A hyperactive deep tendon reflex (DTR) is an abnormally brisk muscle contraction that occurs in response to a sudden stretch induced

by sharply tapping the muscle's tendon of insertion. This elicited sign may be graded as brisk or pathologically hyperactive. Hyperactive DTRs are commonly accompanied by clonus.

The corticospinal tract and other descending tracts govern the reflex arc the relay cycle that produces any reflex response. A corticospinal lesion above the level of the reflex arc being tested may result in hyperactive DTRs. Abnormal neuromuscular transmission at the end of the reflex arc may also cause hyperactive DTRs. For example, a calcium or magnesium deficiency may cause hyperactive DTRs because these electrolytes regulate neuromuscular excitability. (See Tracing the reflex arc

Although hyperactive DTRs typically accompany other neurologic findings, they usually lack specific diagnostic value. For example, they're an early, cardinal sign of hypocalcemia.

History and physical examination

After eliciting hyperactive DTRs, take the patient's history. Ask about spinal cord injury or other trauma and about prolonged exposure to cold, wind, or water. Could the patient be pregnant? A positive response to any of these questions requires prompt evaluation to rule out lifethreatening autonomic hyperreflexia, tetanus, preeclampsia, or hypothermia. Ask about the onset and progression of associated signs and symptoms. Next, perform a neurologic examination. Evaluate the patient's level of consciousness, and test motor and sensory function in the limbs. Ask about paresthesia. Check for ataxia or tremors and for speech and visual deficits. Test for Chvostek's (an abnormal spasm of the facial muscles elicited by light taps on the facial nerve in a patient who has hypocalcemia) and Trousseau's (a carpal spasm induced by inflating a sphygmomanometer cuff on the upper arm to a pressure exceeding systolic blood pressure for 3 minutes in a patient who has hypocalcemia or hypomagnesemia) signs and for carpopedal spasm. Ask about vomiting or altered bladder habits. Make sure to take the patient's vital signs.

Medical causes

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).

Special considerations
Prepare the patient for diagnostic tests to evaluate hyperactive DTRs. These may include laboratory tests for serum calcium, magnesium, and ammonia levels; spinal X-rays; magnetic resonance imaging; a computed tomography scan; lumbar puncture; and myelography.

If motor weakness accompanies hyperactive DTRs, perform or encourage range-of-motion exercises to preserve muscle integrity and prevent deep vein thrombosis. Also, reposition the patient frequently, provide a special mattress, massage his back, and ensure adequate nutrition to prevent skin breakdown. Administer a muscle relaxant and sedative to relieve severe muscle contractions. Keep emergency resuscitation equipment on hand. Provide a quiet, calm atmosphere to decrease neuromuscular excitability. Assist with activities of daily living, and provide emotional support.

Pediatric pointers

Hyperreflexia may be a normal sign in neonates. After age 6, reflex responses are similar to those of adults. When testing DTRs in small children, use distraction techniques to promote reliable results.

Cerebral palsy commonly causes hyperactive DTRs in children. Reye's syndrome causes generalized hyperactive DTRs in stage II; in stage V, DTRs are absent. Adult causes of hyperactive DTRs may also appear in children.

A hypoactive deep tendon reflex (DTR) is an abnormally diminished muscle contraction that occurs in response to a sudden stretch induced by sharply tapping the muscles tendon of insertion. It may be graded as minimal (+) or absent (0). Symmetrically reduced (+) reflexes may be normal.

Normally, a DTR depends on an intact receptor, intact sensory-motor nerve fiber, an intact neuromuscular-glandular junction, and a functional synapse in the spinal cord. Hypoactive DTRs may result from damage to the reflex arc involving the specific muscle, the peripheral nerve, the nerve roots, or the spinal cord at that level. Hypoactive DTRs are an important sign of many disorders, especially when they appear with other neurologic signs and symptoms. (See Documenting deep tendon reflexes.)

History and physical examination

After eliciting hypoactive DTRs, obtain a thorough history from the patient or a family member. Have him describe current signs and symptoms in detail. Then take a family and drug history.

Next, evaluate the patients level of consciousness. Test motor function in his limbs, and palpate for muscle atrophy or increased mass. Test sensory function, including pain, touch, temperature, and vibration sensation. Ask about paresthesia. To observe gait and coordination, have the patient take several steps. To check for Rombergs sign, ask him to stand with his feet together and his eyes closed. During conversation, evaluate his speech. Check for signs of vision or hearing loss. Abrupt onset of hypoactive DTRs accompanied by muscle weakness may occur in life-threatening Guillain-Barr syndrome, botulism, or spinal cord lesions with spinal shock.

Look for autonomic nervous system effects by taking vital signs and monitoring for increased heart rate and blood pressure. Also, inspect the skin for pallor, dryness, flushing, or diaphoresis. Auscultate for hypoactive bowel sounds, and palpate for bladder distention. Ask about nausea, vomiting, constipation, and incontinence.

Medical causes
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 thats most severe in the morning. Weakness improves with mild exercise and worsens with strenuous exercise.

Guillain-Barr syndrome
This disorder causes bilateral hypoactive DTRs that progress from hypotonia to areflexia in several days. Guillain-Barr 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 Rombergs sign; urine retention and urinary incontinence; and arthropathies.

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

Special considerations
Help the patient perform his daily activities. Try to strike a balance between promoting independence and ensuring his safety. Encourage him to walk with assistance. Make sure personal care articles are within easy reach, and provide an obstacle-free course from his bed to the bathroom.

If the patient has sensory deficits, protect him from injury from heat, cold, or pressure. Test his bath water, and reposition him frequently, ensuring a soft, smooth bed surface. Keep his skin clean and dry to prevent breakdown. Perform or encourage range-of-motion exercises. Also encourage a balanced diet with plenty of protein and adequate hydration.

Pediatric pointers
Hypoactive DTRs commonly occur in children with muscular dystrophy, Friedreichs ataxia, syringomyelia, or a spinal cord injury. They also accompany progressive muscular atrophy, which affects preschoolers and adolescents.

Use distraction techniques to test DTRs; assess motor function by watching the infant or child at play

Decerebrate posture is characterized by adduction (internal rotation) and extension of the arms, with the wrists pronated and the fingers flexed. The legs are stiffly extended, with forced plantar flexion of the feet. In severe cases, the back is acutely arched (opisthotonos). This sign indicates upper brain stem damage, which may result from primary lesions, such as infarction, hemorrhage, or tumor; metabolic encephalopathy; head injury; or brain stem compression associated with increased intracranial pressure (ICP).

Decerebrate posture may be elicited by noxious stimuli or may occur spontaneously. It may be unilateral or bilateral. With concurrent brain stem and cerebral damage, decerebrate posture may affect only the arms, with the legs remaining flaccid. Or, decerebrate posture may affect one side of the body and decorticate posture the other. The two postures may also alternate as the patients neurologic status fluctuates. Generally, the duration of each posturing episode correlates with the severity of brain stem damage. (See Comparing decerebrate and decorticate postures, page 224.)

Emergency interventions
Your first priority is to ensure a patent airway. Insert an artificial airway and institute measures to prevent aspiration. (Dont disrupt spinal alignment if you suspect spinal cord injury.) Suction the patient as necessary. Next, examine spontaneous respirations. Give supplemental oxygen, and ventilate the patient with a handheld resuscitation bag if necessary. Intubation and mechanical ventilation may be indicated. Keep emergency resuscitation equipment handy, but be sure to check the patients chart for a do-not-resuscitate order.

History and physical examination

After taking vital signs, determine the patients level of consciousness (LOC). Use the Glasgow Coma Scale (GCS) as a reference. Decerebrate posturing indicates the secondlowest measure of motor response, according to the GCS. Patients exhibiting this abnormal posturing have a decreased LOC and may be in a comatose state. Evaluate the pupils for

size, equality, and response to light. Test deep tendon reflexes (DTRs) and cranial nerve reflexes, and check for dolls eye sign.

Next, explore the history of the patients coma. If youre unable to obtain this information, look for clues to the causative disorder, such as hepatomegaly, cyanosis, diabetic skin changes, needle tracks, or obvious trauma. If a family member is available, find out when the patients LOC began deteriorating. Did it occur abruptly? What did the patient complain of before he lost consciousness? Does he have a history of diabetes, liver disease, cancer, blood clots, or aneurysm? Ask about any accident or traumatic injury responsible for the coma.

Medical causes
Brain stem infarction
Decerebrate posture may be elicited when this primary lesion produces a coma. Associated signs and symptoms vary with the severity of the infarct and may include cranial nerve palsies, bilateral cerebellar ataxia, and sensory loss. In a deep coma, all normal reflexes are usually lost, resulting in absence of dolls eye sign, a positive Babinskis reflex, and flaccidity.

Brain stem tumor

In a brain stem tumor, decerebrate posture is a late sign that accompanies a coma. Early findings commonly include hemiparesis or quadriparesis, cranial nerve palsies, vertigo, dizziness, ataxia, and vomiting.

Cerebral lesion
Whether the cause is trauma, tumor, abscess, or infarction, any cerebral lesion that increases ICP may also produce decerebrate posture, which is typically a late sign. Associated findings vary with the lesions site and extent but commonly include a coma, abnormal pupil size and response to light, and the classic triad of increased ICPbradycardia, increasing systolic blood pressure, and widening pulse pressure.

Hepatic encephalopathy
A late sign in this disorder, decerebrate posture occurs with a coma resulting from increased ICP and ammonia toxicity. Associated signs include fetor hepaticus (foul-smelling breath), a positive Babinskis reflex, and hyperactive DTRs.

Hypoglycemic encephalopathy
Characterized by extremely low blood glucose levels, this disorder may produce decerebrate posture and a coma. It also causes dilated pupils, bradypnea, and bradycardia. Muscle spasms, twitching, and seizures eventually progress to flaccidity.

Hypoxic encephalopathy
Severe hypoxia may produce decerebrate posturethe result of brain stem compression associated with anaerobic metabolism and increased ICP. Other findings include a coma, a positive Babinskis reflex, absence of dolls eye sign, hypoactive DTRs, and possibly fixed pupils and respiratory arrest.

Pontine hemorrhage
Typically, this life-threatening disorder rapidly leads to decerebrate posture with a coma. Accompanying signs include total paralysis, absence of dolls eye sign, a positive Babinskis reflex, and small, reactive pupils.

Posterior fossa hemorrhage

This subtentorial lesion causes decerebrate posture. Its early signs and symptoms include vomiting, headache, vertigo, ataxia, stiff neck, drowsiness, papilledema, and cranial nerve palsies. The patient eventually slips into a coma and may experience respiratory arrest.

Other causes
Diagnostic tests

Removal of spinal fluid during a lumbar puncture to relieve high ICP may precipitate cerebral compression of the brain stem and cause decerebrate posture and a coma.

Special considerations
Help prepare the patient for diagnostic tests that will determine the cause of his decerebrate posture. These include skull X-rays, computed tomography scan, magnetic resonance imaging, cerebral angiography, digital subtraction angiography, EEG, brain scan, and ICP monitoring.

Monitor the patients neurologic status and vital signs every 30 minutes or as indicated. Also, be alert for signs of increased ICP (bradycardia, increasing systolic blood pressure, and widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature).

Inform the patients family that decerebrate posture is a reflex responsenot a voluntary response to pain or a sign of recovery. Offer emotional support.

Pediatric pointers
Children younger than age 2 may not display decerebrate posture because the nervous system is still immature. However, if this posture occurs, its usually the more severe opisthotonos. In fact, opisthotonos is more common in infants and young children than in adults and is usually a terminal sign. In children, the most common cause of decerebrate posture is head injury. It also occurs in Reyes syndromethe result of increased ICP causing brain stem compression.

Pictures

The corneal reflex is tested bilaterally by drawing a fine-pointed wisp of sterile cotton from a corner of each eye to the cornea. Normally, even though only one eye is tested at a time, the patient blinks bilaterally each time either cornea is touched this is the corneal reflex. When this reflex is absent, neither eye-lid closes when the cornea of one is touched. (See Eliciting the corneal reflex.)

The site of the afferent fibers for this reflex is in the ophthalmic branch of the trigeminal nerve (cranial nerve [CN] V); the efferent fibers are located in the facial nerve (CN VII). Unilateral or bilateral absence of the corneal reflex may result from damage to these nerves.

History and physical examination

If you can't elicit the corneal reflex, look for other signs of trigeminal nerve dysfunction. To test the three sensory portions of the nerve, touch each side of the patient's face on the brow, cheek, and jaw with a cotton wisp, and ask him to compare the sensations.

If you suspect facial nerve involvement, note if the upper face (brow and eyes) and lower face (cheek, mouth, and chin) are weak bilaterally. Lower motor neuron facial weakness affects the face on the same side as the lesion, whereas upper motor neuron weakness affects the side opposite the lesion predominantly the lower facial muscles.

Because an absent corneal reflex may signify such progressive neurologic disorders as Guillain-Barr syndrome, ask the patient about associated symptoms facial pain, dysphagia, and limb weakness.

Medical causes
Acoustic neuroma.
Acoustic neuroma affects the trigeminal nerve, causing a diminished or absent corneal reflex, tinnitus, and unilateral hearing impairment. Facial palsy and anesthesia, palate weakness, and signs of cerebellar dysfunction (ataxia, nystagmus) may result if the tumor impinges on the adjacent cranial nerves, brain stem, and cerebellum.

Bell's palsy.
A common cause of diminished or absent corneal reflex, Bell's palsy causes paralysis of CN VII. It can also produce complete hemifacial weakness or paralysis and drooling on the affected side, which also sags and appears masklike. The eye on this side can't be shut and tears constantly.

Brain stem infarction or injury.

An absent corneal reflex can occur on the side opposite the lesion when infarction or injury affects CN V or VII or their connection in the central trigeminal tract. Associated findings include a decreased level of consciousness, dysphagia, dysarthria, contralateral limb weakness, and early signs and symptoms of increased intracranial pressure, such as a headache and vomiting.

With massive brain stem infarction or injury, the patient also displays respiratory changes, such as apneustic breathing or periods of apnea; bilateral pupillary dilation or constriction with decreased responsiveness to light; rising systolic blood pressure; a widening pulse pressure; bradycardia; and coma.

Guillain-Barr syndrome.
With this polyneuropathic disorder, a diminished or absent corneal reflex accompanies ipsilateral loss of facial muscle control. Muscle weakness, the dominant neurologic sign of this disorder, typically starts in the legs, and then extends to the arms and facial nerves within 72 hours. Other findings include dysarthria, dysphagia, paresthesia, respiratory muscle paralysis, respiratory insufficiency, orthostatic hypotension, incontinence, diaphoresis, and tachycardia.

Special considerations
When the corneal reflex is absent, you'll need to take measures to protect the patient's affected eye from injury such as lubricating the eye with artificial tears to prevent drying. Cover the cornea with a shield and avoid excessive corneal reflex testing. Prepare the patient for cranial X-rays or a computed tomography scan.

Pediatric pointers
Brain stem lesions and injuries are usual causes of absent corneal reflexes in children; Guillain-Barr syndrome and trigeminal neuralgia are less common. Infants, especially those born prematurely, may have an absent corneal reflex due to anoxic damage to the brain stem

Babinski's reflex dorsiflexion of the great toe with extension and fanning of the other toes is an abnormal reflex elicited by firmly stroking the lateral aspect of the sole of the foot with a moderately sharp object. (SeeHow to elicit Babinski's reflex, page 70.) In some patients, this reflex can be triggered by noxious stimuli, such as pain, noise, or even bumping the bed. An indicator of corticospinal damage, Babinski's reflex may occur unilaterally or bilaterally and may be temporary or permanent. A temporary Babinski's reflex commonly occurs during the postictal phase of a seizure, whereas a permanent Babinski's reflex occurs with corticospinal damage. A positive Babinski's reflex is normal in neonates and in infants up to 24 months old.

History and physical examination

After eliciting a positive Babinski's reflex, evaluate the patient for other neurologic signs. Evaluate muscle strength in each extremity by having the patient push or pull against your resistance. Passively flex and extend the extremity to assess muscle tone. Intermittent resistance to flexion and extension indicates spasticity, and a lack of resistance indicates flaccidity.

Next, check for evidence of incoordination by asking the patient to perform a repetitive activity. Test deep tendon reflexes (DTRs) in the patient's elbow, antecubital area, wrist, knee, and ankle by striking the tendon with a reflex hammer. An exaggerated muscle response indicates hyperactive DTRs; little or no muscle response indicates hypoactivity.

Then evaluate pain sensation and proprioception in the feet. As you move the patient's toes up and down, ask the patient to identify the direction in which the toes have been moved without looking at his feet.

Medical causes
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-Squard'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.

Special considerations
Babinski's reflex usually occurs with incoordination, weakness, and spasticity, all of which increase the patient's risk of injury. To prevent injury, assist the patient with activity and keep his environment free from obstructions.

Diagnostic tests may include a computed tomography scan or magnetic resonance imaging of the brain or spine, angiography or myelography and, possibly, a lumbar puncture to clarify or confirm the cause of Babinski's reflex. Prepare the patient as necessary.

Pediatric pointers
Babinski's reflex occurs normally in infants ages 18 to 24 months, reflecting immaturity of the corticospinal tract. After age 2, Babinski's reflex is pathologic and may result from hydrocephalus or any of the causes more commonly seen in adults.

The gag reflex a protective mechanism that prevents aspiration of food, fluid, and vomitus normally can be elicited by touching the posterior wall of the oropharynx with a tongue depressor or by suctioning the throat. Prompt elevation of the palate, constriction of the pharyngeal musculature, and a sensation of gagging indicate a normal gag reflex. An abnormal gag reflex either decreased or absent interferes with the ability to swallow and, more important, increases susceptibility to life-threatening aspiration.

An impaired gag reflex can result from a lesion that affects its mediators cranial nerves (CNs) IX (glossopharyngeal) and X (vagus) or the pons or medulla. It can also occur during a coma, in muscle diseases such as severe myasthenia gravis, or as a temporary result of anesthesia.

Emergency interventions
If you detect an abnormal gag reflex, immediately stop the patients oral intake to prevent aspiration. Quickly evaluate his level of consciousness (LOC). If its decreased, place him in a side-lying position to prevent aspiration; if not, place him in Fowlers position. Have suction equipment at hand.

History and physical examination

Ask the patient (or a family member if the patient cant communicate) about the onset and duration of swallowing difficulties, if any. Are liquids more difficult to swallow than solids? Is swallowing more difficult at certain times of the day (as occurs in the bulbar palsy associated

with myasthenia gravis)? If the patient also has trouble chewing, suspect more widespread neurologic involvement because chewing involves different CNs.

Explore the patients medical history for vascular and degenerative disorders. Then assess his respiratory status for evidence of aspiration, and perform a neurologic examination.

Medical causes
Basilar artery occlusion
Basilar artery occlusion may suddenly diminish or obliterate the gag reflex. It also causes diffuse sensory loss, dysarthria, facial weakness, extraocular muscle palsies, quadriplegia, and a decreased LOC.

Brain stem glioma

Brain stem glioma causes a gradual loss of the gag reflex. Related symptoms reflect bilateral brain stem involvement and include diplopia and facial weakness. Common involvement of the corticospinal pathways causes spasticity and paresis of the arms and legs as well as gait disturbances.

Bulbar palsy
Loss of the gag reflex reflects temporary or permanent paralysis of muscles supplied by CNs IX and X. Other indicators of bulbar palsy include jaw and facial muscle weakness, dysphagia, loss of sensation at the base of the tongue, increased salivation, possible difficulty articulating and breathing, and fasciculations.

Wallenbergs syndrome
Paresis of the palate and an impaired gag reflex usually develop within hours to days of thrombosis. The patient may experience analgesia and thermanesthesia, occurring ipsilaterally on the face and contralaterally on the body, and vertigo. He may also display

nystagmus, ipsilateral ataxia of the arm and leg, and signs of Horners syndrome (unilateral ptosis and miosis, hemifacial anhidrosis).

Other causes
Anesthesia
General and local (throat) anesthesia can produce temporary loss of the gag reflex.

Special considerations
Continually assess the patients ability to swallow. If his gag reflex is absent, provide tube feedings; if its merely diminished, try pureed foods. Advise the patient to take small amounts and eat slowly while sitting or in high Fowlers position. Stay with him while he eats and observe for choking. Remember to keep suction equipment handy in case of aspiration. Keep accurate intake and output records, and assess the patients nutritional status daily.

Refer the patient to a therapist to determine his aspiration risk and develop an exercise program to strengthen specific muscles.

Prepare the patient for diagnostic studies, such as swallow studies, a computed tomography scan, magnetic resonance imaging, EEG, lumbar puncture, and arteriography.

An indicator of brain stem dysfunction, the absence of the doll's eye sign is detected by rapid, gentle turning of the patient's head from side to side. The eyes remain fixed in midposition, instead of the normal response of moving laterally toward the side opposite the direction the head is turned. (See Testing for absent doll's eye sign.)

The absence of doll's eye sign indicates injury to the midbrain or pons, involving cranial nerves III and VI. It typically accompanies coma caused by lesions of the cerebellum and brain stem. This sign usually can't be relied upon in a conscious patient because he can control eye movements voluntarily. Absent doll's eye sign is necessary for a diagnosis of brain death.

A variant of absent doll's eye sign that develops gradually is known as abnormal doll's eye sign. Because conjugate eye movement is lost, one eye may move laterally while the other remains fixed or moves in the opposite direction. An abnormal doll's eye sign usually accompanies metabolic coma or increased intracranial pressure (ICP). Associated brain stem dysfunction may be reversible or may progress to deeper coma with absent doll's eye sign.

History and physical examination

After detecting an absent doll's eye sign, perform a neurologic examination. First, evaluate the patient's level of consciousness, using the Glasgow Coma Scale. Note decerebrate or decorticate posture. Examine the pupils for size, equality, and response to light. Check for signs of increased ICPincreased blood pressure, increasing pulse pressure, and bradycardia.

Medical causes
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 signssuch as complete paralysis,

decerebrate posture, a positive Babinski's reflex, and small, reactive pupilsmay 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.

Nursing considerations
Don't attempt to elicit doll's eye sign in a comatose patient with suspected cervical spine injury; doing so risks spinal cord damage.

Monitor vital signs and neurologic status.

Discuss end-of-life issues with the patient's family, if appropriate.

Provide emotional support to the family.

Patient teaching
Explain to the patient the underlying cause and its treatment.

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