventilatory support, if necessary, and monitor
the patient closely.
S
PECIAL CONSIDERATIONS
Depending on the cause, help alleviate your
patient’s spasms by slowly stretching the affected muscle in the direction opposite the
contraction. If necessary, administer a mild
analgesic.
Diagnostic studies may include serum calcium, sodium and carbon dioxide levels, thyroid
function tests, and blood flow studies or arteriography.
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. This disor-
der commonly produces spasticity, spasms,
coarse fasciculations, hyperactive deep tendon
reflexes, and a positive Babinski’s sign. Earlier
effects include progressive muscle weakness
and flaccidity that typically begin in the hands
and arms and eventually spread to the trunk,
neck, larynx, pharynx, and legs; progressive
respiratory muscle weakness leads to respiratory
insufficiency. Other findings include dysphagia,
dysarthria, excessive drooling, and depression.
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How spasticity develops
Motor activity is controlled by pyramidal and
extrapyramidal tracts that originate in the motor cortex, basal ganglia, brain stem, and
spinal cord. Nerve fibers from the various
tracts converge and synapse at the anterior
horn in the spinal cord. Together, they maintain segmental muscle tone by modulating the
stretch reflex arc. This arc, shown in simplified
form below, is basically a negative feedback
Spinal cord
Anterior horn
Proprioceptor nerve
Muscle spindle
loop in which muscle stretch (stimulation)
causes reflexive contraction (inhibition), thus
maintaining muscle length and tone.
Damage to certain tracts results in loss of inhibition and disruption of the stretch reflex arc.
Uninhibited muscle stretch produces exaggerated, uncontrolled muscle activity, accentuating the reflex arc and eventually resulting in
spasticity.
Motor nerve
◆ Epidural hemorrhage. With this disorder,
bilateral limb spasticity is a late and ominous
sign. Other findings include a momentary loss
of consciousness after head trauma, followed
by a lucid interval and then a rapid deterioration in level of consciousness. The patient
may also develop unilateral hemiparesis or
hemiplegia; seizures; fixed, dilated pupils;
high fever; decreased and bounding pulse;
widened pulse pressure; elevated blood pressure; irregular respiratory pattern; and decerebrate posture. A positive Babinski’s sign can
be elicited.
◆ Multiple sclerosis. Muscle spasticity, hyper-
reflexia, and contractures may eventually develop; earlier muscle changes include progressive
weakness and atrophy. Associated signs and
symptoms typically wax and wane and may include diplopia, blurring or loss of vision, nystagmus, sensory loss or paresthesia, dysarthria,
dysphagia, incoordination, ataxic gait, intention
tremors, emotional lability, impotence, and urinary dysfunction.
◆ Spinal cord injury. Spasticity commonly re-
sults from cervical and high thoracic spinal cord
injury, especially from incomplete lesions. Spastic paralysis in the affected limbs follows initial
flaccid paralysis; typically, spasticity and muscle
atrophy increase for up to 1
the injury, then gradually regress to flaccidity.
Associated signs and symptoms vary with the
level of injury but may include respiratory insufficiency or paralysis, sensory losses, bowel and
bladder dysfunction, hyperactive deep tendon
reflexes, positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and
bradycardia.
1
⁄4 to 2 years after
◆ Stroke. Spastic paralysis may develop on the
affected side following the acute stage of a
stroke. Associated findings vary with the site
and extent of vascular damage and may include
dysarthria, aphasia, ataxia, apraxia, agnosia,
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ipsilateral paresthesia or sensory loss, visual
disturbance, altered level of consciousness, amnesia and poor judgment, personality changes,
emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.
◆ Tetanus. This rare, life-threatening disease
produces varying degrees of spasticity. In generalized tetanus, the most common form, early
signs and symptoms include painful jaw and
neck stiffness, trismus, headache, irritability,
restlessness, low-grade fever with chills, tachycardia, diaphoresis, and hyperactive deep tendon reflexes. As the disease progresses, painful
involuntary spasms may spread and cause
boardlike abdominal rigidity, opisthotonos, and
a characteristic grotesque grin known as risus
sardonicus. Reflex spasms may occur in any
muscle group with the slightest stimulus. Glottal, pharyngeal, or respiratory muscle involvement can cause death by asphyxia or cardiac
failure.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, which
may include electromyography, muscle biopsy,
or intracranial or spinal magnetic resonance
imaging or computed tomography. Administer
pain medication and an antispasmodic. Passive
range-of-motion exercises, splinting, traction,
and application of heat may help relieve spasms
and prevent contractures. Maintain a calm, quiet
environment to help relieve spasms and prevent
recurrence, and encourage bed rest. In cases of
prolonged, uncontrollable spasticity, as with
spastic paralysis, nerve blocks or surgical transection may be necessary for permanent relief.
P
EDIATRIC POINTERS
In children, muscle spasticity may be a sign of
cerebral palsy.
Muscle weakness
Muscle weakness is detected by observing and
measuring the strength of an individual muscle
or muscle group. It can result from a malfunction in the cerebral hemispheres, brain stem,
spinal cord, nerve roots, peripheral nerves, or
myoneural junctions and within the muscle itself. Muscle weakness occurs with certain neurologic, musculoskeletal, metabolic, endocrine,
and cardiovascular disorders; as a response to
certain drugs; and after prolonged immobilization.
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by determining the location of the patient’s muscle weakness. Ask if he has difficulty
with specific movements, such as rising from a
chair. Find out when he first noticed the weakness; ask him whether it worsens with exercise
or as the day progresses. Also ask about related
symptoms, especially muscle or joint pain, altered sensory function, and fatigue.
Obtain a medical history, noting especially
chronic disease such as hyperthyroidism; musculoskeletal or neurologic problems, including
recent trauma; family history of chronic muscle
weakness, especially in males; and alcohol and
drug use.
Focus your physical examination on evaluating muscle strength. Test all major muscles bilaterally. (See Testing muscle strength, pages 464
and 465.) When testing, make sure the patient’s
effort is constant; if it isn’t, suspect pain or other
reluctance to make the effort. If the patient
complains of pain, ease or discontinue testing
and have him try the movements again. Remember that the patient’s dominant arm, hand,
and leg are somewhat stronger than their nondominant counterparts. Besides testing individual muscle strength, test for range of motion at
all major joints (shoulder, elbow, wrist, hip,
knee, and ankle). Also test sensory function in
the involved areas, and test deep tendon reflexes bilaterally.
M
EDICAL CAUSES
◆ Amyotrophic lateral sclerosis. This disor-
der typically begins with muscle weakness and
atrophy in one hand that rapidly spread to the
arm and then to the other hand and arm. Eventually, these effects spread to the trunk, neck,
tongue, larynx, pharynx, and legs; progressive
respiratory muscle weakness leads to respiratory insufficiency.
◆ Anemia. Varying degrees of muscle weak-
ness and fatigue are exacerbated by exertion
and temporarily relieved by rest. Other signs
and symptoms include pallor, tachycardia,
paresthesia, and bleeding tendencies.
◆ Brain tumor. Signs and symptoms of muscle
weakness vary with the location and size of the
tumor. Associated findings include headache,
vomiting, diplopia, decreased visual acuity, decreased level of consciousness, pupillary
changes, decreased motor strength, hemiparesis, hemiplegia, diminished sensations, ataxia,
seizures, and behavioral changes.
(Text continues on page 466.)
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Testing muscle strength
Obtain an overall picture of your patient’s motor function by testing strength in 10 selected muscle
groups. Ask the patient to attempt normal range-of-motion movements against your resistance. If
the muscle group is weak, vary the amount of resistance as necessary to permit accurate
assessment. If necessary, position the patient so his limbs don’t have to resist gravity, and repeat
the test.
Arm muscles
Biceps. With your hand on the patient’s hand,
have him flex his forearm against your resistance. Watch for biceps contraction.
Deltoid. With the patient’s arm fully extended,
place one hand over his deltoid muscle and
the other on his wrist. Ask him to abduct his
arm to a horizontal position against your resistance; as he does so, palpate for deltoid
contraction.
Triceps. Have the patient abduct and hold his
arm midway between flexion and extension.
Hold and support his arm at the wrist, and ask
him to extend it against your resistance.
Watch for triceps contraction.
Dorsal interossei. Have the patient extend
and spread his fingers, and tell him to try to resist your attempt to squeeze them together.
Forearm and hand (grip). Have the patient
grasp your middle and index fingers and
squeeze as hard as he can. To prevent pain or
injury to the examiner, the examiner should
cross his fingers.
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Rate muscle strength on a scale from 0 to 5:
0 = No evidence of muscle contraction; no movement
1 = Visible or palpable contraction, but no movement
2 = Full muscle movement with force of gravity eliminated
3 = Full muscle movement against gravity, but no movement against resistance
4 = Full muscle movement against gravity; partial movement against resistance
5 = Full muscle movement against both gravity and resistance—normal strength.
Leg muscles
Anterior tibial. With the patient’s leg extended, place your hand on his foot and ask him to
dorsiflex his ankle against your resistance.
Palpate for anterior tibial contraction.
Psoas. While you support his leg, have the
patient raise his knee and then flex his hip
against your resistance. Watch for psoas contraction.
Extensor hallucis longus. With your finger
on the patient’s great toe, have him dorsiflex
the toe against your resistance. Palpate for extensor hallucis contraction.
Quadriceps. Have the patient bend his knee
slightly while you support his lower leg. Then
ask him to extend the knee against your resistance; as he’s doing so, palpate for quadriceps
contraction.
Gastrocnemius. With the patient on his side,
support his foot and ask him to plantarflex his
ankle against your resistance. Palpate for gastrocnemius contraction.
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◆ Guillain-Barré syndrome. Rapidly progres-
sive, symmetrical weakness and pain ascends
from the feet to the arms and facial nerves and
may progress to total motor paralysis and respiratory failure. Associated findings include sensory loss or paresthesia, muscle flaccidity, loss
of deep tendon reflexes, tachycardia or bradycardia, fluctuating hypertension and orthostatic
hypotension, diaphoresis, bowel and bladder incontinence, facial diplegia, dysphagia,
dysarthria, and hypernasality.
◆ Head trauma. Severe head injury can cause
varying degrees of muscle weakness. Other
findings include decreased level of consciousness, otorrhea or rhinorrhea, raccoon eyes and
Battle’s sign, sensory disturbances, and signs of
increased intracranial pressure.
◆ Herniated disk. Pressure on nerve roots
leads to muscle weakness, disuse, and ultimately, atrophy. The primary symptom is severe low
back pain, possibly radiating to the buttocks,
legs, and feet—usually on one side. Diminished
reflexes and sensory changes may also occur.
◆ Hodgkin’s lymphoma. Muscle weakness
may accompany the classic sign of painless,
progressive lymphadenopathy. Other findings
include paresthesia, fatigue, and weight loss.
◆ Hypercortisolism. This disorder may cause
limb weakness and eventually atrophy. Related
cushingoid features include buffalo hump,
moon face, truncal obesity, purple striae, thin
skin, acne, elevated blood pressure, fatigue, hyperpigmentation, easy bruising, poor wound
healing, and diaphoresis. The male patient may
be impotent; the female patient may exhibit hirsutism and menstrual irregularities.
◆ Hypothyroidism. Reversible weakness and
atrophy of proximal limb muscles may occur in
hypothyroidism. Accompanying findings commonly include muscle cramps; cold intolerance;
weight gain despite anorexia; mental dullness;
dry, pale, doughy skin; puffy face, hands, and
feet; impaired hearing and balance; and bradycardia.
◆ Multiple sclerosis. Muscle weakness in one
or more limbs may progress to atrophy, spasticity, and contractures. Other findings typically
wax and wane and may include diplopia and
blurred vision, vision loss, nystagmus, hyperactive deep tendon reflexes, sensory loss or paresthesia, dysarthria, dysphagia, incoordination,
ataxic gait, intention tremors, emotional lability,
impotence, and urinary dysfunction.
◆ Myasthenia gravis. Gradually progressive
skeletal muscle weakness and fatigue are the
cardinal symptoms of this disorder. Typically,
weakness is mild upon awakening but worsens
during the day. Early signs include weak eye
closure, ptosis, and diplopia; a blank, masklike
facies; difficulty chewing and swallowing; nasal
regurgitation of fluid with hypernasality; and a
hanging jaw and bobbing head. Respiratory
muscle involvement may eventually lead to respiratory failure.
◆ Osteoarthritis. This chronic disorder causes
progressive muscle disuse and weakness that
lead to atrophy.
◆ Paget’s disease. As this disease progresses,
muscle weakness or paralysis may develop,
along with paresthesia and pain. The patient
may also have bowed tibias, frequent fractures,
and kyphosis.
◆ Parkinson’s disease. Muscle weakness ac-
companies rigidity in this degenerative disorder.
Related findings include a unilateral pill-rolling
tremor, propulsive gait, dysarthria, bradykinesia, drooling, dysphagia, masklike facies, and a
high-pitched, monotonic voice.
◆ Peripheral nerve trauma. Prolonged pres-
sure on or injury to a peripheral nerve causes
muscle weakness and atrophy. Other findings
include paresthesia or sensory loss, pain, and
loss of reflexes supplied by the damaged nerve.
◆ Peripheral neuropathy. With this disorder,
muscle weakness progresses slowly to flaccid
paralysis, generally affecting distal extremities
first. It may be accompanied by loss of vibration
sense; paresthesia, hyperesthesia, or anesthesia
in the hands and feet; hypoactive or absent
deep tendon reflexes; mild-to-sharp burning
pain; anhidrosis; and glossy red skin.
◆ Poliomyelitis. Rapidly developing asymmet-
rical muscle weakness, progressing to flaccid
paralysis, occurs with paralytic poliomyelitis.
Associated signs and symptoms include moderate fever, headache, vomiting, lethargy, irritability, and widespread pain. As the disorder progresses, it may produce loss of superficial and
deep reflexes, paresthesia, hyperalgesia, urine
retention, constipation, abdominal distention,
nuchal rigidity, and Hoyne’s, Kernig’s, and
Brudzinski’s signs. Bulbar paralytic poliomyelitis
produces symptoms of encephalitis, along with
facial weakness, dysphasia, dysphagia, and respiratory abnormalities.
◆ Polymyositis. This disorder produces insidi-
ous or acute onset of symmetrical limb and
trunk muscle weakness and tenderness. Weakness may progress to facial, neck, pharyngeal,
and laryngeal muscles. Associated findings include hypoactive deep tendon reflexes, dysphagia, and dysphonia.
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467
◆ Potassium imbalance. With hypokalemia,
temporary generalized muscle weakness may
be accompanied by nausea, vomiting, diarrhea,
decreased mentation, leg cramps, diminished
reflexes, malaise, polyuria, dizziness, hypotension, and arrhythmias.
With hyperkalemia, weakness may progress to
flaccid paralysis accompanied by irritability and
confusion, hyperreflexia, paresthesia or anesthesia, oliguria, anorexia, nausea, diarrhea, abdominal cramps, tachycardia or bradycardia, and
arrhythmias.
◆ Protein deficiency. Prolonged protein defi-
ciency may lead to muscle weakness and wasting, chronic fatigue, apathy, anorexia, lethargy,
dry skin, and dull, sparse, dry hair.
◆ Rhabdomyolysis. Signs and symptoms in-
clude muscle weakness or pain, fever, nausea,
vomiting, malaise, and dark urine. Acute renal
failure, due to renal structure obstruction and
injury from the kidneys’ attempt to filter the
myoglobin from the bloodstream, is a common
complication.
◆ Rheumatoid arthritis. With this disease,
symmetric muscle weakness may accompany
increased warmth, swelling, and tenderness in
involved joints; pain; and stiffness, restricting
motion.
◆ Seizure disorder. Temporary generalized
muscle weakness may occur after a generalized
tonic-clonic seizure; other postictal findings include headache, muscle soreness, and profound
fatigue.
◆ Spinal trauma and disease. Trauma can
cause severe muscle weakness, leading to flaccidity or spasticity and, eventually, paralysis. Infection, tumor, and cervical spondylosis or
stenosis can also cause muscle weakness.
◆ Stroke. Depending on the site and extent of
damage, a stroke may produce contralateral or
bilateral weakness of the arms, legs, face, and
tongue, possibly progressing to hemiplegia and
atrophy. Associated effects include dysarthria,
aphasia, ataxia, apraxia, agnosia, ipsilateral
paresthesia or sensory loss, visual disturbance,
altered level of consciousness, amnesia and
poor judgment, personality changes, bowel and
bladder dysfunction, headache, vomiting, and
seizures.
◆ Thyrotoxicosis. This disorder may produce
insidious, generalized muscle weakness and atrophy. Other effects include anxiety, fatigue, heat
intolerance, diaphoresis, tremors, tachycardia,
palpitations, ventricular or atrial gallop, dyspnea,
weight loss, an enlarged thyroid, and warm,
flushed skin. Exophthalmos may be present.
O
THER CAUSES
◆ Drugs. Generalized muscle weakness can re-
sult from prolonged corticosteroid use, digoxin,
and excessive doses of dantrolene sodium.
Aminoglycoside antibiotics may worsen weakness in patients with myasthenia gravis.
◆ Immobility. Immobilization in a cast, a
splint, or traction can lead to muscle weakness
in the involved extremity; prolonged bed rest or
inactivity results in generalized muscle weakness.
S
PECIAL CONSIDERATIONS
Provide assistive devices as necessary, and protect the patient from injury. If he has concomitant sensory loss, guard against pressure ulcer
formation and thermal injury. With chronic
weakness, provide range-of-motion exercises or
splint limbs as necessary. Arrange therapy sessions to allow for adequate rest periods, and administer pain medications as needed.
Prepare the patient for blood tests, muscle
biopsy, electromyography, nerve conduction
studies, and X-rays or computed tomography
scans.
P
EDIATRIC POINTERS
Muscular dystrophy, usually the Duchenne type,
is a major cause of muscle weakness in children.
Mydriasis
Mydriasis—pupillary dilation caused by contraction of the dilator of the iris—is a normal response to decreased light, strong emotional
stimuli, and topical administration of mydriatic
and cycloplegic drugs. It can also result from
ocular and neurologic disorders, eye trauma,
and disorders that decrease level of consciousness. Mydriasis may be an adverse effect of antihistamines or other drugs.
H
ISTORY AND PHYSICAL
EXAMINATION
Begin by asking the patient about any other eye
problems, such as pain, blurring, diplopia, or visual field defects. Obtain a health history, focusing on eye or head trauma, glaucoma and other
ocular problems, and neurologic and vascular
disorders. In addition, obtain a complete drug
history.
Next, perform a thorough eye and pupil examination. Inspect and compare the pupils’
size, color, and shape—many people normally
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Grading pupil size
To ensure accurate evaluation of pupillary
size, compare your patient’s pupils to the
scale below. Keep in mind that maximum
constriction may be less than 1 mm and
maximum dilation greater than 9 mm.
1 mm 2 mm 3 mm
4 mm 5 mm 6 mm
7 mm 8 mm 9 mm
have unequal pupils. (See Grading pupil size.)
Also, test each pupil for light reflex, consensual
response, and accommodation. Perform a
swinging flashlight test to evaluate a decreased
response to direct light coupled with a normal
consensual response (Marcus Gunn pupil). Be
sure to check the eyes for ptosis, swelling, and
ecchymosis. Test visual acuity in both eyes with
and without correction. Evaluate extraocular
muscle function by checking the six cardinal
fields of gaze.
Keep in mind that mydriasis appears in two
ocular emergencies: acute angle-closure glaucoma and traumatic iridoplegia.
M
EDICAL CAUSES
◆ Adie’s syndrome. This disorder is character-
ized by abrupt unilateral mydriasis, poor or absent pupillary reflexes, visual blurring, and
cramplike eye pain. Deep tendon reflexes may
be hyperactive or absent, especially the ankle
and knee jerk reflexes.
◆ Aortic arch syndrome. Bilateral pupillary
mydriasis commonly occurs late in this syndrome. Other ocular findings include visual
blurring, transient vision loss, and diplopia. Related findings include dizziness and syncope;
neck, shoulder, and chest pain; bruits; loss of
radial and carotid pulses; paresthesia; and intermittent claudication. Blood pressure may be decreased in the arms.
◆ Botulism. Botulism toxin causes bilateral
mydriasis, usually 12 to 36 hours after ingestion. Other early findings are loss of pupillary reflexes, visual blurring, diplopia, ptosis, strabismus and extraocular muscle palsies, anorexia,
nausea, vomiting, diarrhea, and dry mouth. Vertigo, hearing loss, hoarseness, hypernasality,
dysarthria, dysphagia, progressive muscle
weakness, and loss of deep tendon reflexes
soon follow.
◆ Brain stem infarction. This rare disorder
may cause bilateral mydriatic, fixed pupils. Associated signs and symptoms vary but may include paralysis of all extremities, sudden coma,
decerebrate posturing, disconjugate gaze, and
respiratory pattern changes.
◆ Carotid artery aneurysm. With this disor-
der, unilateral mydriasis may be accompanied
by bitemporal hemianopsia, decreased visual
acuity, hemiplegia, decreased level of consciousness, headache, aphasia, behavioral
changes, and hypoesthesia.
◆ Glaucoma (acute angle closure). This ocu-
lar emergency is characterized by moderate mydriasis and loss of pupillary reflex in the affected
eye, accompanied by abrupt onset of excruciating pain, redness, decreased visual acuity, visual blurring, halo vision, conjunctival injection,
and a cloudy cornea. Without treatment, permanent blindness occurs in 2 to 5 days.
◆ Oculomotor nerve palsy. Unilateral mydria-
sis is often the first sign of this disorder. It’s
soon followed by ptosis, diplopia, decreased
pupillary reflexes, exotropia, and complete loss
of accommodation. Focal neurologic signs may
accompany signs of increased intracranial pressure.
◆ Traumatic iridoplegia. Eye trauma can par-
alyze the sphincter of the iris, causing mydriasis
and loss of pupillary reflex; usually, this is transient. Associated findings include a quivering
iris (iridodonesis), ecchymosis, pain, and
swelling.
O
THER CAUSES
◆ Drugs. Mydriasis can be caused by anti-
cholinergics, antihistamines, sympathomimetics, barbiturates (in overdose), estrogens, and
tricyclic antidepressants; it also commonly occurs early in anesthesia induction. Topical mydriatics and cycloplegics, such as phenylephrine, atropine, scopolamine, cyclopentolate,
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469
and tropicamide, are administered specifically
for their mydriatic effects.
◆ Surgery. Traumatic mydriasis commonly re-
sults from ocular surgery.
S
PECIAL CONSIDERATIONS
Diagnostic tests may vary, depending on your
findings, but may include a complete ophthalmologic examination and a thorough neurologic
workup. Explain any diagnostic tests to the patient.
P
EDIATRIC POINTERS
Mydriasis occurs in children as a result of ocular
trauma, drugs, Adie’s syndrome and, most commonly, increased intracranial pressure.
P
ATIENT COUNSELING
If the patient’s mydriasis is the result of mydriatic drugs received during an eye examination,
explain that he’ll likely experience some photophobia and loss of accommodation. Instruct
him to wear dark glasses and to avoid bright
light, and reassure him that the condition is
only temporary.
Myoclonus
Myoclonus—sudden, shocklike contractions of a
single muscle or muscle group—occurs with
various neurologic disorders and may herald
onset of a seizure. These contractions may be
isolated or repetitive, rhythmic or arrhythmic,
symmetrical or asymmetrical, synchronous or
asynchronous, and generalized or focal. They
may be precipitated by bright flickering lights, a
loud sound, or unexpected physical contact.
One type, intention myoclonus, is evoked by intentional muscle movement.
Myoclonus occurs normally just before falling
asleep and as a part of the natural startle reaction. It also occurs with some poisonings and,
rarely, as a complication of hemodialysis.
EMERGENCY INTERVENTIONS If you
observe myoclonus, check for seizure activity. Take vital signs to rule out arrhythmias or a
blocked airway. Have resuscitation equipment on
hand.
If the patient has a seizure, gently help him lie
down. Place a pillow or a rolled-up towel under
his head to prevent concussion. Loosen any constrictive clothing, especially around the neck, and
turn his head (gently, if possible) to one side to
prevent airway occlusion or aspiration of secretions.
H
ISTORY AND PHYSICAL
EXAMINATION
If the patient is stable, evaluate level of consciousness and mental status. Ask about the
frequency, severity, location, and circumstances
of the myoclonus. Has he ever had a seizure? If
so, did myoclonus precede it? Is the myoclonus
ever precipitated by a sensory stimulus? During
the physical examination, check for muscle
rigidity and wasting, and test deep tendon reflexes.
M
EDICAL CAUSES
◆ Alzheimer’s disease. Generalized my-
oclonus may occur in advanced stages of this
slowly progressive dementia. Other late findings
include mild choreoathetoid movements, muscle rigidity, bowel and bladder incontinence,
delusions, and hallucinations.
◆ Creutzfeldt-Jakob disease. Diffuse my-
oclonic jerks appear early in this rapidly progressive dementia. Initially random, they gradually become more rhythmic and symmetrical,
often occurring in response to sensory stimuli.
Associated effects include ataxia, aphasia, hearing loss, muscle rigidity and wasting, fasciculations, hemiplegia, and visual disturbance, or
possibly, blindness.
◆ Encephalitis (viral). With this disease, my-
oclonus is usually intermittent and either localized or generalized. Associated findings vary
but may include rapidly decreasing level of consciousness, fever, headache, irritability, nuchal
rigidity, vomiting, seizures, aphasia, ataxia,
hemiparesis, facial muscle weakness, nystagmus, ocular palsies, and dysphagia.
◆ Encephalopathy. Hepatic encephalopathy
occasionally produces myoclonic jerks in association with asterixis and focal or generalized
seizures.
Hypoxic encephalopathy may produce generalized myoclonus or seizures almost immediately after restoration of cardiopulmonary function. The patient may also have a residual
intention myoclonus.
Uremic encephalopathy commonly produces
myoclonic jerks and seizures. Other signs and
symptoms include apathy, fatigue, irritability,
headache, confusion, gradually decreasing level
of consciousness, nausea, vomiting, oliguria,
edema, and papilledema. The patient may also
exhibit elevated blood pressure, dyspnea, arrhythmias, and abnormal respirations.
◆ Epilepsy. With idiopathic epilepsy, localized
myoclonus is usually confined to an arm or leg
and occurs singly or in short bursts, usually
470 MYOCLONUS
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upon awakening. It’s usually more frequent and
severe during the prodromal stage of a major
generalized seizure, after which it diminishes in
frequency and intensity.
Myoclonic jerks are usually the first signs of
myoclonic epilepsy, the most common cause of
progressive myoclonus. At first, myoclonus is
infrequent and localized, but over a period of
months, it becomes more frequent and involves
the entire body, disrupting voluntary movement
(intention myoclonus). As the disease progresses, myoclonus is accompanied by generalized
seizures and dementia.
O
THER CAUSES
◆ Drug withdrawal. Myoclonus may be seen
in patients with alcohol, opioid, or sedative
withdrawal, or delirium tremens.
◆ Poisoning. Acute intoxication with methyl
bromide, bismuth, or strychnine may produce
an acute onset of myoclonus and confusion.
S
PECIAL CONSIDERATIONS
If your patient’s myoclonus is progressive, take
seizure precautions. Keep an oral airway and
suction equipment at his bedside, and pad the
side rails. Because myoclonus may cause falls,
remove potentially harmful objects from the patient’s environment, and remain with him while
he walks. Be sure to instruct the patient and his
family about the need for safety precautions.
As needed, administer drugs that suppress myoclonus: ethosuximide, L-5-hydroxytryptophan,
phenobarbital, clonazepam, or carbidopa. An
EEG may be needed to evaluate myoclonus and
related brain activity.
P
EDIATRIC POINTERS
Although myoclonus is relatively uncommon in
infants and children, it can result from subacute
sclerosing panencephalitis, severe meningitis,
progressive poliodystrophy, childhood myoclonic epilepsy, and encephalopathies, such as
Reye’s syndrome.
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