Re: Babinski Reflex

[Guest guest]

Babinski reflex is a sign for anyone with a central nervous system

lesion (not just MS but a myriad of other conditions as well) and as

was stated is very hard to perform on oneself. The normal response is

a flexor or curled toes response and the sign of a lesion is an

extensor or flared toes response. BTW any keys will work:-)

As far as other reflexes and central nervous system conditions go,

most people with MS (or other CNS conditions) will be hyperreflexic

when the patellar (tap below knee cap) reflex, achillies, brachial or

other reflexes are tested. Meaning most of the time, the knee (or

whatever area)will be extra " jerky " .

Happy Halloween!

le

[Guest guest]

Wow Gretchen. This is great info whether we've got Babinski Reflex or not. I've

had this done to my feet just thinking it was normal foot testing. Thanks very

much.

Barb

[Guest guest]

I would like to know how many of us with CMT have the presence of the

Babinski reflex. I show it on both feet.

Karon

[Guest guest]

I had no reaction at all. I may have been doing it wrong. Is sensation

required for it to work? If you can't feel the bottom of your feet, do you still

have reflexes?

I wonder if it's like the reflex in my knees. When the doctor hits me with his

hammer, nothing happens then either.

O

[Guest guest]

I don't know if sensation is required. I can feel my feet most of the time.

[Guest guest]

I have the Babinski Reflect in my left foot only. But still have plenty of

sensation in both feet.

Gretchen

[Guest guest]

More info http://en.wikipedia.org/wiki/Plantar_reflex and also this

article below. ~ Gretchen

The Babinski sign--a reappraisal.

Kumar SP, Ramasubramanian D. The Babinski sign--a reappraisal.

Neurol India [serial online] 2000 [cited 2008 Jan 6];48:314.

Available from: http://www.neurologyindia.com/text.asp?

2000/48/4/314/1509

Kumar SP, Ramasubramanian D

Departments of Neurology and Neurosurgery, Madurai Medical College,

Madurai, 625020, India.

In 1896, ph Babinski, a French neurologist, first described the

best known neurologic eponym 'the Babinski sign'. This sign is

characterised by dorsiflexion of the big toe and recruitment of the

extensor hallucis longus muscle, on stimulating the sole of the

foot. He has emphasised from the outset, the intimate relationship

between this sign and the shortening movement in other leg muscles,

which form the flexion synergy of the lower limb. The Babinski sign

is not a new reflex, rather it is released as a result of breakdown

of the harmonious integration of the flexion and extension

components of the normal defence reflex mechanism, due to pyramidal

tract dysfunction. A pathological Babinski sign should be clearly

distinguished from upgoing toes that may not always be a part of the

flexion synergy. This article reviews the Babinski sign in detail,

focusing on the historical perspectives, role of pyramidal tract

dysfunction and art of elicitation and interpretation. The

significance of assessing this phenomenon in the entire leg, and the

clinical clues that will help to dispel the myths regarding the

Babinski sign, have been emphasised.

Introduction

It was on February 22, 1896, that ph Francois Felix Babinski

published his first report on 'reflexe cutane plantaire' [cutaneous

plantar reflex] which became the sign that bears his name: 'the

Babinski sign'.[1] However unknown to Babinski, several painters

like Bortticelli, Raphael, Leonardo da Vinci had previously

demonstrated this phenomenon in their paintings.[2] Later, Babinski

asserted that if others had described the abnormal reflex before

him, they found it fortuitously and did not realize its clinical

implication; while he discovered it by a combination of chance,

careful observation and intuition.[3] Babinski first differentiated

between a normal and pathologic plantar response.[4]

Sketch of the Man

ph Babinski was born in Paris and died at the age of 75 in 1932

[Figure. 1]. Of reticent disposition, he wrote in a very sombre and

serious tone, but his gaze, clear and calm, was penetrating and

scrutinizing.[5] He was a devout bachelor and had two passions in

his life i.e. work and his brother Henri. His objective was always

to find clinical signs that permitted the authentification of the

organic nature of the syndrome; and specify the localisation of the

lesion responsible for the same. Babinski's ambition to establish a

department of neurosurgery at the Hospital de la Pitie in Paris,

where he did most of his work, was realised shortly after his death.

[6]

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. 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 1st year of

life, due to a brisker flexion synergy, the toes being a part of it.

As the nervous system matures and the pyramidal tract gains more

control over spinal motor neurons, the flexion synergy becomes less

brisk and toe 'extensors' are no longer a part of it. The toe then

often goes down, instead of up, as a result of a segmental reflex

involving the 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'.[7]

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 role of pyramidal tract

There seems to be a close association between occurrence of the

Babinski sign and impairment of voluntary foot movement. 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 function of the pyramidal tract may not only be

disturbed by structural lesions of myelin sheaths, axons, or both,

but also by nonneurological conditions [Table I].

The motor neurons of the leg muscles are laminated into separate

columns within the anterior horn of the cord, each of which supply

proximal or distal muscles, flexor or extensor muscles. In addition,

there are important pyramidal tract projections to the intermediate

(interneuronal) zone. This divergence of pyramidal tract projections

allows the following two explanations for the Babinski sign.

The Babinski sign might be released by dysfunction of pyramidal

tract fibres that project on interneuronal zone, at least on those

interneurons that subserve the flexion reflex synergy, of which the

Babinski sign is a part. As these interneurons are necessarily

interconnected across the segments of the lumbosacral spinal cord, a

Babinski sign would always be

Types of Babinski sign

a) Minimal Babinski sign : Contraction of hamstring muscles and

tensor faciae latae.

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.

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.

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

It is the site of stimulation, the intensity of stimulation, and

even the object used for stimulation that has received by far the

most attention. 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.[9] 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].

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.

By stroking the lateral malleolus (Chaddock's sign); squeezing the

calf muscle (Gordon's sign); applying pressure along the shin of

tibia (Oppenheim sign); pressing the 4th toe downwards and then

releasing it with a snap (Gonda's sign); vigorous adduction of the

little toe followed by its sudden release (Stransky sign); squeezing

the Achilles tendon (Schaefer's sign), flexion of the toes, on quick

percussion of the tips of the patients toes with the finger tip

(Rossolimo's sign); flexion of the four outer toes induced by

tapping the dorsum of the foot in the region of cuboid bone (Mendal

Bechtrew sign); giving multiple pinpricks on dorsolateral surface of

the foot (Bing's sign); forceful passive plantar flexion of the

ankle (Moniz sign); pressing over the dorsal aspect of the

metatarsophalangeal joint of the great toe (Throckmortan sign);

application of forceful pressure over anterior tibial region

(Strumpell sign); scratching the dorsum of the foot along the inner

side of the extensor tendon of the great toe (Cornell sign); plantar

flexion and fanning of the toes on tapping the mid plantar region of

the foot or base of the heel.

Interpretation

Incorporation of videotape and electromyography should be welcomed

in the interpretation of plantar response.[10] The following

criteria that have emerged from the comparison of clinical data with

electromyographic results may be applied for interpreting a

pathological Babinski sign.[11]

a) Upward movement of the great toe is pathological only if caused

by contraction of the EHL muscle.

Contraction of the EHL muscle is pathological only if it is

occurring synchronously with reflex activity in other flexor

muscles.

c) A Babinski sign does not necessarily imply that the concurrent

activity of the other flexor muscles should be very brisk and vice

versa.

d) The true Babinski sign is reproducible, unlike voluntary

withdrawal of the toes.

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. Moreover, videotaping and electromyography

could improve the clinical interpretation and help in settling the

argument especially if it is an unexpected finding.

[Guest guest]

Thanks for the article!

 Karon:)

More info http://en.wikipedia.org/wiki/Plantar_reflex and also this

article below. ~ Gretchen

The Babinski sign--a reappraisal.

Kumar SP, Ramasubramanian D. The Babinski sign--a reappraisal.

Neurol India [serial online] 2000 [cited 2008 Jan 6];48:314.

Available from: http://www.neurologyindia.com/text.asp?

2000/48/4/314/1509

Kumar SP, Ramasubramanian D

Departments of Neurology and Neurosurgery, Madurai Medical College,

Madurai, 625020, India.

In 1896, ph Babinski, a French neurologist, first described the

best known neurologic eponym 'the Babinski sign'. This sign is

characterised by dorsiflexion of the big toe and recruitment of the

extensor hallucis longus muscle, on stimulating the sole of the

foot. He has emphasised from the outset, the intimate relationship

between this sign and the shortening movement in other leg muscles,

which form the flexion synergy of the lower limb. The Babinski sign

is not a new reflex, rather it is released as a result of breakdown

of the harmonious integration of the flexion and extension

components of the normal defence reflex mechanism, due to pyramidal

tract dysfunction. A pathological Babinski sign should be clearly

distinguished from upgoing toes that may not always be a part of the

flexion synergy. This article reviews the Babinski sign in detail,

focusing on the historical perspectives, role of pyramidal tract

dysfunction and art of elicitation and interpretation. The

significance of assessing this phenomenon in the entire leg, and the

clinical clues that will help to dispel the myths regarding the

Babinski sign, have been emphasised.

Introduction

It was on February 22, 1896, that ph Francois Felix Babinski

published his first report on 'reflexe cutane plantaire' [cutaneous

plantar reflex] which became the sign that bears his name: 'the

Babinski sign'.[1] However unknown to Babinski, several painters

like Bortticelli, Raphael, Leonardo da Vinci had previously

demonstrated this phenomenon in their paintings.[2] Later, Babinski

asserted that if others had described the abnormal reflex before

him, they found it fortuitously and did not realize its clinical

implication; while he discovered it by a combination of chance,

careful observation and intuition.[3] Babinski first differentiated

between a normal and pathologic plantar response.[4]

Sketch of the Man

ph Babinski was born in Paris and died at the age of 75 in 1932

[Figure. 1]. Of reticent disposition, he wrote in a very sombre and

serious tone, but his gaze, clear and calm, was penetrating and

scrutinizing.[5] He was a devout bachelor and had two passions in

his life i.e. work and his brother Henri. His objective was always

to find clinical signs that permitted the authentification of the

organic nature of the syndrome; and specify the localisation of the

lesion responsible for the same. Babinski's ambition to establish a

department of neurosurgery at the Hospital de la Pitie in Paris,

where he did most of his work, was realised shortly after his death.

[6]

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. 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 1st year of

life, due to a brisker flexion synergy, the toes being a part of it.

As the nervous system matures and the pyramidal tract gains more

control over spinal motor neurons, the flexion synergy becomes less

brisk and toe 'extensors' are no longer a part of it. The toe then

often goes down, instead of up, as a result of a segmental reflex

involving the 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'.[7]

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 role of pyramidal tract

There seems to be a close association between occurrence of the

Babinski sign and impairment of voluntary foot movement. 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 function of the pyramidal tract may not only be

disturbed by structural lesions of myelin sheaths, axons, or both,

but also by nonneurological conditions [Table I].

The motor neurons of the leg muscles are laminated into separate

columns within the anterior horn of the cord, each of which supply

proximal or distal muscles, flexor or extensor muscles. In addition,

there are important pyramidal tract projections to the intermediate

(interneuronal) zone. This divergence of pyramidal tract projections

allows the following two explanations for the Babinski sign.

The Babinski sign might be released by dysfunction of pyramidal

tract fibres that project on interneuronal zone, at least on those

interneurons that subserve the flexion reflex synergy, of which the

Babinski sign is a part. As these interneurons are necessarily

interconnected across the segments of the lumbosacral spinal cord, a

Babinski sign would always be

Types of Babinski sign

a) Minimal Babinski sign : Contraction of hamstring muscles and

tensor faciae latae.

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.

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.

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

It is the site of stimulation, the intensity of stimulation, and

even the object used for stimulation that has received by far the

most attention. 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.[9] 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].

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.

By stroking the lateral malleolus (Chaddock's sign); squeezing the

calf muscle (Gordon's sign); applying pressure along the shin of

tibia (Oppenheim sign); pressing the 4th toe downwards and then

releasing it with a snap (Gonda's sign); vigorous adduction of the

little toe followed by its sudden release (Stransky sign); squeezing

the Achilles tendon (Schaefer's sign), flexion of the toes, on quick

percussion of the tips of the patients toes with the finger tip

(Rossolimo's sign); flexion of the four outer toes induced by

tapping the dorsum of the foot in the region of cuboid bone (Mendal

Bechtrew sign); giving multiple pinpricks on dorsolateral surface of

the foot (Bing's sign); forceful passive plantar flexion of the

ankle (Moniz sign); pressing over the dorsal aspect of the

metatarsophalangeal joint of the great toe (Throckmortan sign);

application of forceful pressure over anterior tibial region

(Strumpell sign); scratching the dorsum of the foot along the inner

side of the extensor tendon of the great toe (Cornell sign); plantar

flexion and fanning of the toes on tapping the mid plantar region of

the foot or base of the heel.

Interpretation

Incorporation of videotape and electromyography should be welcomed

in the interpretation of plantar response.[10] The following

criteria that have emerged from the comparison of clinical data with

electromyographic results may be applied for interpreting a

pathological Babinski sign.[11]

a) Upward movement of the great toe is pathological only if caused

by contraction of the EHL muscle.

Contraction of the EHL muscle is pathological only if it is

occurring synchronously with reflex activity in other flexor

muscles.

c) A Babinski sign does not necessarily imply that the concurrent

activity of the other flexor muscles should be very brisk and vice

versa.

d) The true Babinski sign is reproducible, unlike voluntary

withdrawal of the toes.

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. Moreover, videotaping and electromyography

could improve the clinical interpretation and help in settling the

argument especially if it is an unexpected finding.

________________________________________________________________________

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[Guest guest]

Gretchen,

When I went to UCSF Med Center in July, Dr. Ralph noticed the Babinski Reflex on

both feet. When I tried to find info on WebMD on it, there were no articles on

it. Thank you for the information. I will surely use it as my parents are not

well informed on CMT.

Nina