Random Neuro facts

[Nerdoscience]

In a pitiful attempt to get more people posting, and make this forum more interesting for myself, and in a very sad display of my nerdiness, I want to start a thread for random Neuro facts.

What cool stuff have you learned on Neuro? Any interesting cases or findings? Any cool or totally random or painful pimping questions you've been asked?

If you want you can post questions, and see if people know the answer. Or you can just post the whole fact.

Anything, like "What chromosome is the mutation for NF-1 on, and how can you remember it?" or "I recently learned that Shy Drager Disease is not a synonym for social anxiety disorder in people who cross-dress." or "Doesn't the midbrain look like Mickey Mouse?" or "Did you know that the spinal accessory nerve has no cranial nucleus or nerve roots? They're all spinal!!"

Go for it. It can't be as bad as my examples.

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[Bill59]

"Doesn't the midbrain look like Mickey Mouse?"

2-headed gingerbread man was what I learned.

OK....

How many (really) cranial nerves are there?

What neurologic disease did Edgar Allan Poe (maybe) die from?

What's the longest axon?

 

[Happy613]

What neurological disease did Benjamin Franklin allegedly die from?

 

[Nerdoscience]

Longest axon in the human body, or in nature?

 

[Nerdoscience]

What's the longest axon?

If the human body, it's whichever nerve fiber runs from the tip of the big toe up the sciatic nerve and to the spinal cord.

 

[neurodoc]

OK, I'll bite.

Longest human axon is from the alpha motor nucleus at S1 to the AHL muscle end plate. The abnormal gene for NF-1 is on 17q11.2. It's unclear what Edgar Poe died of, but given the facts of his life it probably was related to alcoholism and/or debauchery... There are allegedly 12 cranial "nerves," but the fact is that the olfactory nerve is a central tract and not really a "nerve." I guess that means that there are only 11 CNs...

Here are some more fascinating neuro brain-teasers:

--Why does the left side of the brain control the right side of the body?

--If you have a patient with Wernicke's encephalopathy who doesn't respond to thiamine, what else would you consider using and why?

--What is the neuroanatomical basis of the palmomental reflex? Why should stroking the patient's palm induce a twitch of the contralateral mentalis muscle?

Nick

 

[Nerdoscience]

Yes, so the olfactory tract is totally different than the CNS or PNS. It has its own distinct glial population, and is capable of regeneration.

Many consider the optic nerve and retina to be extensions of the brain.

And CN XI is not cranial at all; it just sends its spinal fibers up into the skull to join other CN fibers, and comes right back down.

So, I guess it depends on how you count...

And did Poe die of rabies? I think that was a theory going around, but not well-substantiated.

 

[Nerdoscience]

And NF-1 is also known as von recklinghausen dz, which has 17 letters (Chr 17)

 

[Bill59]

FWIW, here's what I thought:

The longest neuron is a fine touch/proprioception neuron that extends from the toe to the caudal aspect of the brainstem (nucleus gracilis). But if you consider the afferent portion a dendrite and not an axon, the longest axon would be an alpha-motor neuron at S1. And if you don’t specify human beings, it would be the counterparts in a blue whale.

There are a number of theories of Poe’s death and I’m not enough of a historian to know which is the most credible. But an interesting analysis by Michael Benitez of the University of Maryland concludes Poe died from rabies.

Cranial nerves I and II are really brain tracts (covered by subarachnoid space, myelinated by oligos). And XI is really a spinal nerve. So by my count, there are 18 cranial nerves. BTW some say that C1 should be a CN but I’m not sure why.

 

[kapMD/PhD]

And NF-1 is also known as von recklinghausen dz, which has 17 letters (Chr 17)

Ok just for kicks- this is how i remember it
NF 1 = 17 (the number 1)
NF 2 = 22 ( the number 2 and b/c you have bilateral (2) acoustic schwanomas if you're lucky)

 

[Nerdoscience]

And 'NF-3", usually called by just its eponym, von HIppel Lindau is on Chr 3, and has 3 words in its name

 

[undecided3yr]

Longest axon in the human body, or in nature?

Giant Squid

 

[Nerdoscience]

The squid giant axon is the thickest known axon, as thick as a pencil lead, and quite long, but I don't think it's the longest. And I don't think a live giant squid has ever been captured, though parts have. The axon is called giant, not the squid it came from.

It was quite important to the discovery of the physiology of neuronal membranes.

 

[Nerdoscience]

It is said by some uppity British Neurologists that this is properly done only with a Bentley key. What is it?

 

[Bill59]

Checking for Babinski is the only thing I can think of.

Who is credited with introducing the first effective anti-seziure drug and why was this particular drug chosen?

 

[Nerdoscience]

Checking for Babinski is the only thing I can think of.

That's right. There are some double digit number amount of alternative signs that use some stimulus to provoke an upgoing toe.

These include Chaddock, Gordon, Oppenheim, Gonda, Stransky, Schaefer, Bing, Moniz, Throckmortan, Cornell, Strumpell, Mendal Bechtrew, and Rossolimo.

 

[Nerdoscience]

Who is credited with introducing the first effective anti-seziure drug and why was this particular drug chosen?

Locock, whose name is quite funny, since that's why he chose the drug. He found that bromide made people less sexually excited, and therefore would curb the desire to masturbate. He thought this was the cause of epilepsy. The drug actually worked for generalized tonic clonic seizures, and is still used in some settings!

 

[Bill59]

That's right.

In the 1800’s, bromide was commonly used as a sedative. One of the known side effects was impotence -- in fact, “bromide” was slang for an ugly woman.

Sir Charles Locock, Queen Vicotria’s obstetrician, used bromide to treat women with “sexual excitement” and found it also helped with catamenial epilepsy. He mentioned this is a discussion following a presentation by Sieveking on epilepsy at a meeting of the Royal Medical and Chirurgical Society in London in 1857.

Gradually, bromide became used for non-catamenial epilepsy. Charles Radcliffe published the use of bromide in 1864 and Samual Wilkes independently reported its use in 1878.

Since Locock never published his observations, some feel Radcliffe and Wilkes deserve equal credit.

Although bromide was largely relegated to historical value when it was replaced by phenobarbital in 1912, it’s still occasionally used, especially in veterinary medicine.

 

[GuP]

OK, I'll bite.

Longest human axon is from the alpha motor nucleus at S1 to the AHL muscle end plate. The abnormal gene for NF-1 is on 17q11.2. It's unclear what Edgar Poe died of, but given the facts of his life it probably was related to alcoholism and/or debauchery... There are allegedly 12 cranial "nerves," but the fact is that the olfactory nerve is a central tract and not really a "nerve." I guess that means that there are only 11 CNs...

Here are some more fascinating neuro brain-teasers:

--Why does the left side of the brain control the right side of the body?

--If you have a patient with Wernicke's encephalopathy who doesn't respond to thiamine, what else would you consider using and why?

--What is the neuroanatomical basis of the palmomental reflex? Why should stroking the patient's palm induce a twitch of the contralateral mentalis muscle?

Nick

Someone answer these!

 

[Nerdoscience]

For Wernicke's encephalopathy, you must give glucose first before giving thiamine. Maybe if you didn't give the glucose, that's why it didn't respond, but I otherwise don't really get the question.

 

[Fantasy Sports]

For Wernicke's encephalopathy, you must give glucose first before giving thiamine. Maybe if you didn't give the glucose, that's why it didn't respond, but I otherwise don't really get the question.

Thiamine before glucose. Learn it, live it, love it.

 

[Nerdoscience]

Thiamine before glucose. Learn it, live it, love it.

Oops. But what's the answer?

 

[neurodoc]

Oops. But what's the answer?

Magnesium. Magnesium is a cofactor for thiamine transkeotolase, and in the setting of insufficient Mg++ thiamine alone may fail to reverse Wernicke's. This fact is not well known.

As the others said, give thiamine before (or at least simultaneous with) glucose, since giving glucose alone would cause a metabolic (oxidative) strain on neurons that could exacerbate their demise.

Nick

 

[Fantasy Sports]

Magnesium. Magnesium is a cofactor for thiamine transkeotolase, and in the setting of insufficient Mg++ thiamine alone may fail to reverse Wernicke's. This fact is not well known.

As the others said, give thiamine before (or at least simultaneous with) glucose, since giving glucose alone would cause a metabolic (oxidative) strain on neurons that could exacerbate their demise.

Nick

Nick brings up a good way to remember one of the more important constituents of a "banana bag" (which for some people think has a lot of K due to its name-- but the most important ion is Mg)

 

[Bill59]

--Why does the left side of the brain control the right side of the body?

The evolutionary argument is, briefly:

The optics of the eye cause images to be inverted on the retina, and the crossing of the optic nerve fibers at the chiasm developed as a way to restore image continuity in the brain.

Crossing of the tactile pathways was then necessary to allow the brain to crate a global sensory representation.

In limbless primitive species, a threatening stimulus on the left side of the body is perceived in the right side of the brain. This elicits an aversion reaction by contracting the axial muscles on the right (uncrossed) side of the body to bend the body away from the threat. That’s why the more primitive vestibulospinal and reticulsopinal pathways don’t cross.

But an evolutionary more advanced organism with limbs would need to extend the left limbs to move away from a threat in the left environment, so the higher pathways (corticospinal, rubriospinal) need to cross.

A good review of all this is:
Jabaudon, et al. Reaching beyond the midline: why are human brains cross wired? Lancet Neurology 4:2: 87-99, 2005.

 

[neurodoc]

The evolutionary argument is, briefly:

The optics of the eye cause images to be inverted on the retina, and the crossing of the optic nerve fibers at the chiasm developed as a way to restore image continuity in the brain.

Crossing of the tactile pathways was then necessary to allow the brain to crate a global sensory representation.

In limbless primitive species, a threatening stimulus on the left side of the body is perceived in the right side of the brain. This elicits an aversion reaction by contracting the axial muscles on the right (uncrossed) side of the body to bend the body away from the threat. That’s why the more primitive vestibulospinal and reticulsopinal pathways don’t cross.

But an evolutionary more advanced organism with limbs would need to extend the left limbs to move away from a threat in the left environment, so the higher pathways (corticospinal, rubriospinal) need to cross.

A good review of all this is:
Jabaudon, et al. Reaching beyond the midline: why are human brains cross wired? Lancet Neurology 4:2: 87-99, 2005.

Good work, Bill.

I'll have to look up the Jabaudon article, but I can imagine the argument, since it seems to be the same one I presented in an article I wrote in Medical Hypotheses1995 45.471-475, Why are Vertebrate Nervous Systems Crossed?...I wrote the article when I was a Neurology resident at UC Davis.

Of course I have to agree with "Jabaudon's" hypothesis....I wonder if he cites my 1995 article? If not, I'll send him a copy...

OK, that leaves the last brain teaser...the neuroanatomy of the palmomental reflex. Go for it guys! If you'd like some more brain teasers, let me know and I'll post some.

Nick

Nick

 

[Bill59]

Of course I have to agree with "Jabaudon's" hypothesis....I wonder if he cites my 1995 article? If not, I'll send him a copy...

I don't think they did. Looks like an inadequate review of the literature

BTW, I made a mistake in my citation -- the first author is Vulliemoz, in case you try to find it.

 

[neurodoc]

I don't think they did. Looks like an inadequate review of the literature

BTW, I made a mistake in my citation -- the first author is Vulliemoz, in case you try to find it.

I found the citation on-line, but it requires a subscription to get the text (too bad not all the articles are free, but the publishers need to make a living too). I'll have to drop by the UCSF Library this week and copy it from the stacks.

I did find a Washington Post report on the article by a D. Brown. If Brown's description is correct, the main points that Jabaudon et al. make seem to have been lifted from my 1995 article and another related one that got published in 1999 Why do we speak with the left hemisphere Medical Hypotheses(1999) 52 (6), 497-503. I note he discusses Ramon y Cajal's work as I did, and this seems more than coincidental...kind of like he read my articles and "forgot" to refer to them...if indeed he failed to do that.

Nick

 

[Nerdoscience]

A few questions without answers. Anyone?

What neurological disease did Benjamin Franklin allegedly die from?

Why do we have the palmomental reflex (should be ipsilateral, though).

 

[neurodoc]

A few questions without answers. Anyone?

What neurological disease did Benjamin Franklin allegedly die from?

Franklin is reputed to have died in 1790, in his mid-80's, of an empyema of the lungs. This has been attributed to some earlier bout(s) of pleurisy. I suppose he could have had tuberculosis, and eventually succumbed to that. Or he could have had a more regular bacterial pneumonia. In his last days were described by his physician as being feverish. He'd been bedridden for a while, apparently recouped briefly, got out of bed and ordered that his bed be remade so that he could return to it and die with dignity...which he did.

If this is accurate, I suppose the "neurological disease" Ben died from was cerebral hypoxia...

 

[neurodoc]

A few questions without answers. Anyone?

Why do we have the palmomental reflex (should be ipsilateral, though).

Come on, guys...

The palmomental reflex is, as you said, "ipsilateral." That is, if you stroke the left palm you get a twitch of the left mentalis muscle. That, however, indicates some lesion of the rightfrontal lobe, which is to say that the peripheral clinical sign represents a "contralateral" central lesion. This is due to the crossed neural circuitry I discussed in my prior posts.

That was not my original question, however. The question is why does the stroking of the palm cause a twitch of the ipsilateral (to the palm) mentalis muscle? In other words, what is the neuroanatomical basis for this reflex?

HINT: Upper motor neuron lesions typically result in reflexes that show a widening of the sensory receptive field for a reflex and a "spread" of the motor reflex response to anatomically adjacent motor output fields. Take a look at the Wilder-Penfield sensory-motor "homunculus," and you will be able to answer this question.

Nick

 

[Nerdoscience]

I'm not quite getting this one. The palm is separated from the chin by the entire hand and face on both homunculi.

 

[Wheezy]

Quote

Magnesium. Magnesium is a cofactor for thiamine transkeotolase, and in the setting of insufficient Mg++ thiamine alone may fail to reverse Wernicke's. This fact is not well known.

----------

Thanks for the pointer. I didn't know that.

Let's say that the magnesium was ok.... would you then consider a co-existing niacin deficiency i.e. pellagra as the cause. would you check you patient's oral mucosa for glossitis, skin for dermatitis... tone for hypertonia.


Ps. I'm not sure how to quote on the forum

 

[Nerdoscience]

did we ever figure out what he neuro condition was for ben franklin?

And what neurologic condition are cellists prone to get?

 

[neurodoc]

did we ever figure out what he neuro condition was for ben franklin?

And what neurologic condition are cellists prone to get?

Carpal Tunnel Syndrome?

 

[Nerdoscience]

nope

 

[neurodoc]

I'm not quite getting this one. The palm is separated from the chin by the entire hand and face on both homunculi.

Yeah, the homunculus map shows some topography between the chin and the palm, but it is the representation of the thumb and the lips that have the most extensive surface representation, and the palmomental reflex is best ellicited by stroking the palm (from the thumb base to the center of the palm). It seems plausible that this frontal release reflex results from a lesion that disrupts the normal inhibition of spread of stimuli from the receptive fields of the hand and face. The inhibitory circuitry develops with normal maturation of the nervous system. The mouth and thumb are closely connected during early development. Infants regularly suck on their thumbs (maybe lateralized...is there a lateralized thumb sucking preference?), and this has even been oberved in utero.

So, I do view the palmomental reflex as due to the loss of developed inhibitory frontal circuits with the consequent spread of the motor response to adjacent receptive-motor representational fields.

Nick

 

[Sir Elroy]

[Mods...feel free to delete this beautifully embarassing duplicate post. I can't figure out how to do it myself.]

 

[Sir Elroy]

Musician's dystonia?

 

[neurodoc]

nope

Well. reptitive strain injuries, such as CTS are the most common complaints among musicians who use stringed instruments. The bow hand or fingering hand can be affected, but the fingering hand is more at risk due to flexion at the wrist. Cellists may be at a higher risk than violinists for focal dystonia, their version of writer's cramp, but I've heard of violinists with the same problem.

 

[Nerdoscience]

Well. reptitive strain injuries, such as CTS are the most common complaints among musicians who use stringed instruments. The bow hand or fingering hand can be affected, but the fingering hand is more at risk due to flexion at the wrist. Cellists may be at a higher risk than violinists for focal dystonia, their version of writer's cramp, but I've heard of violinists with the same problem.

Right on with the dystonia, and repetitive strain injury thing. I was talking more about the latter. Violinists, but more often pianists, get carpal tunnel. Cellist, however, tend to get...

Anyway, I am a violinist, and I have developed trigger finger in my left (finger) hand. I haven't had a neuropathy or anything yet.

 

[NKMU]

Benjamin Franklin-- neurosyphilis?

Interesting thread. A geriatrician taught me about the palmomental reflex, and then I taught him about the Palm(pilot)omental reflex. For those not in the know, it's when students reflexively reach for their PDA while being pimped.

 

[Nerdoscience]

That's right. There are some double digit number amount of alternative signs that use some stimulus to provoke an upgoing toe.

These include Chaddock, Gordon, Oppenheim, Gonda, Stransky, Schaefer, Bing, Moniz, Throckmortan, Cornell, Strumpell, Mendal Bechtrew, and Rossolimo.

Do you know what they all are?

 

[Nerdoscience]

A geriatrician taught me about the palmomental reflex, and then I taught him about the Palm(pilot)omental reflex. For those not in the know, it's when students reflexively reach for their PDA while being pimped.

lol!

 

[neurodoc]

Here's one: what is a "Queen Square Facial?" (No, it is not some sort of beauty treatment for transvestites...).

And when are we going to get the answer on Ben Franklin?

Nick

 

[Sir Elroy]

Uno mas.

Why do some people sneeze when they look into bright light?

 

[llogg]

Uno mas.

Why do some people sneeze when they look into bright light?

Yay! I know one. ACHOO syndrome.

 

[neurodoc]

Yay! I know one. ACHOO syndrome.

For some reason I couldn't open your link. However, I do know that this reflex has a name: the photosnutatory reflex. When you move from darkness to bright light (as in walking out from a dark room into bright sunlight), your pupils constrict, your eyelids close, your frontalis crinkles, and your nasolacrimal glands discharge, the later resulting in a sneeze. This reflex is probably protective, though the only clearlyvprotective part of it would seem to be the pupillary constriction and lacrimation. The sneeze probably just results from the associated neuroanatomy and is a teleologically "extra" response.

No bites on the Queen Square Facial (QSF)? OK, here's the answer. A QSF is facial weakness that is so subtle that only a Queen Square neurologist would notice it...

Nick

 

[Sir Elroy]

For some reason I couldn't open your link. However, I do know that this reflex has a name: the photosnutatory reflex. When you move from darkness to bright light (as in walking out from a dark room into bright sunlight), your pupils constrict, your eyelids close, your frontalis crinkles, and your nasolacrimal glands discharge, the later resulting in a sneeze. This reflex is probably protective, though the only clearlyvprotective part of it would seem to be the pupillary constriction and lacrimation. The sneeze probably just results from the associated neuroanatomy and is a teleologically "extra" response.

I've read that there is some controversy as to the cause. Some say that the photic sneeze reflex happens too quickly for nasolacrimal discharge to have triggered it. What are your thoughts on the theory that the trigeminal nucleus can be triggered by direct overstimulation of the optic nerve?

 

[neurodoc]

I've read that there is some controversy as to the cause. Some say that the photic sneeze reflex happens too quickly for nasolacrimal discharge to have triggered it. What are your thoughts on the theory that the trigeminal nucleus can be triggered by direct overstimulation of the optic nerve?

Fascinating idea. CNs I, II, and V are sensory, and CN II obviously responds to light, so it would be nice to be able to have CN II serve as a direct input to the photosnutatory reflex...but wouldn't the "motor" limb involve CN VII rather than CN V? CN V has has motor output, but this involve branchiomeric musculature. CN VII carries parasympathetic output that seems more involved in the reflex. The nasolacrimal discharge needn't be the "trigger" for the sneeze, though I think it is. It could just be an epiphenomenal component of this protective reflex.

I'm not aware of any proven link between CN II and CN V. And if there is, I don't see how the response (sneeze) would be any faster by virtue of having to go from CN II to CN V (and from thence presumably to CN VII) instead of following a different more direct path from V to VII.

Nick