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.
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).
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 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 results in the gradual onset of generalized hyperactive DTRs accompanied by muscle cramps, hypotension, tachycardia, paresthesia, ataxia, tetany and, possibly, seizures.
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.
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
visual field deficits. Administer a muscle relaxant and sedative to relieve severe muscle contractions. diaphoresis.
If motor weakness accompanies hyperactive DTRs.Incomplete spinal cord lesions cause hyperactive DTRs below the level of the lesion. and myelography. Also. Other signs and symptoms are paralysis and sensory loss below the level of the lesion.
With tetanus. urine retention and overflow incontinence. nasal congestion. The patient may also have unilateral paresis or paralysis. a headache. spasticity. and a positive Babinski's reflex. and risus sardonicus (a masklike grin). magnesium. reposition the patient frequently.
Prepare the patient for diagnostic tests to evaluate hyperactive DTRs.
Stroke. In a traumatic lesion. and ammonia levels. Keep emergency resuscitation equipment on hand. A lesion above T6 may also produce autonomic hyperreflexia with diaphoresis and flushing above the level of the lesion. These may include laboratory tests for serum calcium. calm atmosphere to decrease neuromuscular excitability.
A stroke that affects the origin of the corticospinal tracts causes the sudden onset of hyperactive DTRs on the side opposite the lesion. anesthesia.
. In a neoplastic lesion. Assist with activities of daily living. and ensure adequate nutrition to prevent skin breakdown. spinal X-rays. painful and involuntary muscle contractions.
Tetanus. and provide emotional support. nausea. and alternating constipation and diarrhea. lumbar puncture. Provide a quiet. trismus (lockjaw). massage his back. and bradycardia. hyperactive DTRs follow resolution of spinal shock. hyperactive DTRs gradually replace normal DTRs. a low-grade fever. perform or encourage range-of-motion exercises to preserve muscle integrity and prevent deep vein thrombosis. magnetic resonance imaging. the sudden onset of generalized hyperactive DTRs accompanies tachycardia. provide a special mattress. a computed tomography scan. increased blood pressure.
or the spinal cord at that level. Hypoactive DTRs may result from damage to the reflex arc involving the specific muscle. It may be graded as minimal (+) or absent (0). Ask about paresthesia. ask him to stand with his feet together and his eyes closed. Test motor function in his limbs.
Next. and vibration sensation. an intact neuromuscular-glandular junction.
Cerebral palsy commonly causes hyperactive DTRs in children. (See Documenting deep tendon reflexes.Hyperreflexia may be a normal sign in neonates. especially when they appear with other neurologic signs and symptoms. have the patient take several steps. obtain a thorough history from the patient or a family member. the peripheral nerve. Reye's syndrome causes generalized hyperactive DTRs in stage II. Check for signs of vision or hearing loss. When testing DTRs in small children. reflex responses are similar to those of adults.
Normally. To observe gait and coordination. the nerve roots. During conversation. Then take a family and drug history. in stage V.)
History and physical examination
After eliciting hypoactive DTRs.
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 muscle’s tendon of insertion. intact sensory-motor nerve fiber. Test sensory function. botulism. Symmetrically reduced (+) reflexes may be normal. and palpate for muscle atrophy or increased mass. or spinal cord lesions with spinal shock. use distraction techniques to promote reliable results. temperature. a DTR depends on an intact receptor. including pain. DTRs are absent. evaluate his speech. To check for Romberg’s sign. evaluate the patient’s level of consciousness. and a functional synapse in the spinal cord. touch. After age 6. Hypoactive DTRs are an important sign of many disorders.
. Adult causes of hyperactive DTRs may also appear in children. Have him describe current signs and symptoms in detail. Abrupt onset of hypoactive DTRs accompanied by muscle weakness may occur in life-threatening Guillain-Barré syndrome.
Initially. flushing. vomiting. and walking. generalized hypoactive DTRs accompany progressive descending muscle weakness.Look for autonomic nervous system effects by taking vital signs and monitoring for increased heart rate and blood pressure. and incontinence. anorexia. Early signs include difficulty rising from a chair. to the trunk and neck muscles. inspect the skin for pallor. and vomiting. Weakness improves with mild exercise and worsens with strenuous exercise. the patient usually complains of blurred and double vision and.
This disorder produces generalized hypoactive DTRs. climbing stairs. hearing loss. and dysphagia. Guillain-Barré syndrome typically causes muscle weakness that begins in the legs and then extends to the arms and. Auscultate for hypoactive bowel sounds. occasionally.
In this disorder. paresthesia. Associated clinical findings vary depending on the cause and location of the dysfunction. Ask about nausea. Other early bulbar findings include vertigo. Also. dryness. possibly. The patient may complain of achiness. and muscle weakness that’s most severe in the morning. Occasionally. and palpate for bladder distention.
This disorder may produce hypoactive DTRs by increasing the level of inhibition through long tracts upon spinal motor neurons.
This disorder causes bilateral hypoactive DTRs that progress from hypotonia to areflexia in several days. nausea. weakness may progress to total paralysis. dysarthria. constipation. Other signs and symptoms include cranial nerve
. The patient may have signs of respiratory distress and severe constipation marked by hypoactive bowel sounds. or diaphoresis.
. and alcoholism. deep. Other effects include motor weakness. flushing. and as an adverse effect of various medications. However. their location varies with the affected muscles.
Spinal cord lesions
Spinal cord injury or complete transection produces spinal shock. muscle weakness and hypoactive DTRs peak in severity within 10 to 14 days. fluctuating blood pressure. such as sinus tachycardia or bradycardia. shoulders. peripheral neuropathy results in progressive hypoactive DTRs. constipation. reflex activity may return within several weeks. flaccidity. Hypoactive DTRs and flaccidity are usually transient. renal failure.palsies. resulting in hypoactive DTRs (areflexia) below the level of the lesion. Also characteristic are urine retention with overflow incontinence. and genital reflex loss. tremors and. signs of autonomic dysfunction. sensory loss. possibly. hypoactive bowel sounds. and occasionally the legs. residual hypoactive DTRs and motor weakness may persist. spasms and. paresthesia. pain. neck. hypoactive DTRs accompany muscle weakness. increased size or atrophy. and signs of brief autonomic dysfunction. and anhidrosis or episodic diaphoresis. stiffness.
Permanent bilateral hypoactive DTRs occur early in this slowly progressive disorder. such as orthostatic hypotension and incontinence.
In this disorder. pale skin. paresthesia. then symptoms begin to clear.
Characteristic of end-stage diabetes mellitus. Other signs and symptoms are muscle weakness and atrophy. in severe cases. possibly. loss of sensation below the level of the lesion. and dry. loss of sensation usually extending in a capelike fashion over the arms. back. Associated signs and symptoms include quadriplegia or paraplegia. These effects are usually temporary. pain.
ensuring a soft. which affects preschoolers and adolescents. and unilateral tongue atrophy).
. Make sure personal care articles are within easy reach. and provide an obstacle-free course from his bed to the bathroom. or pressure. Also encourage a balanced diet with plenty of protein and adequate hydration. unilateral vocal cord paralysis or weakness.
If the patient has sensory deficits. may cause hypoactive DTRs. protect him from injury from heat. Try to strike a balance between promoting independence and ensuring his safety. face. ataxic gait with a positive Romberg’s sign. Encourage him to walk with assistance.
Help the patient perform his daily activities. such as pancuronium. and reposition him frequently. They also accompany progressive muscular atrophy. Perform or encourage range-of-motion exercises. Test his bath water. smooth bed surface. and signs of brain stem involvement (nystagmus.
Barbiturates and paralyzing drugs.
Hypoactive DTRs commonly occur in children with muscular dystrophy. urine retention and urinary incontinence. Syringomyelia is more common in males than in females. cold. or trunk. Keep his skin clean and dry to prevent breakdown. facial numbness. or a spinal cord injury. visceral pain with retching and vomiting.
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.boring pain (despite analgesia) in the limbs. and arthropathies. syringomyelia. Friedreich’s ataxia. sensory loss in the legs.
The two postures may also alternate as the patient’s neurologic status fluctuates. which may result from primary lesions. Insert an artificial airway and institute measures to prevent aspiration. Keep emergency resuscitation equipment handy.)
Your first priority is to ensure a patent airway.) Suction the patient as necessary.
History and physical examination
After taking vital signs. Use the Glasgow Coma Scale (GCS) as a reference. or tumor. It may be unilateral or bilateral. assess motor function by watching the infant or child at play
Decerebrate posture is characterized by adduction (internal rotation) and extension of the arms. such as infarction. the back is acutely arched (opisthotonos). with forced plantar flexion of the feet. Generally. examine spontaneous respirations. Or. but be sure to check the patient’s chart for a do-not-resuscitate order. In severe cases. Next. Intubation and mechanical ventilation may be indicated. the duration of each posturing episode correlates with the severity of brain stem damage. or brain stem compression associated with increased intracranial pressure (ICP). (Don’t disrupt spinal alignment if you suspect spinal cord injury. Give supplemental oxygen. decerebrate posture may affect only the arms. Decerebrate posturing indicates the secondlowest measure of motor response.
Decerebrate posture may be elicited by noxious stimuli or may occur spontaneously. hemorrhage. head injury. With concurrent brain stem and cerebral damage. (See Comparing decerebrate and decorticate postures. The legs are stiffly extended.Use distraction techniques to test DTRs. with the legs remaining flaccid. decerebrate posture may affect one side of the body and decorticate posture the other. determine the patient’s level of consciousness (LOC). and ventilate the patient with a handheld resuscitation bag if necessary. Evaluate the pupils for
. metabolic encephalopathy. with the wrists pronated and the fingers flexed. Patients exhibiting this abnormal posturing have a decreased LOC and may be in a comatose state. page 224. according to the GCS. This sign indicates upper brain stem damage.
In a deep coma. or infarction. If a family member is available. which is typically a late sign. all normal reflexes are usually lost.
Next. abscess. cancer. Did it occur abruptly? What did the patient complain of before he lost consciousness? Does he have a history of diabetes. dizziness.
Brain stem tumor
In a brain stem tumor. vertigo. Early findings commonly include hemiparesis or quadriparesis. bilateral cerebellar ataxia. and check for doll’s eye sign. explore the history of the patient’s coma. needle tracks. liver disease. cyanosis. Associated findings vary with the lesion’s site and extent but commonly include a coma. or obvious trauma. and sensory loss. or aneurysm? Ask about any accident or traumatic injury responsible for the coma. blood clots. such as hepatomegaly.
Brain stem infarction
Decerebrate posture may be elicited when this primary lesion produces a coma. equality. a positive Babinski’s reflex. look for clues to the causative disorder. cranial nerve palsies. abnormal pupil size and response to light. If you’re unable to obtain this information.size. any cerebral lesion that increases ICP may also produce decerebrate posture.
. decerebrate posture is a late sign that accompanies a coma. ataxia.
Whether the cause is trauma. Test deep tendon reflexes (DTRs) and cranial nerve reflexes. resulting in absence of doll’s eye sign. and widening pulse pressure. tumor. and flaccidity. and the classic triad of increased ICP—bradycardia. diabetic skin changes. and response to light. Associated signs and symptoms vary with the severity of the infarct and may include cranial nerve palsies. and vomiting. increasing systolic blood pressure. find out when the patient’s LOC began deteriorating.
Posterior fossa hemorrhage
This subtentorial lesion causes decerebrate posture. vertigo.
Typically. ataxia. decerebrate posture occurs with a coma resulting from increased ICP and ammonia toxicity. and small. a positive Babinski’s reflex. a positive Babinski’s reflex.Hepatic encephalopathy
A late sign in this disorder.
Characterized by extremely low blood glucose levels. papilledema. and bradycardia. headache.
. this life-threatening disorder rapidly leads to decerebrate posture with a coma. Muscle spasms. Accompanying signs include total paralysis. Associated signs include fetor hepaticus (foul-smelling breath). absence of doll’s eye sign. stiff neck. and possibly fixed pupils and respiratory arrest. It also causes dilated pupils. and hyperactive DTRs. absence of doll’s eye sign. bradypnea. a positive Babinski’s reflex.
Severe hypoxia may produce decerebrate posture—the result of brain stem compression associated with anaerobic metabolism and increased ICP. this disorder may produce decerebrate posture and a coma. twitching. Its early signs and symptoms include vomiting. and cranial nerve palsies. reactive pupils. hypoactive DTRs. Other findings include a coma. and seizures eventually progress to flaccidity. The patient eventually slips into a coma and may experience respiratory arrest. drowsiness.
be alert for signs of increased ICP (bradycardia. In children. However. Offer emotional support. These include skull X-rays. computed tomography scan.
Monitor the patient’s neurologic status and vital signs every 30 minutes or as indicated. brain scan. EEG.
Inform the patient’s family that decerebrate posture is a reflex response—not a voluntary response to pain or a sign of recovery. and ICP monitoring. It also occurs in Reye’s syndrome—the result of increased ICP causing brain stem compression. digital subtraction angiography. if this posture occurs. the most common cause of decerebrate posture is head injury.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. it’s usually the more severe opisthotonos. and widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature). Also. In fact.
Children younger than age 2 may not display decerebrate posture because the nervous system is still immature. cerebral angiography. increasing systolic blood pressure. opisthotonos is more common in infants and young children than in adults and is usually a terminal sign. magnetic resonance imaging.
Help prepare the patient for diagnostic tests that will determine the cause of his decerebrate posture.
the efferent fibers are located in the facial nerve (CN VII).
History and physical examination
If you can't elicit the corneal reflex. look for other signs of trigeminal nerve dysfunction.)
The site of the afferent fibers for this reflex is in the ophthalmic branch of the trigeminal nerve (cranial nerve [CN] V). When this reflex is absent. Normally. the patient blinks bilaterally each time either cornea is touched — this is the corneal reflex. (See Eliciting the corneal reflex.
. and jaw with a cotton wisp. and ask him to compare the sensations. neither eye-lid closes when the cornea of one is touched. cheek. even though only one eye is tested at a time.The corneal reflex is tested bilaterally by drawing a fine-pointed wisp of sterile cotton from a corner of each eye to the cornea. Unilateral or bilateral absence of the corneal reflex may result from damage to these nerves. To test the three sensory portions of the nerve. touch each side of the patient's face on the brow.
palate weakness. contralateral limb weakness. mouth. Bell's palsy causes paralysis of CN VII.
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.
A common cause of diminished or absent corneal reflex.
. which also sags and appears masklike. Lower motor neuron facial weakness affects the face on the same side as the lesion. Facial palsy and anesthesia. and early signs and symptoms of increased intracranial pressure. dysphagia. Associated findings include a decreased level of consciousness.
Bell's palsy. and chin) are weak bilaterally.
Acoustic neuroma. nystagmus) may result if the tumor impinges on the adjacent cranial nerves. dysarthria. and signs of cerebellar dysfunction (ataxia. such as a headache and vomiting. dysphagia. whereas upper motor neuron weakness affects the side opposite the lesion — predominantly the lower facial muscles. It can also produce complete hemifacial weakness or paralysis and drooling on the affected side.
Because an absent corneal reflex may signify such progressive neurologic disorders as Guillain-Barré syndrome. tinnitus. and cerebellum. ask the patient about associated symptoms — facial pain. causing a diminished or absent corneal reflex.
Brain stem infarction or injury. The eye on this side can't be shut and tears constantly.
Acoustic neuroma affects the trigeminal nerve. and unilateral hearing impairment. and limb weakness.If you suspect facial nerve involvement. note if the upper face (brow and eyes) and lower face (cheek. brain stem.
such as apneustic breathing or periods of apnea.) In some patients.
Brain stem lesions and injuries are usual causes of absent corneal reflexes in children. paresthesia. or even bumping the bed. (SeeHow to elicit Babinski's reflex. Prepare the patient for cranial X-rays or a computed tomography scan. a diminished or absent corneal reflex accompanies ipsilateral loss of facial muscle control. An indicator of corticospinal damage. and tachycardia. respiratory muscle paralysis. Cover the cornea with a shield and avoid excessive corneal reflex testing. this reflex can be triggered by noxious stimuli. dysphagia. and coma. Other findings include dysarthria.
Guillain-Barré syndrome. a widening pulse pressure. especially those born prematurely. noise.
. whereas a permanent Babinski's reflex occurs with corticospinal damage. typically starts in the legs.
With this polyneuropathic disorder. rising systolic blood pressure. diaphoresis.
When the corneal reflex is absent.With massive brain stem infarction or injury. Infants. and then extends to the arms and facial nerves within 72 hours. bilateral pupillary dilation or constriction with decreased responsiveness to light. 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. A positive Babinski's reflex is normal in neonates and in infants up to 24 months old. Guillain-Barré syndrome and trigeminal neuralgia are less common. respiratory insufficiency. the dominant neurologic sign of this disorder. 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. incontinence. the patient also displays respiratory changes. Muscle weakness. page 70. 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. orthostatic hypotension. such as pain. bradycardia.
Passively flex and extend the extremity to assess muscle tone. bilateral Babinski's reflex may occur with hyperactive DTRs and spasticity. Intermittent resistance to flexion and extension indicates spasticity. Progressive bulbar palsy involves the brain stem and may cause episodes of crying or inappropriate laughter. and a lack of resistance indicates flaccidity. and breathing. With this progressive motor neuron disorder. antecubital area. Typically. Evaluate muscle strength in each extremity by having the patient push or pull against your resistance. As you move the patient's toes up and down. Test deep tendon reflexes (DTRs) in the patient's elbow. check for evidence of incoordination by asking the patient to perform a repetitive activity. difficulty chewing. A brain tumor that involves the corticospinal tract may produce Babinski's reflex. swallowing. decreased pain sensation. wrist. choking and excessive drooling. Incoordination makes carrying out activities of daily living difficult for the patient. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral). emotional lability. cranial nerve dysfunction. and ankle by striking the tendon with a reflex hammer. spasticity.
❑ Brain tumor. evaluate the patient for other neurologic signs. urinary frequency and urgency.
. ALS produces fasciculations accompanied by muscle atrophy and weakness. seizures.
❑ Amyotrophic lateral sclerosis (ALS). ask the patient to identify the direction in which the toes have been moved without looking at his feet. headache. and. Associated signs and symptoms include impaired speech.
Next. occasionally.History and physical examination
After eliciting a positive Babinski's reflex. the patient's poor prognosis may cause periodic depression. and a decreased level of consciousness (LOC). incoordination. little or no muscle response indicates hypoactivity. an unsteady gait. Although his mental status remains intact. knee.
Then evaluate pain sensation and proprioception in the feet. An exaggerated muscle response indicates hyperactive DTRs. hemiparesis or hemiplegia.
With acute injury.
❑ Rabies. nuchal rigidity. photophobia. this reflex confirms corticospinal damage. marked by unilateral ptosis. bilaterally when injury affects both sides.
❑ Hepatic encephalopathy. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms. pupillary constriction. As meningitis progresses. The patient may also have weakness and incoordination.
❑ Meningitis. Horner's syndrome. and decreased LOC with abnormal pupillary size and response to light. spasticity.❑ Head trauma. Bilateral Babinski's reflex — possibly elicited by nonspecific noxious stimuli alone — appears in the excitation phase of rabies. vomiting. delirium. may occur with lower cervical cord injury. altered vital signs. malaise. As shock resolves. It's accompanied by hyperactive DTRs. hyperactive DTRs.
❑ Spinal cord injury. spinal shock temporarily erases all reflexes. Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Rather than signaling the return of neurologic function. and facial anhidrosis.
. and opisthotonos. With meningitis. Seizures and hyperactive DTRs may also occur. and deep stupor that may progress to coma. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Unilateral or bilateral Babinski's reflex may occur as the result of primary corticospinal damage or secondary injury associated with increased intracranial pressure. it also causes decreased LOC. and irritability (which occur 30 to 40 days after a bite from an infected animal). chills. bilateral Babinski's reflex commonly follows fever. Associated signs and symptoms include irritability. proprioception. positive Brudzinski's and Kernig's signs. and motor function. behavior changes. Babinski's reflex occurs late in hepatic encephalopathy when the patient slips into a coma. diplopia. Babinski's reflex occurs — unilaterally when injury affects only one side of the spinal cord (Brown-Séquard's syndrome). and malaise and is accompanied by nausea and vomiting. Hyperactive DTRs and spasticity commonly occur with Babinski's reflex. and variable or total loss of pain and temperature sensation. such as fever. It's accompanied by hyperactive DTRs and fetor hepaticus. Other signs and symptoms vary with the type of head trauma and include headache.
later. With spinal cord tumor. bilateral Babinski's reflex occurs with muscle atrophy and weakness that may progress to paralysis. muscle tenderness. proprioception. and aphasia. irritability and. With syringomyelia. assist the patient with activity and keep his environment free from obstructions. vomiting. commonly appears late in the disorder. such as dysphagia and dysarthria. disorientation. It's accompanied by progressive weakness. To prevent injury. paresthesia. If it involves the cerebrum. it produces unilateral Babinski's reflex accompanied by hemiplegia or hemiparesis. and incontinence are also characteristic.
. as are Hoyne's. and absent abdominal reflexes. atrophy.
❑ Spinal paralytic poliomyelitis. It also causes spasticity. seizures. Spasticity. Generalized signs and symptoms of stroke include headache. absent abdominal reflexes. and motor function. If it involves the brain stem. deep pain. hyperactive DTRs. unilateral hyperactive DTRs. occasionally. bilateral Babinski's reflex occurs with variable loss of pain and temperature sensation. and spasticity. DTRs may be hypoactive or hyperactive. Diffuse pain may occur at the level of the tumor. Cranial nerve dysfunction. Kernig's. ataxia and. It's accompanied by spasticity.
❑ Stroke. and Brudzinski's signs. bilateral hyperactive DTRs. Spiral tuberculosis may produce bilateral Babinski's reflex accompanied by variable loss of pain and temperature sensation. spasticity. cranial nerve dysfunction. hemianopsia. and motor function. bladder incontinence. it produces bilateral Babinski's reflex accompanied by bilateral weakness or paralysis. hyperactive DTRs.
❑ Syringomyelia. and an unsteady gait. and coma. all of which increase the patient's risk of injury. Resistance to neck flexion is characteristic. incoordination. nuchal rigidity. proprioception.
Babinski's reflex usually occurs with incoordination.
❑ Spinal tuberculosis. fever. weakness.❑ Spinal cord tumor. Babinski's reflex varies with the site of the stroke. Unilateral or bilateral Babinski's reflex occurs 5 to 7 days after the onset of fever.
possibly. Have suction equipment at hand. if not. Babinski's reflex is pathologic and may result from hydrocephalus or any of the causes more commonly seen in adults. reflecting immaturity of the corticospinal tract. It can also occur during a coma. and vomitus — normally can be elicited by touching the posterior wall of the oropharynx with a tongue depressor or by suctioning the throat. immediately stop the patient’s oral intake to prevent aspiration. place him in Fowler’s position. An abnormal gag reflex — either decreased or absent — interferes with the ability to swallow and. 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
. constriction of the pharyngeal musculature. Quickly evaluate his level of consciousness (LOC). and a sensation of gagging indicate a normal gag reflex. more important. fluid. 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.
Babinski's reflex occurs normally in infants ages 18 to 24 months. Prepare the patient as necessary. Prompt elevation of the palate. angiography or myelography and. a lumbar puncture to clarify or confirm the cause of Babinski's reflex. or as a temporary result of anesthesia.
History and physical examination
Ask the patient (or a family member if the patient can’t communicate) about the onset and duration of swallowing difficulties. If it’s decreased. if any.Diagnostic tests may include a computed tomography scan or magnetic resonance imaging of the brain or spine.
If you detect an abnormal gag reflex.
The gag reflex — a protective mechanism that prevents aspiration of food. After age 2. place him in a side-lying position to prevent aspiration. in muscle diseases such as severe myasthenia gravis.
quadriplegia.with myasthenia gravis)? If the patient also has trouble chewing. dysarthria. Then assess his respiratory status for evidence of aspiration.
Loss of the gag reflex reflects temporary or permanent paralysis of muscles supplied by CNs IX and X.
Paresis of the palate and an impaired gag reflex usually develop within hours to days of thrombosis. and vertigo. and perform a neurologic examination.
Brain stem glioma
Brain stem glioma causes a gradual loss of the gag reflex. loss of sensation at the base of the tongue. facial weakness. dysphagia. Other indicators of bulbar palsy include jaw and facial muscle weakness. and a decreased LOC. possible difficulty articulating and breathing. He may also display
. Related symptoms reflect bilateral brain stem involvement and include diplopia and facial weakness. The patient may experience analgesia and thermanesthesia. It also causes diffuse sensory loss.
Basilar artery occlusion
Basilar artery occlusion may suddenly diminish or obliterate the gag reflex.
Explore the patient’s medical history for vascular and degenerative disorders. occurring ipsilaterally on the face and contralaterally on the body. increased salivation. and fasciculations. extraocular muscle palsies. suspect more widespread neurologic involvement because chewing involves different CNs. Common involvement of the corticospinal pathways causes spasticity and paresis of the arms and legs as well as gait disturbances.
General and local (throat) anesthesia can produce temporary loss of the gag reflex. EEG.)
The absence of doll's eye sign indicates injury to the midbrain or pons. It typically accompanies coma caused by lesions of the cerebellum and brain stem. Remember to keep suction equipment handy in case of aspiration.
Prepare the patient for diagnostic studies. Absent doll's eye sign is necessary for a diagnosis of brain death. Advise the patient to take small amounts and eat slowly while sitting or in high Fowler’s position.
. and arteriography. (See Testing for absent doll's eye sign. The eyes remain fixed in midposition. Stay with him while he eats and observe for choking. provide tube feedings. the absence of the doll's eye sign is detected by rapid.
Refer the patient to a therapist to determine his aspiration risk and develop an exercise program to strengthen specific muscles. involving cranial nerves III and VI. magnetic resonance imaging. gentle turning of the patient's head from side to side. lumbar puncture. and assess the patient’s nutritional status daily.
An indicator of brain stem dysfunction.
Continually assess the patient’s ability to swallow. Keep accurate intake and output records. try pureed foods. a computed tomography scan. hemifacial anhidrosis). This sign usually can't be relied upon in a conscious patient because he can control eye movements voluntarily.nystagmus. such as swallow studies. if it’s merely diminished. instead of the normal response of moving laterally toward the side opposite the direction the head is turned. and signs of Horner’s syndrome (unilateral ptosis and miosis. ipsilateral ataxia of the arm and leg. If his gag reflex is absent.
Examine the pupils for size. tinnitus. Other ominous signs—such as complete paralysis.
Brain stem tumor. increasing pulse pressure. absent doll's eye sign is associated with coma.A variant of absent doll's eye sign that develops gradually is known as abnormal doll's eye sign.Brain stem infarction causes absent doll's eye sign with coma.
Central midbrain infarction. diplopia. nystagmus.Absent doll's eye sign and coma develop within minutes with pontine hemorrhage. a life-threatening disorder. ataxia.Absent doll's eye sign accompanies coma with a brain stem tumor. hearing loss.
Brain stem infarction.With a central midbrain infarction. contralateral ataxic tremor.
History and physical examination
After detecting an absent doll's eye sign. cranial nerve palsies (facial weakness.
. decerebrate posture. and nystagmus). perform a neurologic examination. one eye may move laterally while the other remains fixed or moves in the opposite direction. facial pain or sensory loss. and muscle flaccidity. facial paralysis. First. bilateral cerebellar ataxia. Check for signs of increased ICP—increased blood pressure. evaluate the patient's level of consciousness. a diminished corneal reflex. using the Glasgow Coma Scale. dysphagia. It also causes limb paralysis. Associated brain stem dysfunction may be reversible or may progress to deeper coma with absent doll's eye sign. This sign may be preceded by hemiparesis. blindness or visual field deficits. a positive Babinski's reflex. extraocular nerve palsies. nystagmus. drooling. vertigo. Note decerebrate or decorticate posture. An abnormal doll's eye sign usually accompanies metabolic coma or increased intracranial pressure (ICP). Because conjugate eye movement is lost. equality. and pupillary abnormalities. and vomiting. and bradycardia. Weber's syndrome (oculomotor palsy with contralateral hemiplegia).
Pontine hemorrhage. variable sensory loss. dizziness. and response to light.
▪ Provide emotional support to the family. cranial nerve palsies.Barbiturates may produce severe central nervous system depression.A subdural hematoma at the posterior fossa typically causes absent doll's eye sign and coma. unequal pupils. confusion. drowsiness.
▪ Explain to the patient the underlying cause and its treatment. dysphagia. such as a headache. if appropriate. reactive pupils—may rapidly progress to death. and cerebellar ataxia.
▪ Monitor vital signs and neurologic status. These signs may be preceded by characteristic signs and symptoms.
Posterior fossa hematoma. a positive Babinski's reflex.
▪ Don't attempt to elicit doll's eye sign in a comatose patient with suspected cervical spine injury.
▪ Discuss end-of-life issues with the patient's family. resulting in coma and absent doll's eye sign. and small.decerebrate posture. a stiff neck. doing so risks spinal cord damage.