Classical gait disorders

It is an old saying that a Neurologist can only recognize those diseases that he can mimic. So we play around with various gait disorders, looking at youtube videos and trying to isolate the core examples.

More videos can be found here.


Vibration sense and proprioception

You have an elderly man with gait disturbance, discover B12 deficiency which fits the clinical picture of afferent ataxia, substitute it, he gets better. Then your attending comes along, thrusts his Rydel-Seiffer-fork at the malleoli, comes up with 5/8 and wonders whether your diagnosis is correct. How can that be?

We discuss the peculiar neuroanatomy of vibration sense (as opposed to proprioception) as described in

  • Brazis Localization in Clinical Neurology

to which

We also mention the best way to measure pallesthesia (repeatedly, over skin vs. bone – the former being more sensitive), the bad interobserver reliability of Rydel-Seiffer-fork measurements and indications for doing pallesthesia in your average ER patient. Quite similarly we debate the various ways to examine joint position sense and why it is different from kinesthesia.

Subtle central motor weakness

In a screening neurological examination, you need efficient sensitive examinations to detect subtle motor deficits, e.g. in your basic r/o MS or stroke patient. We usually do pronator drift, but there are some simple additional tests that could be included in your (and my) routine, especially the forearm rolling test and – even better – the finger rolling test.

We use these tests in a few patients to illustrate their practical application and also discuss the relevant data, using 2 of Anderson’s articles, namely

Finally, there is yet another of these tests, which seems even simpler to me: The thumb rolling tests. If you believe the Canadians, then it is the best.

Babinski sign

We have talked about the man Babinski and Charcot’s school, the Salpetriere and other historical figures in the past. Today we talk about the Babinski sign itself. Here are some of my notes on the subject, taken from references below.

Core knowledge:

  • The extensor toe sign is mediated by the extensor hallucis longus (EHL).
  • The extensor toe sign is always part of the flexion reflex (an upgoing toe is anatomically actually a flexion mechanism rather than an extension), you have to look out for that.
  • The Babinski phenomenon competes with
    the brisk toe flexion and dorsal extension of the superficial flexion reflex (which is mediated by L4 to S1-2 and the tibial nerve) which is abolished in pyramidal tract lesions (as other superficial reflexes are)
    a grasp reflex which is a slow tonic flexor movement as part of a complex proximal and distal flexor movement
  • The fanning phenomenon is just an extension of all toes, yet the lateral ones can’t really extend (cf the fingers)
  • Neonates have brisk extensor signs, this becomes less brisk and more subtle over time, yet the tensor fasciae latae may remain.
  • No extensor sign w/o weakness or bradydiadochokinesis in the foot extensors (the converse is not true)

A method^{The formulation “a method” is so typical for Sapira’s art and science of bedside diagnosis, yet Sapira’s description is not too good}

  • Uncover the entire leg
  • Have the pt. lie down and recommend to let the muscles be floppy despite the upcoming scratching(never sit him up and lift the leg!)
  • Use a pointed tool that is not too sharp
  • Start with light touches and strokes, then increase pressure, going up from the lateral heel to the lateral metatarsal pad, going on the pad of the big toe, never touch above the metatarsal pad.
  • If the patient is too ticklish or you have equivocal results, stroke the lateral dorsum of the foot (Chaddock’s sign)
  • Look out for movement of the EHL, the other flexors, touching the hamstrings and the TFL.
  • Remember that the cutaneous field of the sign enlarges (S3 <- S2 <- S1 L5 L4), the threshold reduces, so Babinski’s changes every day after a stroke.

Van Gijn’s [1995] warnings:

1. It’s not Babinski’s if

  • the extension is due to other muscles than the EHL or due to foot dorsiflexion or to flexion of the other toes
  • other muscles (the hamstrings and the TFL) don’t react
  • it’s not reproducible

2. The stimulus need not be painful.

3. Babinski and Chaddock suffice – the other various Babinski variants are not as sensitive or specific.

4. The extensor movement can be early or late, brisk or slow.

5. Fanning of the toes is of historical interest only.

Some historical remarks:

  • Babinski started out with painful pinpricks than switched to stroke the sole.
  • It seems that Remak discovered the sign first, but did not do a good job.
  • Babinski described other signs, such as cocontraction of the platysma on maximal opening of the mouth, the Babinski rising reflex, Babinski’s tonus test and the nowadays quite prominent pronation sign used for latent paresis.
  • Babinski observe the sign in nonfocal situations (epilepsy, intoxication). It actually may occur during physical exertion (soldiers walking for hours in 1,27%), in Cheyne-Stokes-Respiration.


  • Van Gijn. The Babinski reflex. Postgrad Med J 1995: A brilliantly written knowledgeable and concise account from one that has thoroughly studied the reflex and the literature, including a translation of Babinski’s original publications (yet not in this paper but in his monograph on the subject).
  • Haerer. DeJong’s the neurologic examination. As so often, the respective chapter in DeJong has a lot to say but is not very concise.
  • Goetz. History of the extensor plantar response. Sem Neurol 2002. Contains the original 28 lines of Babinski’s first publication in the appendix.
  • Miller & Claiborne Johnston. Should the Babinski sign be part of
    the routine neurologic examination? This article started (once more) a lively discussion on the subject. It is still the best study to investigate the role of the sign in routine practice

 Images on the web