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ULY CLINIC
ULY CLINIC
14 Septemba 2025, 00:35:37
Paralysis
Paralysis is the total loss of voluntary motor function, resulting from severe cortical or pyramidal tract damage. It can occur due to cerebrovascular disorders, degenerative neuromuscular diseases, trauma, tumors, or central nervous system infections. Acute paralysis may indicate life-threatening conditions such as Guillain-Barré syndrome.
Paralysis can be local or widespread, symmetrical or asymmetrical, transient or permanent, and spastic or flaccid. Common classifications include:
Paraplegia: paralysis of the legs (may be transient).
Quadriplegia: paralysis of arms, legs, and body below the lesion (usually permanent).
Hemiplegia: unilateral paralysis of variable severity.
Paresis: incomplete paralysis with profound weakness, which may precede total paralysis.
Emergency interventions
Immediate assessment if paralysis develops suddenly (suspect trauma or acute vascular insult).
Ensure spinal immobilization.
Assess level of consciousness (LOC) and vital signs. Monitor for elevated systolic BP, widened pulse pressure, bradycardia (signs of increased ICP).
Elevate head 30° and maintain neutral alignment.
Assess respiratory function; be prepared for oxygen therapy, airway management, or mechanical ventilation.
Obtain history of precipitating events; seek eyewitness accounts if patient is unable to respond.
History and Physical examination
Obtain a detailed history of onset, duration, progression, and preceding events.
Focus on degenerative neurologic/neuromuscular diseases, infections, STDs, tumors, trauma.
Assess associated symptoms: fever, headache, vision changes, dysphagia, nausea, vomiting, bowel/bladder dysfunction, fatigue, muscle pain/weakness.
Perform a complete neurologic examination:
Cranial nerves (CN I–XII)
Motor function (strength, tone, atrophy)
Sensory function
Deep tendon reflexes (DTRs)
Document all findings as a baseline.
Medical causes
Cause | Features / Associated Findings |
Amyotrophic lateral sclerosis (ALS) | Progressive spastic/flaccid paralysis of major muscle groups, fasciculations, muscle atrophy, hyperreflexia, respiratory muscle involvement → dyspnea, respiratory distress, dysarthria, dysphagia. |
Bell’s palsy | Transient unilateral facial paralysis (CN VII), inability to close eyelid, drooling, increased tearing, diminished corneal reflex. |
Botulism | Rapidly descending paralysis 2–4 days after ingestion of toxin. Early: nausea, vomiting, diarrhea, blurred/double vision, dysarthria, dysphagia, bilateral mydriasis; may progress to respiratory arrest. |
Brain abscess | Hemiplegia, ocular disturbances, unequal pupils, decreased LOC, ataxia, tremors, signs of infection. |
Brain tumor | Gradual contralateral hemiparesis → hemiplegia; early: headache, behavioral changes; later: seizures, aphasia, ICP signs. |
Conversion disorder | Hysterical paralysis; loss of voluntary movement with no physical cause; unpredictable, often accompanied by dramatic or indifferent behavior. |
Encephalitis | Late-stage paralysis; early: decreasing LOC, fever, headache, photophobia, vomiting, meningeal signs, nystagmus, ocular palsies, myoclonus, seizures. |
Guillain-Barré syndrome | Rapidly ascending paralysis, symmetric; cranial nerve involvement → dysphagia, nasal speech, dysarthria; may cause respiratory failure. Transient paresthesia, autonomic dysfunction (orthostatic hypotension, tachycardia), bowel/bladder incontinence. |
Head trauma | Sudden paralysis from cerebral edema, increased ICP. Associated: decreased LOC, sensory disturbances, headache, blurred/double vision, nausea/vomiting, focal deficits. |
Multiple sclerosis (MS) | Fluctuating paralysis, eventual permanent; initial: vision/sensory disturbances; later: weakness, spasticity, hyperreflexia, tremor, ataxia, dysarthria, dysphagia, urinary issues. |
Myasthenia gravis | Muscle weakness → transient paralysis; ocular involvement (ptosis, diplopia), dysphagia, nasal speech, jaw drop, head bobbing; respiratory muscles → distress. |
Parkinson’s disease | Tremors, rigidity, bradykinesia; extreme rigidity may lead to limb paralysis, reversible with treatment. |
Peripheral neuropathy | Muscle weakness → flaccid paralysis and atrophy; sensory deficits, hypoactive/absent reflexes, paresthesia, skin changes. |
Rabies | Acute flaccid paralysis, vascular collapse, coma, death; prodrome: fever, headache, hyperesthesia, paresthesia, photophobia, tachycardia, hypersalivation, hydrophobia. |
Seizure disorders | Todd’s paralysis: transient, local; contralateral to seizure focus. |
Spinal cord injury | Complete transection → permanent spastic paralysis; partial → variable deficits; reflexes may return post spinal shock. |
Spinal cord tumors | Paresis, pain, paresthesia; may progress to spastic paralysis, DTR hyperactivity, bladder/bowel incontinence. |
Stroke | Contralateral paresis/paralysis; sudden or gradual onset; may include headache, vomiting, seizures, dysarthria, dysphagia, sensory deficits, apraxia, aphasia, bowel/bladder dysfunction. |
Subarachnoid hemorrhage | Sudden paralysis; may be temporary or permanent; severe headache, photophobia, mydriasis, decreased LOC, nuchal rigidity, vomiting, seizures. |
Syringomyelia | Segmental paresis → flaccid paralysis of hands/arms; absent reflexes; capelike loss of pain/temp sensation. |
Transient ischemic attack (TIA) | Episodic unilateral paresis/paralysis; associated: paresthesia, vision disturbances, dizziness, aphasia, dysarthria. |
West Nile encephalitis | Mosquito-borne; mild: fever, headache, myalgia, rash; severe: paralysis, tremors, seizures, coma, death. |
Drugs | Neuromuscular blockers (pancuronium, curare) → paralysis. |
Electroconvulsive therapy (ECT) | Acute, transient paralysis. |
Understanding spinal cord syndromes
Syndrome | Features |
Anterior cord syndrome | Motor paralysis, loss of pain/temperature below lesion; touch, proprioception, vibration preserved. |
Brown-Séquard syndrome | Ipsilateral motor paralysis; contralateral pain/temperature loss. |
Central cord syndrome | Greater motor loss in arms than legs; mild sensory loss. |
Posterior cord syndrome | Loss of proprioception/light touch; motor function intact. |
Special considerations
Prevent complications of immobility: position changes, skin care, chest physiotherapy, passive ROM, splints, footboards.
Nutrition: thickened or soft diet; suctioning; feeding tubes/TPN for severe cases.
Safety: impaired vision/ambulation; provide call light and assistance.
Therapy referrals: physical, occupational, speech, swallowing.
Patient counseling
Explain cause and prognosis of paralysis.
Refer to social and psychological support services.
Teach home care: passive ROM exercises, frequent turning, chest physiotherapy, feeding strategies.
Pediatric pointers
Causes may include trauma, infection, tumor, or congenital/hereditary disorders (e.g., Tay-Sachs, Werdnig-Hoffmann disease, spina bifida, cerebral palsy).
References
Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary Care: A Collaborative Practice. St. Louis, MO: Mosby Elsevier; 2008.
Colyar MR. Well-Child Assessment for Primary Care Providers. Philadelphia, PA: F.A. Davis; 2003.
Lehne RA. Pharmacology for Nursing Care. 7th ed. St. Louis, MO: Saunders Elsevier; 2010.
McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Maryland Heights, MO: Mosby Elsevier; 2010.
Sarwark JF. Essentials of Musculoskeletal Care. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2010.
Sommers MS, Brunner LS. Pocket Diseases. Philadelphia, PA: F.A. Davis; 2012.