Brainstem Rules of 4

 

In 2005, Peter Gates published a superb paper titled:

‘The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non-neurologist’.

Gates described a simplified method for answering the question ‘Where is the lesion?’ using only the parts of the brainstem that we actually examine during a clinical examination to understand brainstem vascular syndromes.

Firstly, a quick review of the blood supply of the brainstem. Simply put the blood supply comes from:

1. paramedian branches
2. long circumferential branches (SAP)

• superior cerebellar artery (SCA)
• anterior inferior cerebellar artery (AICA)
• posterior inferior cerebellar artery (PICA)

And occlusion of these two groups of vessels results in two distinct types of brainstem syndrome:

1. medial (or paramedian) brainstem syndromes ( due to para-median branch occlusion)
2. lateral brainstem syndromes ( due to occlusion of the circumferential branches, also occasionally seen in unilateral vertebral occlusion)

And now the rules. If you can remember these rules the  diagnosis of brainstem vascular syndromes becomes a pitifully simple exercise (?!) - here’s how it works:

In the rule of 4 there are 4 rules

1. There are 4 structures in the ‘midline‘ beginning with M
2. There are 4 structures to the ‘side‘ (lateral) beginning with S
3. There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain)
4. The 4 motor nuclei that are in the midline are those that divide equally into 12 except for 1 and 2, that is 3, 4, 6 and 12
   (5, 7, 9 and 11 are in the lateral brainstem)

The 4 medial structures and the associated deficits are:

1. Motor pathway (or corticospinal tract):
   contralateral weakness of the arm and leg
2. Medial Lemniscus:
   contralateral loss of vibration and proprioception in the arm and leg
3. Medial longitudinal fasciculus:
   ipsilateral inter-nuclear ophthalmoplegia
   (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally)
4. Motor nucleus and nerve:
   ipsilateral loss of the cranial nerve that is affected (3, 4, 6 or 12)

The 4 ’side’ (lateral) structures and the associated deficits are:

1. Spinocerebellar pathway:
   ipsilateral ataxia of the arm and leg
2. Spinothalamic pathway:
   contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk
3. Sensory nucleus of the 5th cranial nerve:
   ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve
   (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla)
4. Sympathetic pathway:
   ipsilateral Homer’s syndrome, that is partial ptosis and a small pupil (miosis)

According to Gates:

These pathways pass through the entire length of the brainstem and can be likened to ‘meridians of longitude‘ whereas the various cranial nerves can be regarded as ‘parallels of latitude‘. If you establish where the meridians of longitude and parallels of latitude intersect then you have established the site of the lesion.

The 4 cranial nerves in the medulla are CN9-12:

1. Glossopharyngeal (CN9):
   ipsilateral loss of pharyngeal sensation
2. Vagus (CN10):
   ipsilateral palatal weakness
3. Spinal accessory (CN11):
   ipsilateral weakness of the trapezius and stemocleidomastoid muscles
4. Hypoglossal (CN12):
   ipsilateral weakness of the tongue

The 12th cranial nerve is the motor nerve in the midline of the medulla. Although the 9th, 10th and 11th cranial nerves have motor components, they do not divide evenly into 12 (using our rule) and are thus not the medial motor nerves.

The 4 cranial nerves in the pons are CN5-8:

1. Trigeminal (CN5):
   ipsilateral alteration of pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw.
2. Abducent (CN6):
   ipsilateral weakness of abduction (lateral movement) of the eye (lateral rectus).
3. Facial (CN7):
   ipsilateral facial weakness.
4. Auditory (CN8):
   ipsilateral deafness.

The 6th cranial nerve is the motor nerve in the medial pons.
The 7th is a motor nerve but it also carries pathways of taste, and using the rule of 4 it does not divide equally in to 12 and thus it is not a motor nerve that is in the midline.
The vestibular portion of the 8th nerve is not included in order to keep the concept simple and to avoid confusion. Nausea and vomiting and vertigo are often more common with involvement of the vestibular connections in the lateral medulla.

The 4 cranial nerves above the pons are CN1-4:

1. Olfactory (CN1):
   not in midbrain.
2. Optic (CN2):
   not in midbrain.
3. Oculomotor (CN3):
   impaired adduction, supradduction and infradduction of the ipsilateral eye with or without a dilated pupil.
   The eye is turned out and slightly down.
4. Trochlear (CN4):
   eye unable to look down when the eye is looking in towards the nose (superior oblique).

The 3rd and 4th cranial nerves are the motor nerves in the midbrain.

Thus a medial brainstem syndrome will consist of the 4 M’s and the relevant motor cranial nerves, and a lateral brainstem syndrome will consist of the 4 S’s and either
the 9-11th cranial nerve if the lesion is in the medulla, or the 5th, 7th and 8th cranial nerve if the lesion is in the pons.

Handy tip:
If there are signs of both a lateral and a medial (paramedian) brainstem syndrome, then one needs to consider a basilar artery problem, possibly an occlusion.

I’ll let you mull over these rules until the next ‘brainstem’ post, where you’ll be able to test drive ‘Gates’ Brainstem Rules of 4′ on some clinical scenarios.

Scenario 1

• You are examining a patient with sudden onset left-sided weakness. These are your clinical examination findings:
  weakness of the left upper and lower limbs, with sparing of the face.
  tongue deviation to the right, with no ophthalmoplegia.
  loss of vibration and proprioception in the left upper and lower limbs.
• 
• Where is the lesion?
  weakness of the left upper and lower limbs, with sparing of the face:
  motor (corticospinal pathway) localises the lesion to the contralateral medial brainstem
  (sparing of the face (CN7) means the lesion must be below the upper pons)
  tongue deviation to the right, with no ophthalmoplegia:
  tongue deviation indicates CN12 involvement, localising the lesion to the ipsilateral medulla
  (sparing of CN3 and CN6 means the midbrain and pons are not involved)
  loss of vibration and proprioception in the left upper and lower limbs:
  confirms localisation of the lesion to the contralateral medial brainstem
• Site of the lesion: right medial medulla. Sometimes, due to the peculiar pattern of blood supply to the medulla, bilateral infarction may occur.

Scenario 2

• You are examining a patient with sudden onset right-sided weakness. These are your clinical examination findings:
  weakness of the right face, upper and lower limbs.
  the left eye is turned “down and out” and the pupil is dilated.
• Where is the lesion?
  weakness of the right face, upper and lower limbs:
  motor (corticospinal pathway) localises the lesion to the contralateral medial brainstem
  (involvement of the face means the lesion must be at or above the upper pons)
  the left eye is turned “down and out” and the pupil is dilated:
  CN3 involvement, localising the lesion to the ipsilateral midbrain
  (sparing of CN6 and CN12 means the pons and medulla are not involved)
• Site of the lesion: left medial midbrain. A CN3 palsy (from damage to the CN3 nerve fascicle) and contralateral hemiplegia is known as Weber’s syndrome (”basal” infarction)  - which can be difficult to distinguish from ‘coning’ if you don’t have a CT scanner available.

Scenario 3

• You are examining a patient with vertigo, vomiting, and nystagmus. These are your clinical examination findings:
  left-sided limb ataxia.
  left-sided alteration of pain and temperature on the face.
  left-sided ipsilateral Homer’s syndrome.
  right-sided alteration of pain and temperature affecting the arm and leg.
  dysarthria and decreased gag reflex on the left, with the palate pulling up on the right-side.
• 
• Where is the lesion?
  left-sided limb ataxia:
  spinocerebellar pathway localises the lesion to the ipsilateral lateral brainstem.
  left-sided alteration of pain and temperature on the face:
  Sensory nucleus of the 5th cranial nerve localises the lesion to the ipsilateral lateral brainstem.
  left-sided ipsilateral Homer’s syndrome:
  Sympathetic pathway localises the lesion to the ipsilateral lateral brainstem.
  right-sided alteration of pain and temperature affecting the arm and leg:
  Spinothalamic pathway localises the lesion to the contralateral lateral brainstem.
  dysarthria and decreased gag reflex on the left, with the palate pulling up on the right-side:
  localises the lesion to the medulla affecting the ipsilateral  CN9 and 10.
• Site of the lesion: left lateral medulla. Also known as Wallenberg’s syndrome, caused by a left vertebral or left posterior inferior cerebellar artery occlusion (blood supply is variable to this region).

Scenario 4

• You are examining a patient with right-sided deafness, that was preceded by tinnitus. These are your clinical examination findings:
  right-sided limb ataxia (predominantly affecting the right upper limb).
  right-sided facial numbness with loss of the corneal reflex.
  right-sided hemi-facial spasms.
• Where is the lesion?
  right-sided limb ataxia (predominantly affecting the right upper limb):
  spinocerebellar pathway localises the lesion to the ipsilateral lateral brainstem.
  right-sided facial numbness with loss of the corneal reflex:
  Sensory nucleus of the 5th cranial nerve localises the lesion to the ipsilateral lateral brainstem.
  right-sided hemi-facial spasms:
  the lesion involves the pons affecting the ipsilateral CN7.
• Site of the lesion: The findings indicate a lesion affecting the right lateral pons with evidence of spinocerebellar involvement. In this case the lesion was not vascular in origin but in fact an example of a cerebropontine angle lesion - an acoustic neuroma (or schwannoma). This demonstrates the the broader utility of Gates’ Brainstem Rules of 4.

Scenario 5

• You are examining a patient with sudden onset right-sided weakness. These are your clinical examination findings:
  weakness of the right face, upper and lower limbs.
  failure of abduction of the left eye.
  loss of vibration and proprioception in the right upper and lower limbs.
• Where is the lesion?
  weakness of the right face, upper and lower limbs:
  motor (corticospinal pathway) localises the lesion to the contralateral medial brainstem
  (involvement of the face means the lesion must be at or above the upper pons)
  failure of abduction of the left eye:
  indicates CN6 involvement, localising the lesion to the ipsilateral pons.
  (sparing of CN3 and CN12 means the midbrain and medulla are not involved)
  loss of vibration and proprioception in the right upper and lower limbs:
  confirms localisation of the lesion to the contralateral medial brainstem
• Site of the lesion: left medial pons. Interestingly, the facial nerve runs a strange course - it loops around medial to the CN6 nucleus from its own laterally situated CN7 nucleus. Thus a CN7 palsy tends to coexist with a CN6 lesion despite the CN7 nucleus being in the lateral pons.

Scenario 6

• You are examining a patient with sudden onset intermittent double vision (diplopia). These are your clinical examination findings:
  failure of adduction past the midline (movement towards the nose) of the left eye and leading eye (right) nystagmus on looking laterally to the right. Normal eye movements on looking to the left.
  The patient is hypertensive. There is no hemiparesis and further examination is unremarkable.
• Where is the lesion?
  This finding  suggests a unilateral left-sided internuclear ophthalmoplegia, which localises the lesion to the ipsilateral medial longitudinal fasciculus (MLF). The MLF connects CN3 in the midbrain and the contralateral CN6 in the pons.
  The MLF is not usually affected when there is hemiparesis as it lies further back in the brainstem relative to the motor (corticospinal) pathway.
  Unilateral internuclear ophthalmoplegia can result from a lacunar infarct.
  (Always remember the possibility of multiple sclerosis)
• Site of the lesion: left medial longitudinal fasciculus (connects CN3 in the midbrain and contralateral CN6 in the pons).

Scenario 7

• You are examining a patient with a right-sided Horner’s syndrome. These are your clinical examination findings:
  right-sided Horner’s syndrome.
  right-sided limb ataxia.
  left-sided total loss of sensation.
• Where is the lesion?
  right-sided Horner’s syndrome:
  sympathetic pathway localises the lesion to the ipsilateral lateral brainstem.
  right-sided limb ataxia:
  spinocerebellar pathway localises the lesion to the ipsilateral lateral brainstem.
  left-sided total loss of sensation:
  Spinothalamic pathway localises the lesion to the contralateral lateral brainstem (in the midbrain the medial lemniscal pathway is actually situated more laterally, ventral to the spinothalamic pathway - ie. the two pathways come together… an exception to the Rule of 4!).
• Site of the lesion: Right dorsolateral midbrain. An extensive lesion that also involves CN3 is known by the delightful name of Nothnagel’s syndrome.

Scenario 8

• You are examining a patient with a ‘down and out’ right eye with pupillary dilatation. These are your clinical examination findings:
  right-sided impaired adduction, supradduction and infradduction of the ipsilateral eye with a dilated pupil.
  left-sided limb ataxia.
• Where is the lesion?
  right-sided impaired adduction, supradduction and infradduction of the ipsilateral eye with a dilated pupil:
  CN3 lesion localises the lesion to the ipsilateral medial midbrain.
  left-sided limb ataxia:
  usually this indicates ipsilateral spinocerebellar pathway involvment (a lateral structure). However, in this case we know that the midbrain is affected (CN3 palsy) and the red nucleus lies in the medial midbrain just lateral to the CN3 nerve fascicle. Damage to the red nucleus interrupts the ‘dentatorubrothalamic tract’ from the opposite cerebellar hemisphere causing cerebellar signs in the limbs opposite to the CN3 lesion.
• Site of the lesion: Right medial midbrain. The clinical manifestations of this lesion (affecting the CN3 nucleus or its fascicle as well as the red nucleus) is known as Benedikt’s syndrome.

 

Taken from: Life in the Fast Lane

Babinski sign- Mechanism& other Babinski like responses.

The Babinski sign
This eponym refers to the dorsiflexion of the great toe with or without fanning of the other toes and withdrawal of the leg, on plantar stimulation in patients with pyramidal tract dysfunction.

The characteristic response is dorsiflexion of the great toe by recruitment of extensor hallucis longus (EHL) muscle.

The art of elicitation:
The reflexogenic area for the plantar reflex is the first sacral (S1) dermatome with the receptor nerve endings being located in the skin. The afferent nerve is the tibial nerve, the spinal cord segments involved in the reflex arc being 4th and 5th lumbar and 1st and 2nd sacral.

Position
All the leg muscles should be visible and in a relaxed state. This can be achieved by positioning the patient in a way that the knee is slightly flexed and the thigh is externally rotated. The patient should be warned that the sole is going to be scratched and ask him to try to let his limb remain as floppy as possible. The toes should not be touched at all.

Stimulation
Any part of the leg can be stimulated, but the best technique is to stimulate the lateral plantar surface and the transverse arch in a single movement upto the middle metatarsophalangeal joint with a firm applicator lasting 5 to 6 seconds. Difficulties are bound to arise in certain clinical situations which makes elicitation and interpretation of plantar response inconclusive. It is imperative that one realises these problems and be aware of their solutions in order to arrive at an appropriate clinical conclusion [Table II].

Interpretation of the response
The plantar response may be:
1. Normal flexor plantar response
2. Pathologic or abnormal extensor plantar response (Babinski’s sign)

Normal flexor plantar response
In normal people after infancy, there is a plantar flexion of the foot and toes along with adduction of the toes. The primary movement is a plantar flexion of the great toe at the metatarsophalangeal joint, even if the terminal joint appears to extend. The response is a fairly rapid one and may be accompanied at times by an associated flexion of the hip and knee on the stimulated side.
Abnormal extensor plantar response (Babinski’s sign)
The Babinski’s sign is encountered in patients with pyramidal tract dysfunction and is characterised by a dorsiflexion or extension of the great toe with or without fanning or abduction of the other toes. The fully developed response is also accompanied by dorsiflexion of the ankle and flexion of the hip and knee joint and slight abduction of the thigh, leading to a withdrawal of the leg on plantar stimulation.
The Babinski sign is always pathological. There is no such thing as a negative Babinski sign.

mechanism:

In most mammals the limbs are automatically retracted on painful stimulation as a defence reflex, which is more pronounced in hind limbs. Sherrington called it, the flexion reflex synergy, because activation of all muscles effected shortening of the limb; the toe extensors forming part of this shortening synergy. Confusion has arisen from the application of the term extensor plantar response to a movement which forms part of a flexion synergy of the lower limbs. The toe 'extensors' although named extensors by anatomists, are infact flexors in a physiological sense because their action is to shorten the limb and contract reflexly along with other flexor muscles.

The Babinski sign may be a normal occurrence in the first year of life. In the infant, before  myelination of the nervous system is complete and an upright stance has been achieved, the normal plantar response is extensor, due to a brisker ‘flexion synergy’as part of the withdrawal response to pain. As the nervous system matures and the pyramidal tracts gain more control over spinal motor neurons, the ‘flexion synergy’ becomes less brisk and the toe ‘extensors’ are no longer a part of it. When the child assumes an upright posture, the plantar response becomes part of the postural reflex maintaining the tones of the foot and leg. At this time, the normal response to stimulation becomes a flexor movement of the toes and the ‘withdrawal extensor’ movement is suppressed by the influence of the pyramidal tract over the spinal reflex arc. The toe then goes down instead of up, as a result of a segmental reflex involving small foot muscles and the overlying skin.This is considered to be normal in adults and is termed - flexor plantar response. With lesions of the pyramidal system, structural or functional, this segmental downward response of the toes disappears, the flexion synergy may become disinhibited and the EHL muscle is again recruited into the flexion reflex of the leg producing the sign of 'Babinski'.
The pyramidal tract thus maintains a suppressor action on the ‘flexion reflex’synergy. Pyramidal tract dysfunction however, allows the response to revert to the withdrawal movement by releasing or facilitating the ‘flexion reflex synergy’ of which contraction of the extensor hallucis longus muscle forms an integral part. A Babinski sign can appear only if the intraspinal pathways of the ‘flexion reflex synergy’are operative, however severe the motor deficit in the foot. The motor neurons of the
leg muscles are laminated into separate columns within the anterior horns of the cord, each of which supply proximal or distal flexor or extensor muscles. Both structural as well as functional lesions of the pyramidal tract fibres projecting onto the lumbosacral anterior horn cells and interneurons supplying the leg muscles subserving the ‘flexion reflex synergy’ can release the
Babinski sign. Reversible pathophysiologic conditions result in, or produce, a transient extensor plantar response.Structural lesions produce more lasting effects

The muscles taking part in a fully developed response include extensor hallucis longus, tibialis anterior, extensor digitorum longus, hamstring group of muscles and tensor faciae latae. The characteristic response is dorsiflexion (extension) of the [big toe], which precedes all other movements. It is followed by fanning out and extension of the other toes, dorsiflexion of the ankle and flexion of the hip and knee joint. This response represents 'positive' Babinski sign. There is no such thing as a 'negative' Babinski sign.

The dorsiflexion of the toes may be the only visible effect, but the contraction of the thigh and leg muscles is always present and can be detected by palpation. Contraction of the tensor fasciae
latae has been referred to as Brissaud’s reflex.
So the fully developed extensor plantar response forms part of the primitive ‘flexion reflex synergy’ of the lower limbs designed to withdraw the limb from a painful stimulus.
This spinal defence reflex mechanism described by Sherrington, activates all the muscles involved in
shortening the stimulated limb. It involves flexion of the hip and knee, dorsiflexion of the ankle and extension of the great toe. The ‘toe and foot extensors’ although named extensors by anatomists, are in fact flexor in a physiological sense, because their action is to shorten the limb and
contract reflexly along with other flexor muscles. The physiologist looks on the Babinski sign as simply a part of the ‘primitive flexion reflex’.

The function of the pyramidal tract may not only be disturbed by structural lesions of myelin sheaths, axons, or both, but also by non-neurological conditions [Table I].

Types of Babinski sign
a) Minimal Babinski sign : Contraction of hamstring muscles and tensor faciae latae.

b) True Babinski sign : Includes all the components of the fully developed extensor plantar reflex.

c) Pseudo Babinski sign : One may encounter this type of response in sensitive individuals, plantar hyperaesthesia, and choreo-athetosis due to hyperkinesis. True Babinski can be clinically distinguished from the false Babinski by the contraction of hamstring muscles in the former, and failure to inhibit the extensor response by pressure over the base of the great toe. The true Babinski sign is reproducible, unlike voluntary withdrawal of the toes.

d) Exaggerated Babinski sign : It can either be in the form of 'flexor spasm' or 'extensor spasm', depending upon the muscles i.e. whether flexors or extensors, have excess of tone. Flexor spasms occur in spinal cord disease, bilateral upper motor neuron lesion at a supraspinal level, multiple sclerosis and subacute combined degeneration of the cord, while 'extensor spasm' occurs in patients with corticospinal tract lesion when the posterior column function is normal.

e) Inversion of plantar reflex : If the short flexors of the toe are paralysed or flexor tendons are severed accidentally, an extensor response may be obtained.

f) Tonic Babinski reflex : Characterised by slow prolonged contraction of extensors of toe, seen in frontal lobe lesions and extrapyramidal involvement.

g) Crossed extensor response/bilateral Babinski sign : Unilateral stimulation produces bilateral
Babinski in patients with bilateral cerebral disease and spinal cord disease.

h) Spontaneous Babinski : In infants and children following manipulation of the foot, and in patients with extensive pyramidal tract diseases, passive extension of the knee or passive flexion of the hip and the knee, may produce a positive Babinski sign.

Alternate methods
The late 19th and early 20th century was abound with disclaimers associated with founders of new reflex movements of the great toe. These movements are known by the term 'Babinski like responses'. These responses can be elicited by the following techniques, each with its own eponym.

1. Chaddock's sign:The extension of the big toe may be obtained by stimulating the dorsal lateral aspect of the foot from the posterior portion of the skin beneath the external malleolis anteriorly along the external edge of the foot.
2. Gordon's sign: squeezing the calf muscle
3. Oppenheim sign: applying pressure along the shin of tibia
4. Gonda's sign: pressing the 4th toe downwards and then releasing it with a snap
5. Stransky sign: vigorous adduction of the little toe followed by its sudden release
6. Schaefer's sign: squeezing the Achilles tendon
7. Rossolimo's sign: flexion of the toes, on quick percussion of the tips of the patients toes with the finger tip
8. Mendal Bechtrew sign: flexion of the four outer toes induced by tapping the dorsum of the foot in the region of cuboid bone
9. Bing's sign:  giving multiple pinpricks on dorsolateral surface of the foot
10. Moniz sign: forceful passive plantar flexion of the ankle
11. Throckmortan sign: pressing over the dorsal aspect of the metatarsophalangeal joint of the great toe
12. Strumpell sign: application of forceful pressure over anterior tibial region
13. Cornell sign: scratching the dorsum of the foot along the inner side of the extensor tendon of the great toe
14. plantar flexion and fanning of the toes on tapping the mid plantar region of the foot or base of the heel.

Most of these signs imply an increase in the reflexogenous zone and denote responses from different parts of the receptive field. When sufficiently facilitated, the reflex may be elicited by other stimuli as well. Infact, in extreme cases of UMN deficit, the complete ‘flexion reflex’ may be exhibited spontaneously and continuously; the patient lies in bed, the hip and knee flexed, and the ankle and great toe dorsiflexed. In other cases of severe UMN deficit, almost any unpleasant stimulus, such as scratching, pinching, or pricking, will evoke the ‘flexion reflex’, even when applied as high as the thigh, far from the usual reflexogenous zone.

 

Fallacies
An extensor response may be present when there is no damage to the pyramidal tract. A possible explanation being the excitation of the distal motor neurons and inhibition of the impulses via flexor reflex afferent
nerve fibres can be dissociated because they are mediated by different neurons, however closely linked. On the contrary, cases with proven damage to the pyramidal system have had normal plantar response. We should understand that corticospinal fibres not only originate in different parts of the cortex, but also have different terminations. Babinski sign can be expected only when 'leg fibres' of the pyramidal tract are involved. Plantar areflexia can be noted in cases with loss of sensation of sole due to lesion of the first sacral cutaneous distribution. The same can be observed in paralysis of extensors or long flexors of great toe. In spinal shock, cessation of tonic discharge of spinal neurons by excitatory impulses in descending pathways may explain its non existence. Drugs like parenteral physostigmine in physiological doses may also abolish a plantar response.

    »   Conclusion        

Despite the continuing controversy and observer bias, clinical utility of Babinski sign remains unchallenged. The role of pyramidal system in the pathophysiology of this sign is quite clear. Pyramidal tract dysfunction releases the flexion reflex synergy, of which contraction of the extensor hallucis longus muscle forms an integral part. The most important and vital question in interpreting the plantar response is not, whether the great toe goes up or not, but is whether an upgoing toe is pathological or not. For an appropriate answer the method of observation is much more important than the method of elicitation.

 

Modified From--Kumar SP, Ramasubramanian D. The Babinski sign--a reappraisal. Neurol India 2000;48:314

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Difference b/w spasticity & rigidity{basics in neurology}

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