Paralysis
Paralysis: Excerpt from Professional Guide to Signs & Symptoms (Fifth Edition)
Paralysis, the total loss of voluntary motor function, results from severe cortical or pyramidal tract damage. It can occur with a cerebrovascular disorder, degenerative neuromuscular disease, trauma, tumor, or central nervous system infection. Acute paralysis may be an early indicator of a life-threatening disorder, such as Guillain-Barré syndrome.
Paralysis can be local or widespread, symmetrical or asymmetrical, transient or permanent, and spastic or flaccid. It’s commonly classified according to location and severity as paraplegia (sometimes transient paralysis of the legs), quadriplegia (permanent paralysis of the arms, legs, and body below the level of the spinal lesion), or hemiplegia (unilateral paralysis of varying severity and permanence). Incomplete paralysis with profound weakness (paresis) may precede total paralysis in some patients.
Emergency Interventions
If paralysis has developed suddenly, suspect trauma or an acute vascular insult. After ensuring that the patient’s spine is properly immobilized, quickly determine his level of consciousness (LOC) and take his vital signs. Elevated systolic blood pressure, widening pulse pressure, and bradycardia may signal increasing intracranial pressure (ICP). If possible, elevate the patient’s head 30 degrees to decrease ICP.
Evaluate respiratory status, and be prepared to administer oxygen, insert an artificial airway, or provide intubation and mechanical ventilation, as needed. To help determine the nature of the patient’s injury, ask him for an account of the precipitating events. If he’s unable to respond, try to find an eyewitness.
History and physical examination
If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or recent injury. Explore related signs and symptoms, noting fever, headache, vision disturbances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.
Next, perform a complete neurologic examination, testing cranial nerve, motor, and sensory function and deep tendon reflexes. Assess strength in all major muscle groups, and note any muscle atrophy. (See Testing muscle strength, pages 530 and 531.) Document all findings to serve as a baseline.
Medical causes
Amyotrophic lateral sclerosis
This invariably fatal disorder produces spastic or flaccid paralysis in the body’s major muscle groups, eventually progressing to total paralysis. Earlier findings include progressive muscle weakness, fasciculations, and muscle atrophy, usually beginning in the arms and hands. Cramping and hyperreflexia are also common. Involvement of respiratory muscles and the brain stem produces dyspnea and possibly respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagia, drooling, choking, and difficulty chewing.
Bell’s palsy
Bell’s palsy, a disease of cranial nerve VII, causes transient, unilateral facial muscle paralysis. The affected muscles sag and eyelid closure is impossible. Other signs include increased tearing, drooling, and a diminished or absent corneal reflex.
Botulism
This bacterial toxin infection can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after the ingestion of contaminated food. Respiratory muscle paralysis leads to dyspnea and respiratory arrest. Nausea, vomiting, diarrhea, blurred or double vision, bilateral mydriasis, dysarthria, and dysphagia are some early findings.
Brain abscess
Advanced abscessin the frontal or temporal lobe can cause hemiplegia accompanied by other late findings, such as ocular disturbances, unequal pupils, decreased LOC, ataxia, tremors, and signs of infection.
Brain tumor
A tumor affecting the motor cortex of the frontal lobe may cause contralateral hemiparesis that progresses to hemiplegia. Onset is gradual, but paralysis is permanent without treatment. In early stages, frontal headache and behavioral changes may be the only indicators. Eventually, seizures, aphasia, and signs of increased ICP (decreased LOC and vomiting) develop.
Conversion disorder
Hysterical paralysis, a classic symptom of conversion disorder, is characterized by the loss of voluntary movement with no obvious physical cause. It can affect any muscle group, appears and disappears unpredictably, and may occur with histrionic behavior (manipulative, dramatic, vain, irrational) or a strange indifference.
Encephalitis
Variable paralysis develops in the late stages of this disorder. Earlier signs and symptoms include rapidly decreasing LOC (possibly coma), fever, headache, photophobia, vomiting, signs of meningeal irritation (nuchal rigidity, positive Kernig’s and Brudzinski’s signs), aphasia, ataxia, nystagmus, ocular palsies, myoclonus, and seizures.
Guillain-Barré syndrome
This syndrome is characterized by a rapidly developing, but reversible, ascending paralysis. It commonly begins as leg muscle weakness and progresses symmetrically, sometimes affecting even the cranial nerves, producing dysphagia, nasal speech, and dysarthria. Respiratory muscle paralysis may be life-threatening. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.
Head trauma
Cerebral injury can cause paralysis due to cerebral edema and increased intracranial pressure. Onset is usually sudden. Location and extent vary, depending on the injury. Associated findings also vary but include decreased LOC; sensory disturbances, such as paresthesia and loss of sensation; headache; blurred or double vision; nausea and vomiting; and focal neurologic disturbances.
Migraine headache
Hemiparesis, scotomas, paresthesia, confusion, dizziness, photophobia, or other transient symptoms may precede the onset of a throbbing unilateral headache and may persist after it subsides.
Multiple sclerosis
With this disorder, paralysis commonly waxes and wanes until the later stages, when it may become permanent. Its extent can range from monoplegia to quadriplegia. In most patients, vision and sensory disturbances (paresthesia) are the earliest symptoms. Later findings are widely variable and may include muscle weakness and spasticity, nystagmus, hyperreflexia, intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.
Myasthenia gravis
With this neuromuscular disease, profound muscle weakness and abnormal fatigability may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages but becomes more persistent as the disease progresses. Associated findings depend on the areas of neuromuscular involvement; they include weak eye closure, ptosis, diplopia, lack of facial mobility, dysphagia, nasal speech, and frequent nasal regurgitation of fluids. Neck muscle weakness may cause the patient’s jaw to drop and his head to bob. Respiratory muscle involvement can lead to respiratory distress—dyspnea, shallow respirations, and cyanosis.
Neurosyphilis
Irreversible hemiplegia may occur in the late stages of neurosyphilis. Dementia, cranial nerve palsies, tremors, and abnormal reflexes are other late findings.
Parkinson’s disease
Tremors, bradykinesia, and lead-pipe or cogwheel rigidity are the classic signs of Parkinson’s disease. Extreme rigidity can progress to paralysis, particularly in the extremities. In most cases, paralysis resolves with prompt treatment of the disease.
Peripheral nerve trauma
Severe injury to a peripheral nerve or group of nerves results in the loss of motor and sensory function in the innervated area. Muscles become flaccid and atrophied, and reflexes are lost. If transection isn’t complete, paralysis may be temporary.
Peripheral neuropathy
Typically, this syndrome produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, loss of vibration sensation, hypoactive or absent deep tendon reflexes, neuralgia, and skin changes such as anhidrosis.
Poliomyelitis
This disorder can produce insidious, permanent flaccid paralysis and hyporeflexia. Sensory function remains intact, but the patient loses voluntary muscle control.
Rabies
This acute disorder produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms—fever; headache; hyperesthesia; paresthesia, coldness, and itching at the bite site; photophobia; tachycardia; shallow respirations; and excessive salivation, lacrimation, and perspiration—develop almost immediately. Within 2 to 10 days, a phase of excitement begins, marked by agitation, cranial nerve dysfunction (pupil changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, high fever, urine retention, drooling, and hydrophobia.
Seizure disorders
Seizures, particularly focal seizures, can cause transient local paralysis (Todd’s paralysis). Any part of the body may be affected, although paralysis tends to occur contralateral to the side of the irritable focus.
Spinal cord injury
Complete spinal cord transection results in permanent spastic paralysis below the level of injury. Reflexes may return after spinal shock resolves. Partial transection causes variable paralysis and paresthesia, depending on the location and extent of injury. (See Understanding spinal cord syndromes.)
Spinal cord tumors
Paresis, pain, paresthesia, and variable sensory loss may occur along the nerve distribution pathway served by the affected cord segment. Eventually, these symptoms may progress to spastic paralysis with hyperactive deep tendon reflexes (unless the tumor is in the cauda equina, which produces hyporeflexia) and, perhaps, bladder and bowel incontinence. Paralysis is permanent without treatment.
Stroke
A stroke involving the motor cortex can produce contralateral paresis or paralysis. Onset may be sudden or gradual, and paralysis may be transient or permanent. Associated signs and symptoms vary widely and may include headache, vomiting, seizures, decreased LOC and mental acuity, dysarthria, dysphagia, ataxia, contralateral paresthesia or sensory loss, apraxia, agnosia, aphasia, vision disturbances, emotional lability, and bowel and bladder dysfunction.
Subarachnoid hemorrhage
This potentially life-threatening disorder can produce sudden paralysis. The condition may be temporary, resolving with decreasing edema, or permanent, if tissue destruction has occurred. Other acute effects are severe headache, mydriasis, photophobia, aphasia, sharply decreased LOC, nuchal rigidity, vomiting, and seizures.
Syringomyelia
This degenerative spinal cord disease produces segmental paresis, leading to flaccid paralysis of the hands and arms. Reflexes are absent, and loss of pain and temperature sensation is distributed over the neck, shoulders, and arms in a capelike pattern.
Thoracic aortic aneurysm
Occlusion of spinal arteries by a ruptured thoracic aortic aneurysm may cause sudden onset of transient bilateral paralysis. Severe chest pain radiating to the neck, shoulders, back, and abdomen and a sensation of tearing in the thorax are prominent symptoms. Related findings include syncope, pallor, diaphoresis, dyspnea, tachycardia, cyanosis, diastolic heart murmur, and abrupt loss of radial and femoral pulses or wide variations in pulses and blood pressure between arms and legs. Ironically, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.
Transient ischemic attack (TIA)
Episodic TIAs may cause transient unilateral paresis or paralysis accompanied by paresthesia, blurred or double vision, dizziness, aphasia, dysarthria, decreased LOC, and other site-dependent effects.
West Nile encephalitis
This brain infection is caused by West Nile virus, a mosquito-borne flavivirus endemic to Africa, the Middle East, western Asia, and the United States. Mild infections are common and include fever, headache, and body aches, which are sometimes accompanied by skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.
Other causes
Drugs
Therapeutic use of neuromuscular blockers, such as pancuronium, produces paralysis.
Electroconvulsive therapy
This therapy can produce acute, but transient, paralysis.
Special considerations
Because a paralyzed patient is particularly susceptible to complications of prolonged immobility, provide frequent position changes, meticulous skin care, and frequent chest physiotherapy. He may benefit from passive range-of-motion exercises to maintain muscle tone, application of splints to prevent contractures, and the use of footboards or other devices to prevent footdrop. If his cranial nerves are affected, the patient will have difficulty chewing and swallowing. Provide a liquid or soft diet, and keep suction equipment on hand in case aspiration occurs. Feeding tubes or total parenteral nutrition may be necessary with severe paralysis. Paralysis and accompanying vision disturbances may make ambulation hazardous; provide a call light and show the patient how to call for help. As appropriate, arrange for physical, speech, or occupational therapy.
Pediatric pointers
Although children may develop paralysis from an obvious cause—such as trauma, infection, or tumor—they may also develop it from a hereditary or congenital disorder, such as Tay-Sachs disease, Werdnig-Hoffmann disease, spina bifida, or cerebral palsy.
Pictures
Book Source Details
- Book Title: Professional Guide to Signs & Symptoms (Fifth Edition)
- Author(s): Springhouse
- Year of Publication: 2006
- Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2006 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Vocal cord paralysis (Handbook of Diseases)
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