Causes of Reflex sympathetic dystrophy syndrome
List of causes of Reflex sympathetic dystrophy syndrome
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Reflex sympathetic dystrophy syndrome)
that could possibly cause Reflex sympathetic dystrophy syndrome includes:
Common Causes of Reflex sympathetic dystrophy syndrome
Following is a list of common causes of Reflex sympathetic dystrophy syndrome:
Other Causes of Reflex sympathetic dystrophy syndrome
Following is a list of other causes of Reflex sympathetic dystrophy syndrome:
Causes of Reflex sympathetic dystrophy syndrome (Diseases Database):
The follow list shows some of the possible medical causes of Reflex sympathetic dystrophy syndrome
that are listed by the Diseases Database:
Source: Diseases Database
Reflex sympathetic dystrophy syndrome Causes: Book Excerpts
What causes Reflex sympathetic dystrophy syndrome?
Causes: Reflex sympathetic dystrophy syndrome:
The cause of RSDS is unknown. The disorder is
unique in that it simultaneously affects the nerves, skin, muscles, blood
vessels, and bones.
(Source: excerpt from NINDS Reflex Sympathetic Dystrophy Syndrome Information Page: NINDS)
What triggers Reflex sympathetic dystrophy syndrome?
The following conditions are listed as possible triggers
for Reflex sympathetic dystrophy syndrome:
Related information on causes of Reflex sympathetic dystrophy syndrome:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Reflex sympathetic dystrophy syndrome may be found in:
Causes of Reflex sympathetic dystrophy syndrome: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Reflex sympathetic dystrophy syndrome.
Deep tendon reflexes, hyperactive:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Amyotrophic lateral sclerosis (ALS)
ALS produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor.
A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Hypocalcemia
Hypocalcemia may produce a sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek's and Trousseau's signs, carpopedal spasm, and tetany.
Hypomagnesemia
Hypomagnesemia results in the gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia
Mild hypothermia (90 to 94 F [32.2 to 34.4 C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Preeclampsia.
Occurring in pregnancy of at least 20 weeks' gestation, preeclampsia may cause a gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; a severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, a headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke.
A stroke that affects the origin of the corticospinal tracts causes the sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Tetanus.
With tetanus, the sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, a low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Babinski's reflex [Extensor plantar reflex]:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
❑ Amyotrophic lateral sclerosis (ALS). With this progressive motor neuron disorder, bilateral Babinski's reflex may occur with hyperactive DTRs and spasticity. Typically, ALS produces fasciculations accompanied by muscle atrophy and weakness. Incoordination makes carrying out activities of daily living difficult for the patient. Associated signs and symptoms include impaired speech; difficulty chewing, swallowing, and breathing; urinary frequency and urgency; and, occasionally, choking and excessive drooling. Although his mental status remains intact, the patient's poor prognosis may cause periodic depression. Progressive bulbar palsy involves the brain stem and may cause episodes of crying or inappropriate laughter.
❑ Brain tumor. A brain tumor that involves the corticospinal tract may produce Babinski's reflex. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral), spasticity, seizures, cranial nerve dysfunction, hemiparesis or hemiplegia, decreased pain sensation, an unsteady gait, incoordination, headache, emotional lability, and a decreased level of consciousness (LOC).
❑ Head trauma. Unilateral or bilateral Babinski's reflex may occur as the result of primary corticospinal damage or secondary injury associated with increased intracranial pressure. Hyperactive DTRs and spasticity commonly occur with Babinski's reflex. The patient may also have weakness and incoordination. Other signs and symptoms vary with the type of head trauma and include headache, vomiting, behavior changes, altered vital signs, and decreased LOC with abnormal pupillary size and response to light.
❑ Hepatic encephalopathy. Babinski's reflex occurs late in hepatic encephalopathy when the patient slips into a coma. It's accompanied by hyperactive DTRs and fetor hepaticus.
❑ Meningitis. With meningitis, bilateral Babinski's reflex commonly follows fever, chills, and malaise and is accompanied by nausea and vomiting. As meningitis progresses, it also causes decreased LOC, nuchal rigidity, positive Brudzinski's and Kernig's signs, hyperactive DTRs, and opisthotonos. Associated signs and symptoms include irritability, photophobia, diplopia, delirium, and deep stupor that may progress to coma.
❑ Rabies. Bilateral Babinski's reflex — possibly elicited by nonspecific noxious stimuli alone — appears in the excitation phase of rabies. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms, such as fever, malaise, and irritability (which occur 30 to 40 days after a bite from an infected animal). Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Seizures and hyperactive DTRs may also occur.
❑ Spinal cord injury. With acute injury, spinal shock temporarily erases all reflexes. As shock resolves, Babinski's reflex occurs — unilaterally when injury affects only one side of the spinal cord (Brown-Séquard's syndrome), bilaterally when injury affects both sides. Rather than signaling the return of neurologic function, this reflex confirms corticospinal damage. It's accompanied by hyperactive DTRs, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner's syndrome, marked by unilateral ptosis, pupillary constriction, and facial anhidrosis, may occur with lower cervical cord injury.
❑ Spinal cord tumor. With spinal cord tumor, bilateral Babinski's reflex occurs with variable loss of pain and temperature sensation, proprioception, and motor function. Spasticity, hyperactive DTRs, absent abdominal reflexes, and incontinence are also characteristic. Diffuse pain may occur at the level of the tumor.
❑ Spinal paralytic poliomyelitis. Unilateral or bilateral Babinski's reflex occurs 5 to 7 days after the onset of fever. It's accompanied by progressive weakness, paresthesia, muscle tenderness, spasticity, irritability and, later, atrophy. Resistance to neck flexion is characteristic, as are Hoyne's, Kernig's, and Brudzinski's signs.
❑ Spinal tuberculosis. Spiral tuberculosis may produce bilateral Babinski's reflex accompanied by variable loss of pain and temperature sensation, proprioception, and motor function. It also causes spasticity, hyperactive DTRs, bladder incontinence, and absent abdominal reflexes.
❑ Stroke. Babinski's reflex varies with the site of the stroke. If it involves the cerebrum, it produces unilateral Babinski's reflex accompanied by hemiplegia or hemiparesis, unilateral hyperactive DTRs, hemianopsia, and aphasia. If it involves the brain stem, it produces bilateral Babinski's reflex accompanied by bilateral weakness or paralysis, bilateral hyperactive DTRs, cranial nerve dysfunction, incoordination, and an unsteady gait. Generalized signs and symptoms of stroke include headache, vomiting, fever, disorientation, nuchal rigidity, seizures, and coma.
❑ Syringomyelia. With syringomyelia, bilateral Babinski's reflex occurs with muscle atrophy and weakness that may progress to paralysis. It's accompanied by spasticity, ataxia and, occasionally, deep pain. DTRs may be hypoactive or hyperactive. Cranial nerve dysfunction, such as dysphagia and dysarthria, commonly appears late in the disorder.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Complex regional pain syndrome:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The exact cause of CRPS is unknown. Impaired communication between the damaged nerves of the sympathetic nervous system and the brain may cause interference with normal signals for sensations, temperature, and blood flow. This leads to problems in the nerves, blood vessels, skin, bones, and muscles. Infection or injury to an arm or leg may initiate CRPS. It can also occur after heart attacks and strokes. However, the condition can sometimes appear without obvious injury to the affected limb. This condition is more common in people between ages 40 and 60, but has been seen in younger people too. CRPS may also be seen in postoperative patients and in patients with diseases that can cause chronic pain, such as cancer and arthritis. Annual incidence is unknown because CRPS is often misdiagnosed. However, it has been reported in 1% to 2% of patients with various fractures and in 2% to 5% of patients with peripheral nerve injury.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Posttraumatic stress disorder:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
PTSD occurs in response to an extremely distressing event, including a serious threat of harm to the patient or his family, such as war, abuse, or violent crime. It may be triggered by sudden destruction of his home or community by a bombing, fire, flood, tornado, earthquake, or similar disaster. It may also follow witnessing the death or serious injury of another person by torture, in a death camp, by natural disaster, or by a motor vehicle or airplane crash.
Preexisting psychopathology can predispose some patients to this disorder, but anyone can develop it, especially if the stressor is extreme.
Any person who has experienced traumatic relocation due to such events as rioting or other civil strife, extreme natural disasters, or war should be assessed for signs of PTSD.
PTSD can occur at any age. Most cases resolve 3 months after the traumatic event, but some cases can last for years.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Deep tendon reflexes, hyperactive:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Amyotrophic lateral sclerosis
This disorder produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor
A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Hepatic encephalopathy
Generalized hyperactive DTRs occur late and are accompanied by a positive Babinski’s reflex, fetor hepaticus, and a coma.
Hypocalcemia
This disorder may produce sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek’s and Trousseau’s signs, carpopedal spasm, and tetany.
Hypomagnesemia
This disorder results in gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia
Mild hypothermia (90° to 94° F [32.2° to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Multiple sclerosis
Typically, hyperactive DTRs are preceded by weakness and paresthesia in one or both arms or legs. Associated signs include clonus and a positive Babinski’s reflex. Passive flexion of the patient’s neck may cause a tingling sensation down his back. Later, ataxia, diplopia, vertigo, vomiting, urine retention, or urinary incontinence may occur.
Preeclampsia
Occurring in pregnancy of at least 20 weeks’ duration, preeclampsia may cause gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; dyspnea; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke
Any stroke that affects the origin of the corticospinal tracts causes sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Tetanus
In this disorder, sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Babinski's reflex [Extensor plantar reflex]:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Amyotrophic lateral sclerosis (ALS)
In this progressive motor neuron disorder, bilateral Babinski’s reflex may occur with hyperactive DTRs and spasticity. Typically, ALS produces fasciculations accompanied by muscle atrophy and weakness. Incoordination makes carrying out activities of daily living difficult for the patient. Associated signs and symptoms include impaired speech; difficulty chewing, swallowing, and breathing; urinary frequency and urgency; and, occasionally, choking and excessive drooling. Although his mental status remains intact, the patient’s poor prognosis may cause periodic depression. Progressive bulbar palsy involves the brain stem and may cause episodes of crying or inappropriate laughter.
Brain tumor
A brain tumor that involves the corticospinal tract may produce Babinski’s reflex. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral), spasticity, seizures, cranial nerve dysfunction, hemiparesis or hemiplegia, decreased pain sensation, unsteady gait, incoordination, headache, emotional lability, and decreased level of consciousness (LOC).
Familial spastic paraparesis
Familial spastic paraparesis may produce bilateral Babinski’s reflex accompanied by hyperactive DTRs and progressive spasticity with ataxia and weakness.
Friedreich’s ataxia
Friedreich’s ataxia is a familial disorder that may produce bilateral Babinski’s reflex. Accompanying it are high-arched feet, hypoactive DTRs, hypotonia, ataxia, head tremor, weakness, and paresthesia.
Head trauma
Unilateral or bilateral Babinski’s reflex may occur as the result of primary corticospinal damage or secondary injury associated with increased intracranial pressure. Hyperactive DTRs and spasticity commonly occur with Babinski’s reflex. The patient may also have weakness and incoordination. Other signs and symptoms vary with the type of head trauma and include headache, vomiting, behavior changes, altered vital signs, and decreased LOC with abnormal pupillary size and response to light.
Hepatic encephalopathy
Babinski’s reflex occurs late in hepatic encephalopathy when the patient slips into a coma. It’s accompanied by hyperactive DTRs and fetor hepaticus.
Meningitis
In meningitis, bilateral Babinski’s reflex commonly follows fever, chills, and malaise and is accompanied by nausea and vomiting. As meningitis progresses, it also causes decreased LOC, nuchal rigidity, positive Brudzinski’s and Kernig’s signs, hyperactive DTRs, and opisthotonos. Associated signs and symptoms include irritability, photophobia, diplopia, delirium, and deep stupor that may progress to coma.
Multiple sclerosis (MS)
In most patients with MS—a demyelinating disorder—bilateral Babinski’s reflex eventually follows initial signs and symptoms of paresthesia, nystagmus, and blurred or double vision. Associated signs and symptoms include scanning speech (clipped speech with some pauses between syllables), dysphagia, intention tremor, weakness, incoordination, spasticity, gait ataxia, seizures, paraparesis or paraplegia, bladder incontinence, and emotional lability. Loss of pain and temperature sensation and proprioception occur occasionally.
Pernicious anemia
Bilateral Babinski’s reflex occurs late in pernicious anemia when vitamin B12 deficiency affects the central nervous system. Anemia may eventually cause widespread GI, neurologic, and cardiovascular effects. Characteristic GI signs and symptoms include nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation. Gingival bleeding and a sore, inflamed tongue may make eating painful and intensify anorexia. The lips, gums, and tongue appear markedly pale. Jaundice may cause pale to bright yellow skin.
Characteristic neurologic signs and symptoms include neuritis, weakness, peripheral paresthesia, disturbed position sense, incoordination, ataxia, positive Romberg’s sign, light-headedness, bowel and bladder incontinence, and altered vision (diplopia, blurred vision), taste, and hearing (tinnitus). Pernicious anemia may also produce irritability, poor memory, headache, depression, impotence, and delirium. Characteristic cardiovascular signs and symptoms include palpitations, wide pulse pressure, dyspnea, orthopnea, and tachycardia.
Rabies
Bilateral Babinski’s reflex—possibly elicited by nonspecific noxious stimuli alone—appears in the excitation phase of rabies. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms, such as fever, malaise, and irritability (which occur 30 to 40 days after a bite from an infected animal). Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Seizures and hyperactive DTRs may also occur.
Spinal cord injury
In an acute injury, spinal shock temporarily erases all reflexes. As shock resolves, Babinski’s reflex occurs—unilaterally when the injury affects only one side of the spinal cord (Brown-Séquard syndrome) and bilaterally when the injury affects both sides. Rather than signaling the return of neurologic function, this reflex confirms corticospinal damage. It’s accompanied by hyperactive DTRs, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner’s syndrome, marked by unilateral ptosis, pupillary constriction, and facial anhidrosis, may occur in a lower cervical cord injury.
Spinal cord tumor
In a spinal cord tumor, bilateral Babinski’s reflex occurs with variable loss of pain and temperature sensation, proprioception, and motor function. Spasticity, hyperactive DTRs, absent abdominal reflexes, and incontinence are also characteristic. Diffuse pain may occur at the level of the tumor.
Spinal paralytic poliomyelitis
Unilateral or bilateral Babinski’s reflex occurs 5 to 7 days after the onset of fever. It’s accompanied by progressive weakness, paresthesia, muscle tenderness, spasticity, irritability and, later, atrophy. Resistance to neck flexion is characteristic, as are Hoyne’s, Kernig’s, and Brudzinski’s signs.
Spinal tuberculosis
Spinal tuberculosis may produce bilateral Babinski’s reflex accompanied by variable loss of pain and temperature sensation, proprioception, and motor function. It also causes spasticity, hyperactive DTRs, bladder incontinence, and absent abdominal reflexes.
Stroke
Babinski’s reflex varies with the site of the stroke. A stroke involving the cerebrum produces unilateral Babinski’s reflex accompanied by hemiplegia or hemiparesis, unilateral hyperactive DTRs, hemianopsia, and aphasia. A stroke involving the brain stem produces bilateral Babinski’s reflex accompanied by bilateral weakness or paralysis, bilateral hyperactive DTRs, cranial nerve dysfunction, incoordination, and unsteady gait. Generalized signs and symptoms of stroke include headache, vomiting, fever, disorientation, nuchal rigidity, seizures, and coma.
Syringomyelia
In syringomyelia, bilateral Babinski’s reflex occurs with muscle atrophy and weakness that may progress to paralysis. It’s accompanied by spasticity, ataxia and, occasionally, deep pain. DTRs may be hypoactive or hyperactive. Cranial nerve dysfunction, such as dysphagia and dysarthria, commonly appears late in the disorder.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Complex regional pain syndrome:
Causes
(Handbook of Diseases)
The exact cause of CRPS is unknown. Impaired communication between the damaged nerves of the sympathetic nervous system and the brain may cause interference with normal signals for sensations, temperature, and blood flow. Infection or injury to an area or leg may initiate CRPS.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Posttraumatic stress disorder:
Causes
(Handbook of Diseases)
Posttraumatic stress disorder occurs in response to an extremely distressing event, including a serious threat of harm to the patient or his family, such as war, abuse, violent crime, or natural disaster. It may be triggered by sudden destruction of his home or community by a bombing, fire, flood, tornado, earthquake, or similar disaster. It may also occur after the patient witnesses the death or serious injury of another person by torture, in a death camp, by natural disaster, or by a motor vehicle or airplane crash.
Preexisting psychopathology can predispose some patients to this disorder, but anyone can develop it, especially if the stressor is extreme.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Deep tendon reflexes, hyperactive:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS), which is also known as Lou Gehrig disease, produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor
A cerebral brain tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Hepatic encephalopathy
Generalized hyperactive DTRs occur late in the comatose stage of hepatic encephalopathy and are accompanied by a positive Babinski’s reflex, fetor hepaticus (a musty, sweet odor to the breath), and coma.
Hypocalcemia
Hypocalcemia may produce sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek’s and Trousseau’s signs, carpopedal spasm, and tetany. Other signs and symptoms include abdominal cramps, muscle cramps, arrhythmias, and diarrhea.
Hypomagnesemia
Hypomagnesemia results in gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures. Other signs and symptoms include Chvostek’s sign, confusion, delusions, hallucinations, arrhythmias, and hypotension.
Hypothermia
Mild hypothermia (90°F to 94° F [32.2° C to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Multiple sclerosis
Typically, hyperactive DTRs are preceded by weakness and paresthesia in one or both arms or legs in patients with multiple sclerosis. Associated signs include clonus and a positive Babinski’s reflex. Passive flexion of the patient’s neck may cause a tingling sensation down his back. Later, ataxia, diplopia, vertigo, vomiting, urine retention, or urinary incontinence may occur.
Preeclampsia
Occurring in pregnancy of at least 20 weeks’ duration, preeclampsia may cause gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion
Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms of spinal cord lesion include paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke
Any stroke that affects the origin of the corticospinal tracts causes sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski’s reflex.
Tetanus
With tetanus, sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Babinski's reflex:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Amyotrophic lateral sclerosis
With amyotrophic lateral sclerosis (ALS), a progressive motor neuron disorder, bilateral Babinski’s reflex may occur with hyperactive DTRs and spasticity. Typically, ALS produces fasciculations accompanied by muscle atrophy and weakness. Incoordination makes carrying out activities of daily living difficult for the patient. Associated signs and symptoms include impaired speech; difficulty chewing, swallowing, and breathing; urinary frequency and urgency; and, occasionally, choking and excessive drooling. Although his mental status remains intact, the patient’s poor prognosis may cause periodic depression.
Brain tumor
A brain tumor that involves the corticospinal tract may produce Babinski’s reflex. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral), spasticity, seizures, cranial nerve dysfunction, hemiparesis or hemiplegia, decreased pain sensation, unsteady gait, incoordination, headache, emotional lability, and decreased level of consciousness (LOC).
Head trauma
In a patient with head trauma, unilateral or bilateral Babinski’s reflex may occur as the result of primary corticospinal damage or secondary injury associated with increased intracranial pressure. Hyperactive DTRs and spasticity commonly occur with Babinski’s reflex. The patient may also have weakness and incoordination. Other signs and symptoms vary with the type of head trauma and include headache, vomiting, behavior changes, altered vital signs, and decreased LOC with abnormal pupillary size and response to light.
Meningitis
With meningitis, bilateral Babinski’s reflex commonly follows fever, chills, and malaise and is accompanied by nausea and vomiting. As meningitis progresses, it also causes decreased LOC, nuchal rigidity, positive Brudzinski’s and Kernig’s signs, hyperactive DTRs, and opisthotonos. Associated signs and symptoms include irritability, photophobia, diplopia, delirium, and deep stupor that may progress to coma.
Multiple sclerosis
In most patients with multiple sclerosis, a demyelinating disorder, Babinski’s reflex eventually occurs bilaterally. It follows initial signs and symptoms of multiple sclerosis — usually, paresthesia, nystagmus, and blurred or double vision. Associated signs and symptoms include scanning speech (clipped speech with some pauses between syllables), dysphagia, intention tremor, weakness, incoordination, spasticity, gait ataxia, seizures, paraparesis or paraplegia, bladder incontinence and, occasionally, loss of pain and temperature sensation and proprioception. Emotional lability is also characteristic.
Pernicious anemia
Bilateral Babinski’s reflex occurs late in pernicious anemia when vitamin B12 deficiency affects the central nervous system. Anemia may eventually cause widespread GI, neurologic, and cardiovascular effects. Characteristic GI signs and symptoms include nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation. Gingival bleeding and a sore, inflamed tongue may make eating painful and intensify anorexia. The lips, gums, and tongue also appear markedly pale. Jaundice may cause pale to bright yellow skin.
Characteristic neurologic signs and symptoms include neuritis, weakness, peripheral paresthesia, disturbed position sense, incoordination, ataxia, positive Romberg’s sign, light-headedness, bowel and bladder incontinence, and altered vision (diplopia, blurred vision), taste, and hearing (tinnitus). The disorder may also produce irritability, poor memory, headache, depression, impotence, and delirium. Characteristic cardiovascular signs and symptoms include palpitations, wide pulse pressure, dyspnea, orthopnea, and tachycardia.
Rabies
Bilateral Babinski’s reflex — possibly elicited by nonspecific noxious stimuli alone — appears in the excitation phase of rabies. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms, such as fever, malaise, and irritability (which occur 30 to 40 days after a bite from an infected animal). Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Seizures and hyperactive DTRs may also occur.
Spinal cord injury
With acute injury, spinal shock temporarily erases all reflexes. As shock resolves, Babinski’s reflex occurs — unilaterally when injury affects only one side of the spinal cord (Brown-Séquard’s syndrome), bilaterally when injury affects both sides. Rather than signaling the return of neurologic function, this reflex confirms corticospinal damage. It’s accompanied by hyperactive DTRs, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner’s syndrome, marked by unilateral ptosis, pupillary constriction, and facial anhidrosis, may occur with lower cervical cord injury.
Spinal cord tumor
With spinal cord tumor, bilateral Babinski’s reflex occurs with variable loss of pain and temperature sensation, proprioception, and motor function. Spasticity, hyperactive DTRs, absent abdominal reflexes, and incontinence are also characteristic. Diffuse pain may occur at the level of the tumor.
Stroke
Babinski’s reflex varies with the site of a stroke. If it involves the cerebrum, it produces unilateral Babinski’s reflex accompanied by hemiplegia or hemiparesis, unilateral hyperactive DTRs, hemianopsia, and aphasia. If it involves the brain stem, it produces bilateral Babinski’s reflex accompanied by bilateral weakness or paralysis, bilateral hyperactive DTRs, cranial nerve dysfunction, incoordination, and unsteady gait. Generalized signs and symptoms of stroke include headache, vomiting, fever, disorientation, nuchal rigidity, seizures, and coma.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Deep tendon reflexes, hyperactive:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Amyotrophic lateral sclerosis (ALS).ALS produces generalized hyperactive DTRs accompanied by weakness of the hands and forearms and spasticity of the legs. Eventually, the patient develops atrophy of the neck and tongue muscles, fasciculations, weakness of the legs and, possibly, bulbar signs (for example, dysphagia, dysphonia, facial weakness, and dyspnea).
Brain tumor.A cerebral tumor causes hyperactive DTRs on the side opposite the lesion. Associated signs and symptoms develop slowly and may include unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Hypocalcemia.Hypocalcemia may produce a sudden or gradual onset of generalized hyperactive DTRs with paresthesia, muscle twitching and cramping, positive Chvostek's and Trousseau's signs, carpopedal spasm, and tetany.
Hypomagnesemia.Hypomagnesemia results in the gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
Hypothermia.Mild hypothermia (90° to 94° F [32.2° to 34.4° C]) produces generalized hyperactive DTRs. Other signs and symptoms include shivering, fatigue, weakness, lethargy, slurred speech, ataxia, muscle stiffness, tachycardia, diuresis, bradypnea, hypotension, and cold, pale skin.
Preeclampsia.Occurring in pregnancy of at least 20 weeks' gestation, preeclampsia may cause a gradual onset of generalized hyperactive DTRs. Accompanying signs and symptoms include increased blood pressure; abnormal weight gain; edema of the face, fingers, and abdomen after bed rest; albuminuria; oliguria; a severe headache; blurred or double vision; epigastric pain; nausea and vomiting; irritability; cyanosis; shortness of breath; and crackles. If preeclampsia progresses to eclampsia, the patient develops seizures.
Spinal cord lesion.Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. In a traumatic lesion, hyperactive DTRs follow resolution of spinal shock. In a neoplastic lesion, hyperactive DTRs gradually replace normal DTRs. Other signs and symptoms are paralysis and sensory loss below the level of the lesion, urine retention and overflow incontinence, and alternating constipation and diarrhea. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion, a headache, nasal congestion, nausea, increased blood pressure, and bradycardia.
Stroke.A stroke that affects the origin of the corticospinal tracts causes the sudden onset of hyperactive DTRs on the side opposite the lesion. The patient may also have unilateral paresis or paralysis, anesthesia, visual field deficits, spasticity, and a positive Babinski's reflex.
Tetanus.With tetanus, the sudden onset of generalized hyperactive DTRs accompanies tachycardia, diaphoresis, a low-grade fever, painful and involuntary muscle contractions, trismus (lockjaw), and risus sardonicus (a masklike grin).
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Babinski's reflex [Extensor plantar reflex]:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Amyotrophic lateral sclerosis (ALS).With this progressive motor neuron disorder, bilateral Babinski's reflex may occur with hyperactive DTRs and spasticity. Typically, ALS produces fasciculations accompanied by muscle atrophy and weakness. Incoordination makes carrying out activities of daily living difficult for the patient. Associated signs and symptoms include impaired speech; difficulty chewing, swallowing, and breathing; urinary frequency and urgency; and, occasionally, choking and excessive drooling. Although his mental status remains intact, the patient's poor prognosis may cause periodic depression. Progressive bulbar palsy involves the brain stem and may cause episodes of crying or inappropriate laughter.
Brain tumor.A brain tumor that involves the corticospinal tract may produce Babinski's reflex. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral), spasticity, seizures, cranial nerve dysfunction, hemiparesis or hemiplegia, decreased pain sensation, an unsteady gait, incoordination, headache, emotional lability, and a decreased level of consciousness (LOC).
Head trauma.Unilateral or bilateral Babinski's reflex may occur as the result of primary corticospinal damage or secondary injury associated with increased intracranial pressure. Hyperactive DTRs and spasticity commonly occur with Babinski's reflex. The patient may also have weakness and incoordination. Other signs and symptoms vary with the type of head trauma and include headache, vomiting, behavior changes, altered vital signs, and decreased LOC with abnormal pupillary size and response to light.
Hepatic encephalopathy.Babinski's reflex occurs late in hepatic encephalopathy when the patient slips into a coma. It's accompanied by hyperactive DTRs and fetor hepaticus.
Meningitis.With meningitis, bilateral Babinski's reflex commonly follows fever, chills, and malaise and is accompanied by nausea and vomiting. As meningitis progresses, it also causes decreased LOC, nuchal rigidity, positive Brudzinski's and Kernig's signs, hyperactive DTRs, and opisthotonos. Associated signs and symptoms include irritability, photophobia, diplopia, delirium, and deep stupor that may progress to coma.
Rabies.Bilateral Babinski's reflex—possibly elicited by nonspecific noxious stimuli alone—appears in the excitation phase of rabies. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms, such as fever, malaise, and irritability (which occur 30 to 40 days after a bite from an infected animal). Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Seizures and hyperactive DTRs may also occur.
Spinal cord injury.With acute injury, spinal shock temporarily erases all reflexes. As shock resolves, Babinski's reflex occurs—unilaterally when injury affects only one side of the spinal cord (Brown-Séquard's syndrome), bilaterally when injury affects both sides. Rather than signaling the return of neurologic function, this reflex confirms corticospinal damage. It's accompanied by hyperactive DTRs, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner's syndrome, marked by unilateral ptosis, pupillary constriction, and facial anhidrosis, may occur with lower cervical cord injury.
Spinal cord tumor.With spinal cord tumor, bilateral Babinski's reflex occurs with variable loss of pain and temperature sensation, proprioception, and motor function. Spasticity, hyperactive DTRs, absent abdominal reflexes, and incontinence are also characteristic. Diffuse pain may occur at the level of the tumor.
Spinal paralytic poliomyelitis.Unilateral or bilateral Babinski's reflex occurs 5 to 7 days after the onset of fever. It's accompanied by progressive weakness, paresthesia, muscle tenderness, spasticity, irritability and, later, atrophy. Resistance to neck flexion is characteristic, as are Hoyne's, Kernig's, and Brudzinski's signs.
Spinal tuberculosis.Spiral tuberculosis may produce bilateral Babinski's reflex accompanied by variable loss of pain and temperature sensation, proprioception, and motor function. It also causes spasticity, hyperactive DTRs, bladder incontinence, and absent abdominal reflexes.
Stroke.Babinski's reflex varies with the site of the stroke. If it involves the cerebrum, it produces unilateral Babinski's reflex accompanied by hemiplegia or hemiparesis, unilateral hyperactive DTRs, hemianopsia, and aphasia. If it involves the brain stem, it produces bilateral Babinski's reflex accompanied by bilateral weakness or paralysis, bilateral hyperactive DTRs, cranial nerve dysfunction, incoordination, and an unsteady gait. Generalized signs and symptoms of stroke include headache, vomiting, fever, disorientation, nuchal rigidity, seizures, and coma.
Syringomyelia.With syringomyelia, bilateral Babinski's reflex occurs with muscle atrophy and weakness that may progress to paralysis. It's accompanied by spasticity, ataxia and, occasionally, deep pain. DTRs may be hypoactive or hyperactive. Cranial nerve dysfunction, such as dysphagia and dysarthria, commonly appears late in the disorder.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
"I authorize the release of any medical or other information necessary to process this claim." Do you recognize these words? You should, if...
Germs are a fact of life and catching an infectious disease like a cold may seem inevitable. But there are simple ways to protect yourself against...
Sexual contact can sometimes result in problems. An unwanted pregnancy or sexually transmitted diseases may be some of those consequences. But by...
Health insurance is important to everyone, especially people with chronic conditions like Crohn's disease and ulcerative colitis. Tune in to...
See full list of 4 related videos
» Next page: Symptoms of Reflex sympathetic dystrophy syndrome
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
