Causes of Brown-Sequard Syndrome

List of causes of Brown-Sequard Syndrome

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Brown-Sequard Syndrome) that could possibly cause Brown-Sequard Syndrome includes:

• Spinal cord tumor
• Spinal cord trauma
• Degenerative disease
• Ischemia (obstruction of a blood vessel)
• Meningitis
• Shingles
• Tuberculosis
• Multiple sclerosis

Related information on causes of Brown-Sequard Syndrome:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Brown-Sequard Syndrome may be found in:

• Hidden causes of Brown-Sequard Syndrome

Causes of Brown-Sequard Syndrome: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Brown-Sequard Syndrome.

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

❑ Anterior cord syndrome. With anterior cord syndrome, analgesia and thermanesthesia occur bilaterally below the level of the lesion, along with flaccid paralysis and hypoactive deep tendon reflexes.

❑ Central cord syndrome. Typically, analgesia and thermanesthesia occur bilaterally in several dermatomes, in many cases extending in a capelike fashion over the arms, back, and shoulders. Early weakness in the hands progresses to weakness and muscle spasms in the arms and shoulder girdle. Hyperactive deep tendon reflexes and spastic weakness of the legs may develop. However, if the lesion affects the lumbar spine, hypoactive deep tendon reflexes and flaccid weakness may persist in the legs.

With brain stem involvement, additional findings include facial analgesia and thermanesthesia, vertigo, nystagmus, atrophy of the tongue, and dysarthria. The patient may also have dysphagia, urine retention, anhidrosis, decreased intestinal motility, and hyperkeratosis.

❑ Spinal cord hemisection. Contralateral analgesia and thermanesthesia occur below the level of the lesion. In addition, loss of proprioception, spastic paralysis, and hyperactive deep tendon reflexes develop ipsilaterally. The patient may also experience urine retention with overflow incontinence.

Other causes

❑ Drugs. Analgesia may occur with use of a topical or local anesthetic, although numbness and tingling are more common.

» 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

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

Anterior cord syndrome

In anterior cord syndrome, analgesia and thermoanesthesia occur bilaterally below the level of the lesion along with flaccid paralysis and hypoactive DTRs.

Central cord syndrome

In central cord syndrome, analgesia and thermoanesthesia typically occur bilaterally in several dermatomes and may extend in a capelike fashion over the arms, back, and shoulders. Early weakness in the hands progresses to weakness and muscle spasms in the arms and shoulder girdle. Hyperactive DTRs and spastic weakness of the legs may develop. However, if the lesion affects the lumbar spine, hypoactive DTRs and flaccid weakness may persist in the legs.

With brain stem involvement, additional findings include facial analgesia and thermoanesthesia, vertigo, nystagmus, atrophy of the tongue, and dysarthria. The patient may also have anhidrosis, dysphagia, urine retention, decreased intestinal motility, and hyperkeratosis.

Spinal cord hemisection

Contralateral analgesia and thermoanesthesia occur below the level of the lesion. In addition, loss of proprioception, spastic paralysis, and hyperactive deep tendon reflexes develop ipsilaterally. The patient may also experience urine retention with overflow incontinence.

Other causes

Drugs

Analgesia may occur with use of a topical or local anesthetic, although numbness and tingling are more common.

» 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

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

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

Anterior cord syndrome

Analgesia and thermanesthesia occur bilaterally below the level of the lesion, along with flaccid paralysis and hypoactive DTRs.

Central cord syndrome

Analgesia and thermanesthesia occur bilaterally in several dermatomes, in many cases extending in a capelike fashion over the arms, back, and shoulders. Early weakness in the hands is evident and progresses to weakness and muscle spasms in the arms and shoulder girdle. Hyperactive DTRs and spastic weakness of the legs may develop. (If hypoactive, DTRs and flaccid weakness persist in the legs, a lesion in the lumbar spine may be suspected.)

With brain stem involvement, additional findings include facial analgesia and thermanesthesia, vertigo, nystagmus, atrophy of the tongue, dysarthria, dysphagia, urine retention, anhidrosis, decreased intestinal motility, and hyperkeratosis.

Spinal cord hemisection

Contralateral analgesia and thermanesthesia occur below the level of the lesion. In addition, loss of proprioception, spastic paralysis, and hyperactive DTRs develop ipsilaterally. Urine retention with overflow incontinence may be present.

Other causes

Drugs

Analgesia may occur with the use of a topical or local anesthetic, although numbness and tingling are more common.

» READ BOOK EXCERPT ONLINE »

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

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

Anterior cord syndrome.With anterior cord syndrome, analgesia and thermanesthesia occur bilaterally below the level of the lesion, along with flaccid paralysis and hypoactive deep tendon reflexes.

Central cord syndrome.Typically, analgesia and thermanesthesia occur bilaterally in several dermatomes, in many cases extending in a capelike fashion over the arms, back, and shoulders. Early weakness in the hands progresses to weakness and muscle spasms in the arms and shoulder girdle. Hyperactive deep tendon reflexes and spastic weakness of the legs may develop. If the lesion affects the lumbar spine, hypoactive deep tendon reflexes and flaccid weakness may persist in the legs.

With brain stem involvement, additional findings include facial analgesia and thermanesthesia, vertigo, nystagmus, atrophy of the tongue, and dysarthria. The patient may also have dysphagia, urine retention, anhidrosis, decreased intestinal motility, and hyperkeratosis.

Spinal cord hemisection.Contralateral analgesia and thermanesthesia occur below the level of the lesion. In addition, loss of proprioception, spastic paralysis, and hyperactive deep tendon reflexes develop ipsilaterally. The patient may also experience urine retention with overflow incontinence.

Other causes

Drugs.Analgesia may occur with use of a topical or local anesthetic, although numbness and tingling are more common.

» 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 Brown-Sequard Syndrome

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