Causes of Adie syndrome

Causes of Adie syndrome (Diseases Database):

The follow list shows some of the possible medical causes of Adie syndrome that are listed by the Diseases Database:

• Ross syndrome
• Treponema pallidum
• Diabetes mellitus type 2
• Systemic lupus erythematosus
• Miller Fisher syndrome
• Holmes-Adie syndrome
• Diabetes mellitus type 1
• Sicca syndrome
• Guillain-Barre syndrome
• Temporal arteritis

Source: Diseases Database

Causes of Adie syndrome: Online Medical Books

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

Deep tendon reflexes, hypoactive: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Botulism.

With botulism, generalized hypoactive DTRs accompany progressive descending muscle weakness. Initially, the patient usually complains of blurred and double vision and, occasionally, anorexia, nausea, and vomiting. Other early bulbar findings include vertigo, hearing loss, dysarthria, and dysphagia. The patient may have signs of respiratory distress and severe constipation marked by hypoactive bowel sounds.

Eaton-Lambert syndrome

Eaton-Lambert syndrome produces generalized hypoactive DTRs. Early signs include difficulty rising from a chair, climbing stairs, and walking. The patient may complain of achiness, paresthesia, and muscle weakness that's most severe in the morning. Weakness improves with mild exercise and worsens with strenuous exercise.

Guillain-Barré syndrome.

Guillain-Barré syndrome causes bilateral hypoactive DTRs that progress rapidly from hypotonia to areflexia in several days. This disorder typically causes muscle weakness that begins in the legs and then extends to the arms and, possibly, to the trunk and neck muscles. Occasionally, weakness may progress to total paralysis. Other signs and symptoms include cranial nerve palsies, pain, paresthesia, and signs of brief autonomic dysfunction, such as sinus tachycardia or bradycardia, flushing, fluctuating blood pressure, and anhidrosis or episodic diaphoresis.

Usually, muscle weakness and hypoactive DTRs peak in severity within 10 to 14 days, and then symptoms begin to clear. However, in severe cases, residual hypoactive DTRs and motor weakness may persist.

Peripheral neuropathy

Characteristic of end-stage diabetes mellitus, renal failure, and alcoholism and as an adverse effect of various medications, peripheral neuropathy results in progressive hypoactive DTRs. Other effects include motor weakness, sensory loss, paresthesia, tremors, and possible autonomic dysfunction, such as orthostatic hypotension and incontinence.

Polymyositis

With polymyositis, hypoactive DTRs accompany muscle weakness, pain, stiffness, spasms and, possibly, increased size or atrophy. These effects are usually temporary; their location varies with the affected muscles.

Spinal cord lesions

Spinal cord injury or complete transection produces spinal shock, resulting in hypoactive DTRs (areflexia) below the level of the lesion. Associated signs and symptoms include quadriplegia or paraplegia, flaccidity, a loss of sensation below the level of the lesion, and dry, pale skin. Also characteristic are urine retention with overflow incontinence, hypoactive bowel sounds, constipation, and genital reflex loss. Hypoactive DTRs and flaccidity are usually transient; reflex activity may return within several weeks.

Syringomyelia

Permanent bilateral hypoactive DTRs occur early in syringomyelia, which is a slowly progressive disorder. Other signs and symptoms include muscle weakness and atrophy; loss of sensation, usually extending in a capelike fashion over the arms, shoulders, neck, back, and occasionally the legs; deep, boring pain (despite analgesia) in the limbs; and signs of brain stem involvement (nystagmus, facial numbness, unilateral vocal cord paralysis or weakness, and unilateral tongue atrophy). It's more common in males than in females.

Other causes

Drugs

Barbiturates and paralyzing drugs, such as pancuronium and curare, may cause hypoactive DTRs.

» READ BOOK EXCERPT ONLINE »

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

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

Doll's eye sign, absent [Negative oculocephalic reflex]: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Brain stem infarction

This infarction causes absent doll’s eye sign with a coma. It also causes limb paralysis, cranial nerve palsies (facial weakness, diplopia, blindness or visual field deficits, and nystagmus), bilateral cerebellar ataxia, variable sensory loss, a positive Babinski’s reflex, decerebrate posture, and muscle flaccidity.

Brain stem tumor

Absent doll’s eye sign accompanies a coma in this type of tumor. This sign may be preceded by hemiparesis, nystagmus, extraocular nerve palsies, facial pain or sensory loss, facial paralysis, diminished corneal reflex, tinnitus, hearing loss, dysphagia, drooling, vertigo, dizziness, ataxia, and vomiting.

Central midbrain infarction

Accompanying absent doll’s eye sign are a coma, Weber’s syndrome (oculomotor palsy with contralateral hemiplegia), contralateral ataxic tremor, nystagmus, and pupillary abnormalities.

Cerebellar lesion

Whether associated with abscess, hemorrhage, or tumor, a cerebellar lesion that progresses to a coma may also cause an absent doll’s eye sign. The coma may be preceded by headache, nystagmus, ocular deviation to the side of the lesion, unequal pupils, dysarthria, dysphagia, ipsilateral facial paresis, and cerebellar ataxia. Characteristic signs of increased ICP may also occur, including decreased LOC, abnormal pupillary responses, increased systolic blood pressure, widening pulse pressure, bradycardia, altered respiratory pattern, papilledema, and vomiting.

Pontine hemorrhage

Absent doll’s eye sign and a coma develop within minutes in this life-threatening disorder. Other ominous signs—such as complete paralysis, decerebrate posture, a positive Babinski’s reflex, and small, reactive pupils—may rapidly progress to death.

Posterior fossa hematoma

A subdural hematoma at this location typically causes absent doll’s eye sign and a coma. These signs may be preceded by characteristic signs and symptoms, such as headache, vomiting, drowsiness, confusion, unequal pupils, dysphagia, cranial nerve palsies, stiff neck, and cerebellar ataxia.

Other causes

Drugs

Barbiturates may produce severe central nervous system depression, resulting in a coma and absent doll’s eye sign.

» READ BOOK EXCERPT ONLINE »

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

Deep tendon reflexes, hypoactive: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Botulism

In this disorder, generalized hypoactive DTRs accompany progressive descending muscle weakness. Initially, the patient usually complains of blurred and double vision and, occasionally, anorexia, nausea, and vomiting. Other early bulbar findings include vertigo, hearing loss, dysarthria, and dysphagia. The patient may have signs of respiratory distress and severe constipation marked by hypoactive bowel sounds.

Cerebellar dysfunction

This disorder may produce hypoactive DTRs by increasing the level of inhibition through long tracts upon spinal motor neurons. Associated clinical findings vary depending on the cause and location of the dysfunction.

Eaton-Lambert syndrome

This disorder produces generalized hypoactive DTRs. Early signs include difficulty rising from a chair, climbing stairs, and walking. The patient may complain of achiness, paresthesia, and muscle weakness that’s most severe in the morning. Weakness improves with mild exercise and worsens with strenuous exercise.

Guillain-Barré syndrome

This disorder causes bilateral hypoactive DTRs that progress from hypotonia to areflexia in several days. Guillain-Barré syndrome typically causes muscle weakness that begins in the legs and then extends to the arms and, possibly, to the trunk and neck muscles. Occasionally, weakness may progress to total paralysis. Other signs and symptoms include cranial nerve palsies, pain, paresthesia, and signs of brief autonomic dysfunction, such as sinus tachycardia or bradycardia, flushing, fluctuating blood pressure, and anhidrosis or episodic diaphoresis.

Usually, muscle weakness and hypoactive DTRs peak in severity within 10 to 14 days; then symptoms begin to clear. However, in severe cases, residual hypoactive DTRs and motor weakness may persist.

Peripheral neuropathy

Characteristic of end-stage diabetes mellitus, renal failure, and alcoholism, and as an adverse effect of various medications, peripheral neuropathy results in progressive hypoactive DTRs. Other effects include motor weakness, sensory loss, paresthesia, tremors and, possibly, signs of autonomic dysfunction, such as orthostatic hypotension and incontinence.

Polymyositis

In this disorder, hypoactive DTRs accompany muscle weakness, pain, stiffness, spasms and, possibly, increased size or atrophy. These effects are usually temporary; their location varies with the affected muscles.

Spinal cord lesions

Spinal cord injury or complete transection produces spinal shock, resulting in hypoactive DTRs (areflexia) below the level of the lesion. Associated signs and symptoms include quadriplegia or paraplegia, flaccidity, loss of sensation below the level of the lesion, and dry, pale skin. Also characteristic are urine retention with overflow incontinence, hypoactive bowel sounds, constipation, and genital reflex loss. Hypoactive DTRs and flaccidity are usually transient; reflex activity may return within several weeks.

Syringomyelia

Permanent bilateral hypoactive DTRs occur early in this slowly progressive disorder. Other signs and symptoms are muscle weakness and atrophy; loss of sensation usually extending in a capelike fashion over the arms, shoulders, neck, back, and occasionally the legs; deep, boring pain (despite analgesia) in the limbs; and signs of brain stem involvement (nystagmus, facial numbness, unilateral vocal cord paralysis or weakness, and unilateral tongue atrophy). Syringomyelia is more common in males than in females.

Tabes dorsalis

This progressive disorder results in bilateral hypoactive DTRs in the legs and occasionally the arms. Associated signs and symptoms include sharp pain and paresthesia of the legs, face, or trunk; visceral pain with retching and vomiting; sensory loss in the legs; ataxic gait with a positive Romberg’s sign; urine retention and urinary incontinence; and arthropathies.

Other causes

Drugs

Barbiturates and paralyzing drugs, such as pancuronium, may cause hypoactive DTRs.

» READ BOOK EXCERPT ONLINE »

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

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

Deep Tendon Reflex Abnormalities: Differential Overview
(Field Guide to Bedside Diagnosis)

Hyporeflexia

❑ Nerve root compression

❑ Hypothyroidism

❑ Acute stroke

❑ Diabetes

❑ Alcoholism

❑ Vitamin B₁₂ deficiency

❑ Uremia

❑ Myopathy

❑ Occult cancer

❑ Toxins

❑ Guillain-Barré syndrome

❑ Amyloidosis

❑ Spinal shock

❑ Adie syndrome

❑ Botulism

❑ Charcot-Marie-Tooth

Hyperreflexia

❑ Cervical spondylosis

❑ Spinal cord compression

❑ Multiple small strokes

❑ Multiple sclerosis

❑ Metabolic encephalopathy

❑ Amyotrophic lateral sclerosis

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Deep tendon reflexes, hypoactive: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Botulism

With botulism, generalized hypoactive DTRs accompany progressive descending muscle weakness. Initially, the patient usually complains of blurred and double vision and, occasionally, of anorexia, nausea, and vomiting. Other early bulbar findings include vertigo, hearing loss, dysarthria, and dysphagia. The patient may have signs of respiratory distress and severe constipation marked by hypoactive bowel sounds.

Cerebellar dysfunction

Cerebellar dysfunction may produce hypoactive DTRs by increasing the level of inhibition through long tracts upon spinal motor neurons. Associated clinical findings vary depending on the cause and location of the dysfunction.

Guillain-Barré syndrome

Guillain-Barré syndrome causes bilateral hypoactive DTRs that progress rapidly from hypotonia to areflexia in several days. Guillain-Barré syndrome typically causes muscle weakness that begins in the legs and then extends to the arms and, possibly, to the trunk and neck muscles. Occasionally, weakness may progress to total paralysis. Other signs and symptoms include cranial nerve palsies, pain, paresthesia, and signs of brief autonomic dysfunction, such as sinus tachycardia or bradycardia, flushing, fluctuating blood pressure, and anhidrosis or episodic diaphoresis.

Usually, muscle weakness and hypoactive DTRs peak in severity within 10 to 14 days; then symptoms begin to clear. However, in severe cases, residual hypoactive DTRs and motor weakness may persist.

Peripheral neuropathy

Characteristic of end-stage diabetes mellitus, renal failure, alcoholism, and an adverse effect of various medications, peripheral neuropathy results in progressive hypoactive DTRs. Other effects include motor weakness, sensory loss, paresthesia, tremors, and possible autonomic dysfunction, such as orthostatic hypotension and incontinence.

Polymyositis

With polymyositis, hypoactive DTRs accompany muscle weakness, pain, stiffness, spasms and, possibly, increased size or atrophy. These effects are usually temporary; their location varies with the affected muscles.

Spinal cord lesions

Spinal cord injury or complete transection produces spinal shock, resulting in hypoactive DTRs (areflexia) below the level of the lesion. Associated signs and symptoms include quadriplegia or paraplegia, flaccidity, loss of sensation below the level of the lesion, and dry, pale skin. Also characteristic are urine retention with overflow incontinence, hypoactive bowel sounds, constipation, and genital reflex loss. Hypoactive DTRs and flaccidity are usually transient; reflex activity may return within several weeks.

Syringomyelia

Permanent bilateral hypoactive DTRs occur early in syringomyelia, a slowly progressive disorder. Other signs and symptoms of syringomyelia are muscle weakness and atrophy; loss of sensation, usually extending in a capelike fashion over the arms, shoulders, neck, back, and occasionally the legs; deep, boring pain (despite analgesia) in the limbs; and signs of brain stem involvement (nystagmus, facial numbness, unilateral vocal cord paralysis or weakness, and unilateral tongue atrophy).

Other causes

Drugs

Barbiturates and paralyzing drugs, such as pancuronium and curare, may cause hypoactive DTRs.

» READ BOOK EXCERPT ONLINE »

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

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

Doll's eye sign, absent [Negative oculocephalic reflex]: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Brain stem infarction.Brain stem infarction causes absent doll's eye sign with coma. It also causes limb paralysis, cranial nerve palsies (facial weakness, diplopia, blindness or visual field deficits, and nystagmus), bilateral cerebellar ataxia, variable sensory loss, a positive Babinski's reflex, decerebrate posture, and muscle flaccidity.

Brain stem tumor.Absent doll's eye sign accompanies coma with a brain stem tumor. This sign may be preceded by hemiparesis, nystagmus, extraocular nerve palsies, facial pain or sensory loss, facial paralysis, a diminished corneal reflex, tinnitus, hearing loss, dysphagia, drooling, vertigo, dizziness, ataxia, and vomiting.

Central midbrain infarction.With a central midbrain infarction, absent doll's eye sign is associated with coma, Weber's syndrome (oculomotor palsy with contralateral hemiplegia), contralateral ataxic tremor, nystagmus, and pupillary abnormalities.

Pontine hemorrhage.Absent doll's eye sign and coma develop within minutes with pontine hemorrhage, a life-threatening disorder. Other ominous signs—such as complete paralysis, decerebrate posture, a positive Babinski's reflex, and small, reactive pupils—may rapidly progress to death.

Posterior fossa hematoma.A subdural hematoma at the posterior fossa typically causes absent doll's eye sign and coma. These signs may be preceded by characteristic signs and symptoms, such as a headache, vomiting, drowsiness, confusion, unequal pupils, dysphagia, cranial nerve palsies, a stiff neck, and cerebellar ataxia.

Other causes

Drugs.Barbiturates may produce severe central nervous system depression, resulting in coma and absent doll's eye sign.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Deep tendon reflexes, hypoactive: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Botulism.With botulism, generalized hypoactive DTRs accompany progressive descending muscle weakness. Initially, the patient usually complains of blurred and double vision and, occasionally, anorexia, nausea, and vomiting. Other early bulbar findings include vertigo, hearing loss, dysarthria, and dysphagia. The patient may have signs of respiratory distress and severe constipation marked by hypoactive bowel sounds.

Eaton-Lambert syndrome.Eaton-Lambert syndrome produces generalized hypoactive DTRs. Early signs include difficulty rising from a chair, climbing stairs, and walking. The patient may complain of achiness, paresthesia, and muscle weakness that's most severe in the morning. Weakness improves with mild exercise and worsens with strenuous exercise.

Guillain-Barré syndrome.Guillain-Barré syndrome causes bilateral hypoactive DTRs that progress rapidly from hypotonia to areflexia in several days. This disorder typically causes muscle weakness that begins in the legs and then extends to the arms and, possibly, to the trunk and neck muscles. Occasionally, weakness may progress to total paralysis. Other signs and symptoms include cranial nerve palsies, pain, paresthesia, and signs of brief autonomic dysfunction, such as sinus tachycardia or bradycardia, flushing, fluctuating blood pressure, and anhidrosis or episodic diaphoresis.

Usually, muscle weakness and hypoactive DTRs peak in severity within 10 to 14 days, and then symptoms begin to clear. However, in severe cases, residual hypoactive DTRs and motor weakness may persist.

Peripheral neuropathy.Characteristic of end-stage diabetes mellitus, renal failure, and alcoholism and as an adverse effect of various medications, peripheral neuropathy results in progressive hypoactive DTRs. Other effects include motor weakness, sensory loss, paresthesia, tremors, and possible autonomic dysfunction, such as orthostatic hypotension and incontinence.

Polymyositis.With polymyositis, hypoactive DTRs accompany muscle weakness, pain, stiffness, spasms and, possibly, increased size or atrophy. These effects are usually temporary; their location varies with the affected muscles.

Spinal cord lesions.Spinal cord injury or complete transection produces spinal shock, resulting in hypoactive DTRs (areflexia) below the level of the lesion. Associated signs and symptoms include quadriplegia or paraplegia, flaccidity, a loss of sensation below the level of the lesion, and dry, pale skin. Also characteristic are urine retention with overflow incontinence, hypoactive bowel sounds, constipation, and genital reflex loss. Hypoactive DTRs and flaccidity are usually transient; reflex activity may return within several weeks.

Syringomyelia.Permanent bilateral hypoactive DTRs occur early in syringomyelia, which is a slowly progressive neurologic disorder. Other signs and symptoms include muscle weakness and atrophy; loss of sensation, usually extending in a capelike fashion over the arms, shoulders, neck, back, and occasionally the legs; deep, boring pain (despite analgesia) in the limbs; and signs of brain stem involvement (nystagmus, facial numbness, unilateral vocal cord paralysis or weakness, and unilateral tongue atrophy).

Other causes

Drugs.Barbiturates and paralyzing drugs, such as pancuronium and curare, may cause hypoactive DTRs.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 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).

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Source: Nursing: Interpreting Signs and Symptoms, 2007

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