Babinski Sign - method, principles, types, pathway and alternative methods
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Babinski’s sign Chairperson: dr Praveen kusubi Student: dr Vigneshwar m
Introduction Joseph Jules François Félix Babinski (1857-1932) Made Hôpital de Salpêtrière in Paris a world famous medical centre in the late nineteenth and early twentieth century . The others being, among others, Jean-Martin Charcot, Claude Bernard, and Joseph Jules Dejerine
Babinski took an interest in the pathogenesis of hysteria and was the first to present acceptable differential diagnostic criteria for separating hysteria from organic diseases.
Method Stroking the lateral part of the sole of the foot with a fairly sharp object produces plantar flexion of the big toe; often there is also flexion and adduction of the other toes. This normal response is termed the flexor plantar reflex.
Technique
In some patients, stroking the sole produces extension (dorsiflexion) of the big toe, often with extension and abduction ("fanning") of the other toes. This abnormal response is termed the extensor plantar reflex , or Babinski reflex.
Anatomical considerations The reflex arc for the PR comprises of the afferent and efferent fibres in the tibial nerve and the L4-5 to S1-2 cord segments. The reflexogenic area is the first sacral dermatome, with the receptor nerve endings being located in the skin on the sole of the foot.
The afferent fibres travel in the tibial nerve which is a branch of the sciatic nerve, to relay in the L4-5 to S1-2 cord segments. The efferent fibres from the spinal cord travel back in the sciatic nerve which divides into two large branches just proximal to the knee.
Fibres supplying the toe flexors travel in the tibial nerve while those supplying the toe extensors travel in the peroneal nerve to reach the foot. Injury or transection of the tibial nerve therefore, would interrupt the afferent and efferent arcs of the normal plantar response, leaving the toe extensor muscles innervated. Interruption of the reflex arc can cause a diminution or absence of the reflex.
Supraspinal influences from the cortex also influence and modify the spinal reflex or response. A lesion anywhere along the corticospinal pathway can modify the response on the contralateral side of the body if the lesion is above the pyramidal decussation, and on the same or homolateral side of the body if the lesion is below the medullary decussation in the cord itself.
The PR being a polysynaptic reflex, the interneurons in the reflex arc connect with motor neurons at several segmental levels, leading to a co-ordinated motor response or movement of the foot and lower limb following cutaneous stimulation of the sole of the foot.
C omplex reflexes like plantar flexion use more of inhibitory interneurons, sometimes referred to as the internuncial pool. The axons of the Renshaw cells contact the alpha motor neuron . An action potential down the axon of the alpha motor neuron also excites the Renshaw cell through the recurrent collateral.
The Renshaw cell in turn inhibits the same alpha motor neuron and other alpha motor neurons that innervate agonists. The Renshaw cell also inhibits the inhibitory interneuron mediating the reciprocal inhibition.
In this way, the Renshaw cell shortens the reflex contraction of the agonist and, at the same time, shortens the reciprocal inhibition of the antagonist. Through this mechanism, the motor neurons can inhibit their own activity.
This seems to be important in preventing alpha motor neurons from sending long trains of action potentials in response to a brief stimulus. The Renshaw cell and other internuncial neurons receive input from the higher motor centers , which can modulate the activity of these neurons and fine-tune the reflex movements.
In case of plantar reflex The sensory limb of this reflex arc is mediated by cutaneous receptors of fast-conducting 1a afferents that converge on the internuncial pool of inhibitory interneurons. While the motor neurons to the flexor muscles are excited, the extensor muscles are inhibited through reciprocal inhibition.
At the same time, motor neurons to the extensors of the contralateral leg are activated and the flexors are relaxed to compensate for the shift of weight to the contralateral leg while the ipsilateral leg is withdrawn from the painful stimulus. This crossed extensor reflex maintains postural support during withdrawal from a painful stimulus.
As with other reflexes, the strength of the response corresponds to the strength of the stimulus. In a normal individual only a painful stimulus elicits the reflex. When descending motor pathways that suppress and modulate the reflex are damaged, a lighter, non-painful stimulus may elicit the reflex. This was discovered by Babinski when he scratched the sole of the foot of a patient with central nervous system lesions. With the light non-painful stimulus, the strength of the response parallels the extent to which the upper motor neuron lesion has allowed up regulation of the reflex.
There are three responses possible: Flexor : the toes curve inward and the foot everts; this is the response seen in healthy adults (aka a "negative" Babinski ) . Indifferent : there is no response. Extensor : the hallux dorsiflexes and the other toes fan out – the "positive Babinski's sign" indicating damage to the central nervous system.
Types of Babinski sign True Babinski sign – includes all the components of the fully developed extensor plantar response. Minimal Babinski sign – is characterised by contraction of the hamstring muscles and the tensor fasciae latae which can be detected by palpation of the thigh.
Spontaneous Babinski sign – is encountered in patients with extensive pyramidal tract lesions. Passive flexion of the hip and knee or passive extension of the knee may produce a positive Babinski sign in adults, as may foot manipulation in infants and children. Crossed extensor response/bilateral Babinski sign – may be encountered in cases with bilateral cerebral or spinal cord disease. Unilateral foot stimulation elicits a bilateral response in such cases.
Tonic Babinski reflex – is characterised by a slow prolonged contraction of the toe extensors. It is encountered in patients with combined frontal lobe lesions and extrapyramidal involvement. Exaggerated Babinski sign – may take the form of a flexor or extensor spasm.
Causes Pyramidal tract lesions Normal children upto one year of age Deep sleep Coma General Anaesthesia Post-ictal stage of epilepsy
Causes Electroconvulsive therapy (ECT) Hypoglycaemia Alcohol intoxication Narcosis Hypnosis Following severe physical exhaustion Head trauma with concussion.
Additional maneuvers for eliciting superficial toe reflexes These maneuvers, in particular those outside the S1 dermatome, generally are less effective than stimuli within the S1 dermatome. In normal persons, these stimuli usually fail to elicit toe flexion, but after UMN lesions, they may elicit toe extension, just as with Babinski’s maneuver.
References Bickerstaff ER, Spillane A. Neurological Examination in Clinical Practice. 7th edition. Mayo Clinic. Clinical Examination in Neurology. Asian edition. Fourth edition. W.B. Saunders company, 1976; Reflexes. Chapter 8, pg 169-80. DeJong's The Neurologic Examination, 7th edition. DeMyer's the Neurologic Examination,6th edition.