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.
Determine 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 assessment on evaluating muscle strength. Test all major muscles bilaterally. (See Testing muscle strength, pages 428 and 429.)
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 (ROM) at all major joints (shoulder, elbow, wrist, hip, knee, and ankle). Also test sensory function in the involved areas, and test deep tendon reflexes (DTRs) bilaterally.
Amyotrophic lateral sclerosis (ALS) 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.
Signs and symptoms of muscle weakness vary with the tumor’s location and size. Associated findings include headache, vomiting, diplopia, decreased visual acuity, decreased level of consciousness (LOC), pupillary changes, decreased motor strength, hemiparesis, hemiplegia, diminished sensations, ataxia, seizures, and behavioral changes.
With Guillain-Barré syndrome, rapidly progressive, 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 DTRs, tachycardia or bradycardia, fluctuating hypertension and orthostatic hypotension, diaphoresis, bowel and bladder incontinence, facial diplegia, dysphagia, dysarthria, and hypernasality.
Severe head trauma can cause varying degrees of muscle weakness. Other findings include decreased LOC, otorrhea or rhinorrhea, raccoon eyes and Battle’s sign, sensory disturbances, and signs of increased intracranial pressure.
Pressure on nerve roots from a herniated disk 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.
With Hodgkin’s lymphoma, muscle weakness may accompany the classic sign of painless, progressive lymphadenopathy. Other findings include paresthesia, fatigue, persistent fever, night sweats, and weight loss.
Hypercortisolism may cause limb weakness and, eventually, atrophy. Related cush-ingoid 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.
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.
With 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.
Gradually progressive skeletal muscle weakness and fatigue are the cardinal symptoms of myasthenia gravis. 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 is a chronic disorder that causes progressive muscle disuse and weakness that lead to atrophy. Other findings include crepitation; enlarged edematous joints; Heberden’s nodes; increased pain in damp, cold weather; joint stiffness; limited range of motion; pain relieved by resting joints; and smooth, taunt, shiny skin.
As Paget’s disease progresses, muscle weakness or paralysis may develop, along with paresthesia and pain. The patient may also have bowed tibias, frequent fractures, and kyphosis.
Muscle weakness accompanies rigidity in patients with Parkinson’s disease. Related findings include a unilateral pill-rolling tremor, propulsive gait, dysarthria, bradykinesia, drooling, dysphagia, a masklike facies, and a high-pitched, monotonic voice.
Prolonged pressure 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.
With peripheral neuropathy, 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 DTRs; mild to sharp burning pain; anhidrosis; and glossy red skin.
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.
Signs and symptoms of rhabdomyolysis include 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.
With rheumatoid arthritis, symmetric muscle weakness may accompany increased warmth, swelling, and tenderness in involved joints; pain; and stiffness that restrict motion. These findings typically occur bilaterally.
Temporary generalized muscle weakness may occur after a generalized tonic-clonic seizure; other postictal findings include headache, muscle soreness, and profound fatigue. The patient may experience an aura before the seizure.
Spinal 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.
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 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.
Generalized muscle weakness can result from prolonged corticosteroid use, digoxin, and excessive doses of dantrolene. Aminoglycoside antibiotics may worsen weakness in patients with myasthenia gravis.
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.
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 ROM 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.
Muscular dystrophy, usually the Duchenne type, is a major cause of muscle weakness in children.
Teach the patient how to safely use assistive devices. Make sure he understands the importance of frequent position changes to reduce the risk of pressure ulcer formation. Encourage him to plan frequent rest periods throughout the day.
Read excerpts from these other book chapters related to Muscle tension:
Copyright Details: Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright © 2008 Williams & Wilkins.
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More About This Book:
Title: Signs & Symptoms: A 2-in-1 Reference for Nurses Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-318-1 
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