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Diseases » Hereditary Spastic Paraplegia » Causes

Causes of Hereditary Spastic Paraplegia

Contents

Hereditary Spastic Paraplegia Causes: Book Excerpts

Related information on causes of Hereditary Spastic Paraplegia:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Hereditary Spastic Paraplegia may be found in:

Hidden causes of Hereditary Spastic Paraplegia

Causes of Hereditary Spastic Paraplegia: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Hereditary Spastic Paraplegia.

Facial Paralysis & Bell's Palsy: Differential Diagnosis
(In a Page: Signs and Symptoms)

Bell's palsy (idiopathic facial palsy of lower motor neuron type)
–Most common cause of facial nerve paralysis

Lyme disease

Tumors that invade the temporal bone (e.g., cholesteatoma, carotid body tumor)

Ramsay Hunt's syndrome
–Association of facial palsy with herpes zoster eruption in the pharynx and external auditory canal
–Eighth cranial nerve often affected as well

Acoustic neuroma
–May compress the facial nerve
Pontine lesions
–Secondary to infarcts, demyelinating processes, or tumors
–Signs of brainstem involvement may be associated
Facial diplegia or bilateral facial palsy
–Guillain-Barré syndrome (associated with ascending areflexic motor paralysis)
–Heerfordt's syndrome (a form of sarcoidosis; also known as uveoparotid fever)

Diabetic neuropathy

Leprosy

Melkersson-Rosenthal syndrome
–Recurrent facial palsy, labial edema, and tongue plication

Sarcoidosis

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Paraplegia: Differential Diagnosis
(In a Page: Signs and Symptoms)

Myelopathy
–Compressive (e.g., spondylytic, spinal epidural abscess or hematoma)
–Traumatic
–Metabolic (e.g., vitamin B₁₂deficiency)
–Infectious (e.g., HIV or other viral myelitis, botulism)
–Inflammatory (e.g., multiple sclerosis, SLE, vasculitis, transverse myelitis)
–Vascular (spinal cord or cerebral infarct)
–Neoplastic
Congenital
–Dysraphism: Spina bifida, tethered cord
–Cerebral palsy
Syringomyelia
Cauda equina syndrome
–Caused by compression of the cauda equina, often by a central disc herniation
–Variable presentation with lower extremity weakness, sensory loss, pain, lower motor neuron findings on examination, and bowel/bladder disturbances
Polyradiculopathy
Peripheral neuropathy
–Usually results in a chronic or insidious onset of lower extremity weakness (except Guillain-Barré syndrome, which may result in weakness over hours to days)
–Guillain-Barré syndrome: Also results in upper extremity weakness
–Myasthenia gravis
–Eaton-Lambert syndrome
–Amyotrophic lateral sclerosis
- HTLV-I associated myelopathy
- Hereditary spastic paraparesis
- Spinocerebellar or Friedreich's ataxia
- Myopathies (e.g., muscular dystrophy) may result in paraparesis, but usually also result in upper extremity weakness
- Parafalcine meningioma
  –May result in bilateral lower extremity weakness by compressive effects on the medial frontal lobe bilaterally
- Bilateral anterior cerebral artery infarction
- Medications (e.g., pancuronium)
- Periodic paralysis (secondary to hyper- or hypokalemia)
- Tick paralysis
- Lyme disease
- Psychogenic (e.g., conversion disorder)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Facial Paralysis: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Acquired

Bell palsy
–A diagnosis of exclusion; 40% of cases
Acute otitis media
–From erosion or dehiscence of facial canal
Chronic otitis media
–Nerve compression from granulation tissue

Herpes zoster oticus
–Often infects eighth nerve as well, with hearing loss and vertigo

Lyme disease
–Usually several weeks after inoculation

Tumors
–Temporal bone leukemia, rhabdomyosarcoma of head and neck

Melkersson-Rosenthal syndrome
–Relapsing alternating facial paralysis
–Recurrent facial edema
–Fissured tongue

Temporal bone fracture
–Although most cases involve longitudinal fractures, transverse may also result in hearing loss and vertigo

Facial wounds
–Early repair if clean wound
–Tag nerve for delayed repair if dirty wound

Iatrogenic
–After otologic or parotid surgery

Congenital

Traumatic (associated with prolonged and difficult labor)
Inherited disorders
–Myotonic dystrophy: Progressive muscle weakness, facial paresis at birth
–Albers-Schönberg disease: Osteopetrosis increases bone density, compresses nerve
- Developmental abnormalities
  –Möbius syndrome: Facial paralysis with 6th cranial nerve palsy
  –Association with coloboma, heart defect, choanal atresia, genital hypoplasia, ear anomalies (CHARGE)
  –Goldenhar syndrome, also known as oculoauriculovertebral (OAV) syndrome: First and second branchial arch abnormalities
  –Asymmetric crying facies: Also called congenital unilateral lower lip palsy (CULLP)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Paralysis: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

ALS is an invariably fatal disorder that 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, a disease of CN 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

Botulism is a bacterial toxin infection that 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, a 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 (a 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 a rapidly decreasing LOC (possibly coma), a fever, a 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 also vary, but include a decreased LOC; sensory disturbances, such as paresthesia and loss of sensation; a 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 is an acute disorder that produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms — a fever; a 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

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 a headache, vomiting, seizures, a 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 a severe headache, mydriasis, photophobia, aphasia, a sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

Syringomyelia is a degenerative spinal cord disease that 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, a decreased LOC, and other site-dependent effects.

West Nile encephalitis

West Nile encephalitis is a brain infection that’s 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 a fever, a headache, and body aches, which are sometimes accompanied by a skin rash and swollen lymph glands. More severe infections are marked by a headache, a 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.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Muscle spasticity [Muscle hypertonicity]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

ALS commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), 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.

Epidural hemorrhage

With epidural hemorrhage, 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 the level of consciousness (LOC). The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; a high fever; a decreased and bounding pulse; a widened pulse pressure; elevated blood pressure; an irregular respiratory pattern; and decerebrate posture. A positive Babinski’s sign can be elicited.

Spinal cord injury

Spasticity commonly results 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 1¼ to 2 years after the injury, and 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 DTRs, a positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.

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, ipsilateral paresthesia or sensory loss, vision disturbances, an altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, a headache, vomiting, and seizures.

Tetanus

Tetanus is a rare, life-threatening disease that produces varying degrees of spasticity. In generalized tetanus — the most common form — early signs and symptoms include painful jaw and neck stiffness, trismus, a headache, irritability, restlessness, a low-grade fever with chills, tachycardia, diaphoresis, and hyperactive DTRs. 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.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Gait, spastic [Hemiplegic gait]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Brain abscess

In brain abscess, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): a headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, visual disturbances, nystagmus, and pupillary inequality. The patient’s level of consciousness may range from drowsiness to stupor.

Brain tumor

Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (a headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.

Head trauma

Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, a headache, and focal neurologic signs, such as aphasia and visual field deficits.

Multiple sclerosis

Spastic gait begins insidiously and follows multiple sclerosis’ characteristic cycle of remission and exacerbation. The gait, as well as other signs and symptoms, commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include facial pain, paresthesia, incoordination, loss of proprioception and vibration sensation in the ankle and toes, and vision disturbances.

Stroke

Spastic gait usually appears after a period of muscle weakness and hypotonicity on the affected side. Associated effects may include unilateral muscle atrophy, sensory loss, and footdrop; aphasia; dysarthria; dysphagia; visual field deficits; diplopia; and ocular palsies.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Vocal cord paralysis: Causes
(Professional Guide to Diseases (Eighth Edition))

Vocal cord paralysis commonly results from the accidental severing of the recurrent laryngeal nerve, or of one of its extralaryngeal branches, during thyroidectomy. Other causes include pressure from a thoracic aortic aneurysm or from an enlarged atrium (in patients with mitral stenosis), bronchial or esophageal carcinoma, hypertrophy of the thyroid gland, trauma (such as neck injuries) and intubation, and neuritis due to infections or metallic poisoning. Vocal cord paralysis can also result from hysteria and, rarely, lesions of the central nervous system.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Paralysis: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

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

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

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

Spinal cord injury

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.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Muscle spasticity [Muscle hypertonicity]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Amyotrophic lateral sclerosis

This disorder 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.

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, hyperreflexia, 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 results 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 1¼ to 2 years after 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.

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, 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.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Gait, spastic [Hemiplegic gait]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Brain abscess

In this disorder, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, visual disturbances, nystagmus, and pupillary inequality. The patient’s level of consciousness may range from drowsiness to stupor.

Brain tumor

Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.

Head trauma

Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, headache, and focal neurologic signs, such as aphasia and visual field deficits.

Multiple sclerosis (MS)

Spastic gait begins insidiously and follows this disorder’s characteristic cycle of remission and exacerbation. Like other signs and symptoms of MS, the gait commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include vision disturbances, facial pain, paresthesia, incoordination, and loss of proprioception and vibration sensation in the ankle and toes.

Stroke

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Vocal cord paralysis: Causes
(Handbook of Diseases)

Vocal cord paralysis commonly results from the accidental severing of the recurrent laryngeal nerve or of one of its extralaryngeal branches during thyroidectomy.

Other causes include pressure from an aortic aneurysm or from an enlarged atrium (in patients with mitral stenosis), bronchial or esophageal carcinoma, hypertrophy of the thyroid gland, trauma (such as neck injuries) and intubation, and neuritis due to infections or metallic poisoning. Vocal cord paralysis can also result from hysteria and, rarely, lesions of the central nervous system.

CLINICAL TIP: In some cases, cause isn’t identified and spontaneous recovery can occur within a year.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Paralysis: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Amyotrophic lateral sclerosis (ALS)

ALS, an 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 respiratory distress. Progressive cranial nerve paralysis causes dysarthria, dysphagia, drooling, choking, and difficulty chewing.

Bell’s palsy

Transient, unilateral facial muscle paralysis occurs in Bell’s palsy, a disease of cranial nerve VII. (See Recognizing unilateral Bell’s palsy.) The affected muscles sag, and eyelid closure may be impossible. Other signs include increased tearing, drooling, diminished or absent corneal reflex, and possible difficulty with hearing or pain in the ear.

Botulism

Botulism, a bacterial toxin infection, can cause rapidly descending muscle weakness that progresses to paralysis within 2 to 4 days after eating 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, a 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, 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

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. Other effects include transient paresthesia, orthostatic hypotension, tachycardia, diaphoresis, and bowel and bladder incontinence.

ALERT: Respiratory muscle paralysis may be life-threatening.

Head trauma

Cerebral injury can cause paralysis due to cerebral edema and increased ICP. The onset is usually sudden. Location and extent vary, depending on the injury. Associated findings also vary, but include a decreased LOC, headache, blurred or double vision, nausea and vomiting, and focal neurologic disturbances. Sensory disturbances, such as paresthesia and loss of sensation, may also occur.

Migraine headache

Hemiparesis, scotomas, paresthesia, confusion, dizziness, photophobia, nausea and vomiting, or other transient symptoms may precede the onset of a throbbing unilateral headache and may persist after it subsides.

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, intention tremor, gait ataxia, dysphagia, dysarthria, impotence, and constipation. Urinary frequency, urgency, and incontinence may also occur.

Myasthenia gravis

With myasthenia gravis, a 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

Peripheral nerve trauma

Peripheral neuropathy

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

Poliomyelitis

Poliomyelitis can produce insidious, permanent flaccid paralysis, muscle wasting, and hyporeflexia. Sensory function remains intact, but the patient loses voluntary muscle control. Signs and symptoms before paralysis also include muscle weakness, headache, fever, nuchal rigidity, and nausea and vomiting.

Rabies

Rabies, an acute disorder, produces progressive flaccid paralysis, vascular collapse, coma, and death within 2 weeks of contact with an infected animal. Prodromal signs and symptoms — paresthesia and itching at the bite site accompanied by fever, headache, hyperesthesia, photophobia, tachycardia, malaise, alternating rage and calm, hydrophobia, 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 (pupillary changes, hoarseness, facial weakness, ocular palsies), tachycardia or bradycardia, cyclic respirations, high fever, urine retention, and drooling.

Seizure disorders

Spinal cord injury

Spinal cord tumors

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

A potentially life-threatening disorder, subarachnoid hemorrhage 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, a sharply decreased LOC, nuchal rigidity, vomiting, and seizures.

Syringomyelia

Syringomyelia, a 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 the 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 the arms and legs. Paradoxically, however, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.

Transient ischemic attack (TIA)

West Nile encephalitis

A brain infection, West Nile encephalitis 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 a 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 or curare, produces paralysis.

Electroconvulsive therapy (ECT)

ECT can produce acute, but transient, paralysis.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Paralysis: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is an invariably fatal disorder that 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, 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.

Brain tumor

Conversion disorder

Encephalitis

Guillain-Barré syndrome

Head trauma

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. The patient may also experience nausea and vomiting.

Multiple sclerosis

With multiple sclerosis, 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

Myasthenia gravis is a neuromuscular disease that causes profound muscle weakness and abnormal fatigability that may produce paralysis of certain muscle groups. Paralysis is usually transient in early stages but becomes more persistent as the disease progresses. Associated findings in myasthenia gravis 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, meningitis, personality changes, tremors, and abnormal reflexes are other late findings.

Parkinson’s disease

Peripheral nerve trauma

Peripheral neuropathy

Typically, peripheral neuropathy 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.

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, high fever, urine retention, drooling, and hydrophobia.

Seizure disorders

Spinal cord injury

Spinal cord tumor

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 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

Subarachnoid hemorrhage

A 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

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. Paradoxically, however, the patient appears to be in shock, and his systolic blood pressure is either normal or elevated.

Transient ischemic attack

Episodic transient ischemic attacks (TIA) 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

Mild infections of West Nile encephalitis, a mosquito-borne flavivirus, 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 or curare, produces paralysis.

Electroconvulsive therapy

Electroconvulsive therapy can produce acute, but transient, paralysis.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Muscle spasticity: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), 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.

Epidural hemorrhage

Bilateral limb spasticity is a late and ominous sign of epidural hemorrhage. 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 (LOC). 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, hyperreflexia, and contractures may eventually develop in patients with multiple sclerosis; 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 results 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 2 years after 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 DTRs, positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.

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, ipsilateral paresthesia or sensory loss, visual disturbance, altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Paralysis: Medical causes
(Nursing: Interpreting Signs and Symptoms)

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.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Muscle spasticity [Muscle hypertonicity]: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Amyotrophic lateral sclerosis (ALS).ALS commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), 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.

Epidural hemorrhage.With epidural hemorrhage, 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 the level of consciousness (LOC). The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; a high fever; a decreased and bounding pulse; a widened pulse pressure; elevated blood pressure; an irregular respiratory pattern; and decerebrate posture. A positive Babinski's sign can be elicited.

Spinal cord injury.Muscle spasticity commonly results 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 11⁄2 to 2 years after the injury, and 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 DTRs, a positive Babinski's sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.

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, ipsilateral paresthesia or sensory loss, vision disturbances, altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.

Tetanus.Tetanus is a rare, life-threatening disease that produces varying degrees of muscle spasticity. In generalized tetanus—the most common form—early signs and symptoms include painful jaw and neck stiffness, trismus, headache, irritability, restlessness, a low-grade fever with chills, tachycardia, diaphoresis, and hyperactive DTRs. 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.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Gait, spastic [Hemiplegic gait]: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Brain abscess.In brain abscess, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): a headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, vision disturbances, nystagmus, and pupillary inequality. The patient's level of consciousness may range from drowsiness to stupor.

Brain tumor.Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (a headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.

Head trauma.Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, a headache, and focal neurologic signs, such as aphasia and visual field deficits.

Multiple sclerosis.Spastic gait begins insidiously and follows multiple sclerosis' characteristic cycle of remission and exacerbation. The gait, as well as other signs and symptoms, commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include facial pain, paresthesia, incoordination, loss of proprioception and vibration sensation in the ankle and toes, and vision disturbances.

Stroke.With a stroke, spastic gait usually appears after a period of muscle weakness and hypotonicity on the affected side. Associated effects may include unilateral muscle atrophy, sensory loss, and footdrop; aphasia; dysarthria; dysphagia; visual field deficits; diplopia; and ocular palsies.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

» Next page: Symptoms of Hereditary Spastic Paraplegia

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Causes of Hereditary Spastic Paraplegia

Hereditary Spastic Paraplegia Causes: Book Excerpts

Related information on causes of Hereditary Spastic Paraplegia:

Causes of Hereditary Spastic Paraplegia: Online Medical Books

Facial Paralysis & Bell's Palsy: Differential Diagnosis (In a Page: Signs and Symptoms)

Paraplegia: Differential Diagnosis (In a Page: Signs and Symptoms)

Facial Paralysis: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Paralysis: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

Bell’s palsy

Botulism

Brain abscess

Brain tumor

Conversion disorder

Encephalitis

Guillain-Barré syndrome

Head trauma

Multiple sclerosis (MS)

Myasthenia gravis

Parkinson’s disease

Peripheral neuropathy

Rabies

Seizure Disorders

Spinal cord injury

Spinal cord tumors

Stroke

Subarachnoid hemorrhage

Syringomyelia

Transient ischemic attack (TIA)

West Nile encephalitis

Other causes

Drugs

Electroconvulsive therapy (ECT)

Muscle spasticity [Muscle hypertonicity]: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Amyotrophic lateral sclerosis (ALS)

Epidural hemorrhage

Spinal cord injury

Stroke

Tetanus

Gait, spastic [Hemiplegic gait]: Medical causes (Handbook of Signs & Symptoms (Third Edition))

Brain abscess

Brain tumor

Head trauma

Multiple sclerosis

Stroke

Vocal cord paralysis: Causes (Professional Guide to Diseases (Eighth Edition))

Paralysis: Medical causes (Professional Guide to Signs & Symptoms (Fifth Edition))

Amyotrophic lateral sclerosis

Bell’s palsy

Botulism

Brain abscess

Brain tumor

Conversion disorder

Encephalitis

Guillain-Barré syndrome

Head trauma

Migraine headache

Multiple sclerosis

Myasthenia gravis

Neurosyphilis

Parkinson’s disease

Peripheral nerve trauma

Peripheral neuropathy

Poliomyelitis

Rabies

Seizure disorders

Spinal cord injury

Spinal cord tumors

Stroke

Subarachnoid hemorrhage

Syringomyelia

Thoracic aortic aneurysm

Transient ischemic attack (TIA)

West Nile encephalitis

Other causes

Drugs

Electroconvulsive therapy

Muscle spasticity [Muscle hypertonicity]: Medical causes (Professional Guide to Signs & Symptoms (Fifth Edition))

TREATMENTS &
RESEARCH

Dr. Huntley's
Diagnosis
Checklist

Facial Paralysis & Bell's Palsy: Differential Diagnosis
(In a Page: Signs and Symptoms)

Paraplegia: Differential Diagnosis
(In a Page: Signs and Symptoms)

Facial Paralysis: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Paralysis: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Muscle spasticity [Muscle hypertonicity]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Gait, spastic [Hemiplegic gait]: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Vocal cord paralysis: Causes
(Professional Guide to Diseases (Eighth Edition))

Paralysis: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Muscle spasticity [Muscle hypertonicity]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Gait, spastic [Hemiplegic gait]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Vocal cord paralysis: Causes
(Handbook of Diseases)

Paralysis: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Paralysis: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)