Paralysis

Paralysis: Excerpt from Nursing: Interpreting Signs and Symptoms

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.

Action stat!

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, and attempt to keep his head straight and facing forward.

Evaluate the patient's respiratory status, and be prepared to administer oxygen, insert an artificial airway, or provide endotracheal 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 can't 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 fevers, headaches, vision distur-bances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

Next, perform a complete neurologic examination, testing cranial nerve (CN), motor, and sensory function and deep tendon reflexes (DTRs). Assess strength in all major muscle groups, and note muscle atrophy. (See Testing muscle strength, pages 410 and 411.) Document all findings to serve as a baseline.

Medical causes

Amyotrophic lateral sclerosis (ALS).ALS 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, dysphagial drooling, choking, and difficulty chewing.

Bell's palsy.Bell's palsy 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.Botulism 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 abscess in 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. The onset is gradual, but paralysis is permanent without treatment. In early stages, a 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 encephalitis. 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.Guillain-Barré 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 ICP. The onset is usually sudden. The location and extent vary, depending on the injury. Associated findings 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.

Multiple sclerosis (MS).With MS, 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, an intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis.With myasthenia gravis, 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.

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 neuropathy.Typically, peripheral neuropathy produces muscle weakness that may lead to flaccid paralysis and atrophy. Related effects include paresthesia, a loss of vibration sensation, hypoactive or absent DTRs, neuralgia, and skin changes such as anhidrosis.

Rabies.Rabies 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, a 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.With a spinal cord tumor, 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 DTRs (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. The 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.Subarachnoid hemorrhage is a potentially life-threatening disorder that 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.Syringomyelia 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.

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.Symptoms of West Nile encephalitis include fever, headache, and body aches, which are sometimes accompanied by a skin rash and swollen lymph glands. More severe infections are marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Drugs.The therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.

Electroconvulsive therapy (ECT).ECT can produce acute, but transient, paralysis.

Nursing considerations

▪ Provide frequent position changes and meticulous skin care to prevent skin breakdown.

▪ Administer frequent chest physiotherapy.

▪ Perform passive range-of-motion exercises to maintain muscle tone.

▪ Apply splints to prevent contractures and footboards or other devices to prevent footdrop.

▪ Provide a thickened liquid or soft diet, and keep suction equipment on hand in case aspiration occurs, if the patient has difficulty chewing or swallowing.

▪ As appropriate, arrange for physical, speech, swallowing, or occupational therapy.

Patient teaching

▪ Explain all diagnostic tests and procedures.

▪ Explain the disorder and treatment plan.

▪ Teach the patient and his family how to prevent complications.

▪ Provide referrals to social and psychological services.

Pictures

Book Source Details

• Book Title: Nursing: Interpreting Signs and Symptoms
• Author(s): Springhouse
• Year of Publication: 2007
• Copyright Details: Nursing: Interpreting Signs and Symptoms, Copyright © 2007 Lippincott Williams & Wilkins.

More About Paraplegia

• Back to disease: Paraplegia: Introduction
• Next Book Extract About Paraplegia: FACIAL PARALYSIS (Differential Diagnosis in Primary Care)
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Nursing: Interpreting Signs and Symptoms Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-668-7

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