Professional Guide to Signs and Symptoms
5th Edition

Babinski’s reflex [Extensor plantar reflex]
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 blunt object. (See How to elicit Babinski’s reflex.) In some patients, this reflex can be triggered by noxious stimuli, such as pain, noise, or even bumping of 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 age 24 months.
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 him to identify the direction in which the toes have been moved without looking at his feet.
  • Amyotrophic lateral sclerosis (ALS). In this progressive motor neuron disorder, bilateral Babinski’s reflex may occur with hyperactive DTRs and spasticity. Typically, ALS produces fasciculations accompanied by muscle atrophy and weakness. Incoordination makes carrying out activities of daily living difficult for the patient. Associated signs and symptoms include impaired speech; difficulty chewing, swallowing, and breathing; urinary frequency and urgency; and, occasionally, choking and excessive drooling. Although his mental status remains intact, the patient’s poor prognosis may cause periodic depression. Progressive bulbar palsy involves the brain stem and may cause episodes of crying or inappropriate laughter.
  • Brain tumor. A brain tumor that involves the corticospinal tract may produce Babinski’s reflex. The reflex may be accompanied by hyperactive DTRs (unilateral or bilateral), spasticity, seizures, cranial nerve dysfunction, hemiparesis or hemiplegia, decreased pain sensation, unsteady gait, incoordination, headache, emotional lability, and decreased level of consciousness (LOC).
  • Familial spastic paraparesis. Familial spastic paraparesis may produce bilateral Babinski’s reflex accompanied by hyperactive DTRs and progressive spasticity with ataxia and weakness.
  • Friedreich’s ataxia. Friedreich’s ataxia is a familial disorder that may produce bilateral Babinski’s reflex. Accompanying it are high-arched feet, hypoactive DTRs, hypotonia, ataxia, head tremor, weakness, and paresthesia.
  • Head trauma. Unilateral or bilateral Babinski’s reflex may occur as the result of primary corticospinal damage or secondary

    injury associated with increased intracranial pressure. Hyperactive DTRs and spasticity commonly occur with Babinski’s reflex. The patient may also have weakness and incoordination. Other signs and symptoms vary with the type of head trauma and include headache, vomiting, behavior changes, altered vital signs, and decreased LOC with abnormal pupillary size and response to light.
  • Hepatic encephalopathy. Babinski’s reflex occurs late in hepatic encephalopathy when the patient slips into a coma. It’s accompanied by hyperactive DTRs and fetor hepaticus.
  • Meningitis. In meningitis, bilateral Babinski’s reflex commonly follows fever, chills, and malaise and is accompanied by nausea and vomiting. As meningitis progresses, it also causes decreased LOC, nuchal rigidity, positive Brudzinski’s and Kernig’s signs, hyperactive DTRs, and opisthotonos. Associated signs and symptoms include irritability, photophobia, diplopia, delirium, and deep stupor that may progress to coma.
  • Multiple sclerosis (MS). In most patients with MS—a demyelinating disorder—bilateral Babinski’s reflex eventually follows initial signs and symptoms of paresthesia, nystagmus, and blurred or double vision. Associated signs and symptoms include scanning speech (clipped speech with some pauses between syllables), dysphagia, intention tremor, weakness, incoordination, spasticity, gait ataxia, seizures, paraparesis or paraplegia, bladder incontinence, and emotional lability. Loss of pain and temperature sensation and proprioception occur occasionally.
  • Pernicious anemia. Bilateral Babinski’s reflex occurs late in pernicious anemia when vitamin B12 deficiency affects the central nervous system. Anemia may eventually cause widespread GI, neurologic, and cardiovascular effects. Characteristic GI signs and symptoms include nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation. Gingival bleeding and a sore, inflamed tongue may make eating painful and intensify anorexia. The lips, gums, and tongue appear markedly pale. Jaundice may cause pale to bright yellow skin.
    Characteristic neurologic signs and symptoms include neuritis, weakness, peripheral paresthesia, disturbed position sense, incoordination, ataxia, positive Romberg’s sign, light-headedness, bowel and bladder incontinence, and altered vision (diplopia, blurred vision), taste, and hearing (tinnitus). Pernicious anemia may also produce irritability, poor memory, headache, depression, impotence, and delirium. Characteristic cardiovascular signs and symptoms include palpitations, wide pulse pressure, dyspnea, orthopnea, and tachycardia.
  • Rabies. Bilateral Babinski’s reflex—possibly elicited by nonspecific noxious stimuli alone—appears in the excitation phase of rabies. This phase occurs 2 to 10 days after the onset of prodromal signs and symptoms, such as fever, malaise, and irritability (which occur 30 to 40 days after a bite from an infected animal). Rabies is characterized by marked restlessness and extremely painful pharyngeal muscle spasms. Difficulty swallowing causes excessive drooling and hydrophobia in about 50% of affected patients. Seizures and hyperactive DTRs may also occur.
  • Spinal cord injury. In an acute injury, spinal shock temporarily erases all reflexes. As shock resolves, Babinski’s reflex occurs—unilaterally when the injury affects only one side of the spinal cord (Brown-Séquard syndrome) and bilaterally when the injury affects both sides. Rather than signaling the return of neurologic function, this reflex confirms corticospinal damage. It’s accompanied by hyperactive DTRs, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner’s syndrome, marked by unilateral ptosis, pupillary constriction, and facial anhidrosis, may occur in a lower cervical cord injury.
  • Spinal cord tumor. In a spinal cord tumor, bilateral Babinski’s reflex occurs with variable loss of pain and temperature sensation, proprioception, and motor function.

    Spasticity, hyperactive DTRs, absent abdominal reflexes, and incontinence are also characteristic. Diffuse pain may occur at the level of the tumor.
  • Spinal paralytic poliomyelitis. Unilateral or bilateral Babinski’s reflex occurs 5 to 7 days after the onset of fever. It’s accompanied by progressive weakness, paresthesia, muscle tenderness, spasticity, irritability and, later, atrophy. Resistance to neck flexion is characteristic, as are Hoyne’s, Kernig’s, and Brudzinski’s signs.
  • Spinal tuberculosis. Spinal tuberculosis may produce bilateral Babinski’s reflex accompanied by variable loss of pain and temperature sensation, proprioception, and motor function. It also causes spasticity, hyperactive DTRs, bladder incontinence, and absent abdominal reflexes.
  • Stroke. Babinski’s reflex varies with the site of the stroke. A stroke involving the cerebrum produces unilateral Babinski’s reflex accompanied by hemiplegia or hemiparesis, unilateral hyperactive DTRs, hemianopsia, and aphasia. A stroke involving the brain stem produces bilateral Babinski’s reflex accompanied by bilateral weakness or paralysis, bilateral hyperactive DTRs, cranial nerve dysfunction, incoordination, and unsteady gait. Generalized signs and symptoms of stroke include headache, vomiting, fever, disorientation, nuchal rigidity, seizures, and coma.
  • Syringomyelia. In syringomyelia, bilateral Babinski’s reflex occurs with muscle atrophy and weakness that may progress to paralysis. It’s accompanied by spasticity, ataxia and, occasionally, deep pain. DTRs may be hypoactive or hyperactive. Cranial nerve dysfunction, such as dysphagia and dysarthria, commonly appears late in the disorder.
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 activities 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.
Babinski’s reflex occurs normally in infants up to age 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 commonly seen in adults.