Causes: Mobius syndrome:
Absence or defect to facial nerves.
As with all medical conditions, there may be many causal factors. Further relevant information on causes of Mobius syndrome may be found in:
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Mobius syndrome.
Source: In a Page: Signs and Symptoms, 2004
Acquired
Source: In A Page: Pediatric Signs and Symptoms, 2007
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, 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 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.
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.
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.
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.
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 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.
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.
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.
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.
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.
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 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.
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.)
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.
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 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 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.
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 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.
The therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.
ECT can produce acute, but transient, paralysis.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Some forms of absence seizure are accompanied by learning disabilities.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
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.
Source: Professional Guide to Diseases (Eighth Edition), 2005
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, 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Irreversible hemiplegia may occur in the late stages of neurosyphilis. Dementia, cranial nerve palsies, tremors, and abnormal reflexes are other late findings.
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.
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.
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.
This disorder can produce insidious, permanent flaccid paralysis and hyporeflexia. Sensory function remains intact, but the patient loses voluntary muscle control.
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.
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.
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.)
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.
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.
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.
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.
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.
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.
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.
Therapeutic use of neuromuscular blockers, such as pancuronium, produces paralysis.
This therapy can produce acute, but transient, paralysis.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Some forms of absence seizure are accompanied by learning disabilities.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
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.
Source: Handbook of Diseases, 2003
ALERT: Respiratory muscle paralysis may be life-threatening.
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.
Therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.
Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
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, 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.
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.
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, or irrational) or a strange indifference.
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 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.
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.
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.
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 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.
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.
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.
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.
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 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.
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 ae side of the irritable focus. Seizures may be preceded by an aura.
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.)
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.
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.
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, 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.
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.
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.
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.
Therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.
Electroconvulsive therapy can produce acute, but transient, paralysis.
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
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.
Drugs.The therapeutic use of neuromuscular blockers, such as pancuronium or curare, produces paralysis.
Electroconvulsive therapy (ECT).ECT can produce acute, but transient, paralysis.
Source: Nursing: Interpreting Signs and Symptoms, 2007
Idiopathic epilepsy.Some forms of absence seizure are accompanied by learning disabilities.
Drugs.Drugs that lower the threshold for seizures, such as alcohol, cocaine, penicillin in high doses, isoniazid, and phenothiazines may trigger seizures in patients with preexisting epilepsy.
Source: Nursing: Interpreting Signs and Symptoms, 2007
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