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one update regarding online evaluations
you will have to 
do three online course evaluations
please do them all.

Dr Steinberg

small animal neuro again

one thing we were asked to do before was to 
read the handout in advance of this lecture, because each lecturer for 
the next lecture series will show a lot of illustrative material that is 
easier to understand if you already have a sense of the material. 

but 
probably no one did this.

so, a quick refresher: last week, we talked 
about the fact that the clinical signs we see are manifestations of 
abnormal function, and relate directly to an anatomic site that doesn't 
work, so signs give you the neuroanatomic diagnosis. 

the other aspects 
of the disease process give you answers to other questions: what is the 
nature of the process, what caused it, what do I do about it?

you have 
to have some sense of what normal neuroanatomy and neurophysiology is - 
need to know what the parts are, where they are, and what they do 
normally. this part of the issue is a personal problem for Dr. S. 
sometimes he thinks that what he is saying is also rather trivial, b/c 
some of you have solid neuro backgrounds, and those who do not have neuro 
only derived from your experience here, which is a broad/short experience 
that inadequately prepares you for functional neuroanatomy/functional 
neurophysiology. so they will try to share the essentials with you during 
the lectures. it is pretty primitive stuff.

much of this is 17th-19th 
century stuff! it's fundamental, useful, uncomplicated and shouldn't be 
mysterious to you. [yeah, right]
rest of lecture comes from first 17 
pages of handout, which includes a good outline of postural and segmental 
reflexes you should read at your leisure.

The neurological examination:

when you do this, it's useful to divide it into several parts, and do 
them in a routine fashion so you become facile and do not overlook 
anything. the first thing is your sense of the animal's behavior, his 
mental state - you casually observe this while looking at animal - is he 
aware? responsive? sniffing around normally? very agitated? pacing? calm? 
excited? clearly, you learn this by watching animals including your own 
pets. we often ask clients if the animals are conscious, during suspected 
seizures for example. many owners are "sure" that the animal is conscious 
b/c the animal will cock and ear or turn head when owner calls his name. 
but we know that lifting the ear in response to noise isn't indicative of 
awareness per se. it is difficult to be sure that you are reaching the 
correct conclusion.
next, we look at:

Posture and Gait:

ability to rise 
and stand
observe gait
observe general strength
observe respiratory 
pattern
observe body/head position

is it steady? is it short strided? is 
it long strided? is it ataxic? does it wobble side to side? is there 
weakness, proprioceptive deficit, other? recently dr s.  found that the 
word "ataxic" comes from the same root as "taxonomy," meaning order - 
ataxic = without order. 

how to assess posture and gait:
postural rxns

placing - visual and tactile
hemistand, hemiwalk, hopping, wheelbarrowing

extensor postural thrust

posture and gait require a lot of peripheral 
and central pathways, sensory and motor integrity including peripheral 
nerve, spinal cord, brainstem, often hemispheres; segmental reflexes only 
require intact reflex arcs. 

cranial nerves:
the point is, these 
reflexes are on the one hand simple segmental reflexes not unlike the 
knee jerk; very simple segmental reflexes - whereas say the visual 
response is as complicated as postural response. 
CN reflexes help to 
localize dz along the brainstem

segmental reflexes: 
unconscious, often 
quick, always something, and functional looking responses easily elicited 
in animals (difficult to hear everything due to annoying hammering).


reflexes: 
myotactic (stretch) reflexes - simple, monosynaptic
flexor 
withdrawal
cutaneous trunci (panniculus)
perineal


reflex pathway:

sensory branch
a segmental reflex is a simple pathway, requiring afferent 
input - receptor in skin or wherever, the afferent includes the cell body 
in DRG, and a synapse in the spinal cord in the simplest form in the 
ventral horn of grey matter. 
other reflexes have an interneuron 
interposed b/w afferent and efferent neurons. 

motor branch: cell body 
ventral grey matter; axon to periphery, motor end plate to muscle. 


notice the only cord segments being referenced are those at the 
restricted level where afferent enters and efferent exits.

we're 
interested in whether the reflexes (stretch, withdrawal) are:
normal

depressed
exaggerated (when they are irritated, or there has been release 
from inhibition)
are the reflexes clearly pathological? crossed extension 
is abnormal.

sensation:
cutaneous sensation
pain (toe pinch)
sensation 
is NOT the same as flexor withdrawal. the flexor withdrawal requires only 
local cord segment and has nothing to do with sensation. animals will 
withdraw when you pinch the limb even if the limb is anesthetic, if the 
segmental reflex pathway is intact. ok? so anesthetic animals can 
withdraw the limb; paralyzed animals can withdraw the limb. 

now. he 
will show a brief and old example of doing a neuro exam; the process of 
doing one. it starts with a quick overview of the cranial nerve function 
exam. he will try to narrate it usefully. tomorrow dr vite will repeat 
much of the CN exam part so do not panic if it is too fast. the next 
thing is the examples of postural responses, and contrast b/w them and 
segmental reflexes. the message today is postural responses are not the 
same as segmental reflexes, which he has already said four or five times. 
one requires local cord segment only, one requires intact central and 
entire cord pathway.

first look at general behavior as discussed

recognize that olfaction is very hard to test
now, a visual test - moving 
fingers in front of eyes - menace reflex - threatening gesture is made, 
response is animal blinks. a very complex response giving you a sense 
that there is vision, occipital cortex is working, etc. 
contrast that 
with the pupillary light reflex - shining light in eye produces a direct, 
consensual response - both pupils constrict in response to light in one 
eye. 
then dilate the eye, causing mydriasis, to examine the fundus of 
the eye. can see optic nerve, the retina. 
then check extraocular muscle 
function. as you turn the head horizontally you evoke spontaneous eye 
movements; the eye stays fixed - he has a slow eye movement opposite the 
direction of movement, and a rapid correction- physiologic nystagmus, 
relating to vestibular function. then owner calls him from around the 
room while you hold head fixed - you see him moving eyes so you know he 
can move his eyes and see and you know he can hear. 

check temporal 
masseters, innervated by trigeminal - check for atrophy
check facial 
sensation, jaw tone, resistance to opening (trigeminal)

palpebral 
response - touch skin, cause blink CN V, VII
dogs with vestibular 
disorders often want to lie in lateral recumbency on the side of the 
lesion. put dog in lateral recumbency, see how he responds to that. 

check gag reflex, tongue movements - learn about posterior CNs. of 
course, history of being able to eat, drink w/o gagging and no vocal 
changes also gives info about that.

postural responses video:

hold dog 
in front of table - he reaches out with a foot -sometimes left, sometimes 
right. when you cover his eyes, he knows the table is there so he reaches 
out with his legs anyway. this is a telltale maneuver telling you 
something about dogs. if you spin him around a few times and then try 
again, he doesn't reach anymore because he no longer knows where he is. 
if the dog reaches with the same foot each time, often the other foot is 
stuck in your labcoat pocket. if you hold the foot they are using they 
will use the other foot perfectly well. 
these postural responses require 
afferent and efferent integrity of sensory and motor axons, cord segment, 
brainstem, and higher centers. 
hopping - also postural response
neck 
turning, others...
extensor postural thrust - stand him on hind legs, 
shift weight (opposite of wheelbarrowing)
postural responses are 
complicated and require coordinated efforts.

in contrast to segmental 
reflexes, here is a stretch reflex - extend quadriceps, stimulate 
intramuscular end organ, evoke response. also stretch achilles tendon. 
some are easier to elicit than others. 
pinching skin - withdrawal of 
limb  - dno't know if he feels it or not, though, unless you see him 
react in other ways.

these are segmental - from hind limb to lumbar 
intumescence, and back down.

anal sphincter -should have some reflex 
tone
triceps jerk - hard to elicit, not often present - response is 
extension of elbow, if you do elicit it.

in every instance, we assess 
sensory function by looking at animal's motor response.
questions?

the 
rest of this tape is an animal with a lumbar cord injury and we don't 
talk about cords til wednesday but this may be interesting anyway. 

we 
see rads showing vertebral length is shorter than adjacent bones; animal 
has hx of being hit by car. there is a chip missing from vertebra, and 
the caudal end is dorsally displaced, and there has been a compressive 
fracture. 

note the appearance of foreleg extension and hindleg 
flaccidity in this laterally recumbent dog. the forelimbs are sitff, 
extended, toes pointed - they resist compression or flexion. the 
hindlimbs seem flaccid. pinching foot results in no obvious withdrawal. 
there is no resistance to flexion. there is diminished tone. a knee jerk 
is present with greater excursion than normal.
there is an intact 
perineal reflex, and there is reasonable tail tone. 

so the lesion 
involves the 3rd/4th lumbar vertebra; animal has foreleg extension, but 
his hindlegs are flaccid with diminished tone and no good withdrawal, but 
exaggerated knee jerks and perineal reflexes.

what's going on? why are 
the hind limb reflexes missing? 
well. he has release of inhibition 
causing exaggerated patellar response; why does he lack 
flexion/withdrawal? probably has a lesion within the intumescence. but, 
it's not complete; the nerve supply at the rostral end of the lumbar 
intumescence which goes to quadriceps seems to have been spared. those at 
caudal end going to tail/perineum were spared. those in between have a 
problem, so there is no extensor tone or flexor withdrawal. that's our 
guess. 


---break---

after first 17 pages, there is a section in the 
handout on peripheral nerve studies which we're skipping for now, and 
moving on to peripheral nerve diseases.

some peripheral nerve diseases:


one important point - this 12-13 hr lecture series is not intended to be 
a catalog of all neural diseases animals get, but rather diseases that 
occur relatively frequently and that illustrate important points the 
clinician should know about.

we will focus mainly on the material that 
is accessible to clinicians, but often the postmortem specimens are most 
dramatic and useful.

peripheral nerve diseases may be focal or 
generalized.
a very common lesion, esp of the dog, is the nerve sheath 
tumor - a localized lesion. first of all, you may have heard of the term 
"schwannoma." recall that peripheral nerves are myelinated by schwann 
cells. in some spp, especially man, the schwann cell may undergo 
neoplastic transformation. in dogs, who commonly get these tumors, it 
isn't clear what the cell of origin is. it may be the schwann cell. it 
may be a fibroblast. what's important is that it is locally invasive. it 
destroys axons. in people, these tumors tend to be compressive lesions, 
but in the dog it is invasive. so we call this a "nerve sheath tumor."

another important point is that for unknown reasons, this tumor mainly 
occurs in the nerves of the brachial limbs. though they may occur on 
peripheral nerves anywhere along the neuraxis, it is at least 30x more 
common for a nerve to the forelimb to be affected than any other nerves. 

there is no useful tx; although not seen here usually the nerve will 
squeeze through and enter the vertebral canal and compress the cord. so 
removing the tumor is generally very difficult, and the outlook is not 
good, because even after removing the peripheral component, you usually 
still have tumor in the adjacent cord.

another slide - not uncommon for 
multiple nerve roots to be affected, usually on the same side - here we 
see tumor that has invaded the cord or compressed the cord - there is a 
narrow area of the tumor which is where it went through the neural 
foramen into the spinal column. 

about 75 of these were studied - the 
prognosis was related to position along the nerve. the more distal the 
tumor, the better a chance for the animal surviving amputation. 
amputation is the tx of choice to remove these tumors, but generally 
leaves behind tumor in the cord. 

clinically, radiography has some value 
- a DV of the spinal column here is viewed in order to check the size of 
the neural foramina - here this oblique view shoes one neural foramen is 
much larger than the other ones. this kind of bony remodeling can occur 
as these tumors spread centrally. another way to dx this is to look for 
central involvement - here we have a myelogram - a radioopaque agent 
injected into cisterna magna, continuous with subarachnoid space, fills 
the space along the cord - compressing lesions obstruct flow - here we 
see interruption in dye flow where tumor is invading. this is good 
evidence that the lesion has entered the spinal canal. but we can't 
eliminate the possibility of entrance of tumor into the canal by NOT 
seeing interruption of flow. normal myelogram isn't definitive. MRI is 
valuable for demonstration of tumors not showing up on myelogram. 
sometimes reaching into the axilla allows you to palpate the tumor, or 
provokes a pain response. 

slide: extradural vs intradural lesions


slide: postmortem cord sections which have been painted with iodine - the 
white matter is the brighter yellow, the grey matter and compressed cord 
is paler. 

cats can get these too. due to location of tumor, sometimes 
we see signs other than those relating to the peripheral nerves in the 
legs - we may see horner's syndrome or cutaneous trunci reflex 
abnormalities.

expected signs: limb paresis, limb paralysis, limb 
anesthesia, depressed or absent limb reflexes
also: horner's syndrome, 
abnormal cutaneous trunci response

slide; cat with horner's syndrome - 
3rd eyelid is up, lids are droopy, pupil is small (miosis); in man, we 
see endophthalmos (eye sunken in) but in these animals the more obvious 
third sign is prolapse of the nictitans. we see this ipsilateral to the 
affected limb. why? the syndrome reflects a deficit of sympathetic supply 
to the eye. it is the cervical sympathetic trunk that brings sympathetic 
influences to the head/eye.the origin of this sympathetic trunk is the 
nerve root of C8 T1, T2, T3, T4 but the point is the roots that 
contribute to this may be simultaneously affected by tumor, so the lesion 
affecting nerve roots may also affect the sympathetic trunk. 

based on 
neuroanatomy this is rather simple. 

also, a cutaneous trunci reflex 
abnormality may be seen - here, we're talking about stimulating the skin 
over the thorax and upper lumbar area, and provoking a contraction of 
cutaneous trunci muscle. this is  a reflex, it is however multisegmental, 
and a key feature is that sensory input is segmental, but motor outflow 
(innervation to cutaneous trunci) originates in cervical/thoracic 
junction. so that if the animal has an abnormality of these nerve roots 
they may lack the cutaneous trunci reflex response due to lack of motor 
integrity required for that response. but this is a peripheral lesion - a 
nerve sheath tumor of nerve roots - so even if there is no response, when 
you stimulate the skin, the animal is still likely to feel it. the 
sensation is there, you've just lost the motor input to the muscle. 
sensory pathway is intact. 

a second kind of peripheral nerve 
abnormality - 
there was a canadian company making a product that would 
"stop bleeding wherever it occurred in the body." you gave this stuff IM, 
and it would stop the bleeding. so they said. what they didn't tell you 
was, this stuff was very noxious, and when you made the IM injection it 
could necrose tissue, and here we see a necrotized sciatic nerve - there 
was permanent paralysis from this. this type of damage is always a risk 
of IM injection in the region around the sciatic. it's common to use the 
hind limb of animals to make IM injections. certain agents are more 
noxious than others. repository drugs with alcoholic vehicles can be a 
problem. one injectable anthelmintic is known to do this. it's not the 
physical trauma of sticking a needle in the nerve...it's the stuff 
injected. the animal will respond at the moment of injection - they act 
like it hurts, and then they experience anesthesia/paralysis along 
distribution of the nerve.

slide - intramedullary pin threaded down the 
sciatic nerve.
oops.

slide: neuroma - remember, nerves can regenerate - 
schwann cells regenerate easily and axoplasm grows in general in mammals 
at about an inch a month. that's a proliferative process. but if the 
axons aren't organized to reach their targets, you form a neuroma. 
particularly serious in horses. in people after limb amputations, we see 
neuromas forming in the stump. sensory nerve neuromas are very painful, 
and pressure causes a lot of pain. many tx to prevent these - many rest 
on burying the nerve stump somewhere where it isn't likely to be 
compressed. however, though you see these histologically - in small 
animals, we haven't seen an amputation result in a painful neuroma - 
maybe due to no prosthesis, no pressure on it??? just curious.
oh, but he 
says it is common in horses with transected nerves.


slide: cat with 
necrotic feet due to ischemia. cat was brought in because wife didn't 
like cat walking across tablecloth with those feet. oy. they had it like 
this for a year. ischemia is disruptive to nerves is the point. 

we 
often produce ischemia by crossing our legs. that tingling feeling when 
your foot goes to sleep is b/c you interrupted the blood supply to the 
nerves. "ischemic reversible neuropathy," also caused by reading in the 
bathroom.
honeymoon paralysis - in people, the man who cradles the head 
of his loved one wakes up with an absolutely useless arm due to ischemia. 


slide: neuroma formation - little neuromata at the end of nerve roots - 
this cord belonged to an animal who had bilateral brachial plexus 
avulsion secondary to trauma - both plexi were ripped from the cord, 
leaving these little stumps which proliferated. 

slide: dog lying on 
brick patio

generalized peripheral nerve disorders:


polyradiculoneuritis (sp?)  most common example is coonhound paralysis. 
this is a generalized problem affecting spinal nerves, usually producing 
paresis and paralysis with ascending distribution, progressive weakness 
over hours/days, and is left not uncommonly with tetraplegia; considered 
an immune mediated problem, associated with raccoon saliva as the 
antigenic agent. we also recognize what appears to be a clinically 
similar if not identical situation in which raccoons are not part of th 
ehistory or pathogenesis, but some other allergen is. the important part 
of this syndrome is that it carries a generally favorable prognosis, 
recovery is not rare but rather it is very encouraging, most animals do 
recover. the dx is based on history, clinical signs, electrodiagnostic 
methods, and spinal fluid protein usually is elevated in the absence of 
any cellular pleocytosis. this disorder may be analogous to the human 
Guillaine-Barre syndrome, which also produces an ascending paralysis with 
generally good px. typically sensation is preserved in these animals, and 
they often act as though modest stimuli are exceptionally painful - 
sensory system may be enhanced, hard to know that for sure though. could 
be just frustrated by inability to get around. 

steroids are often 
recommended, but it is by no means essential to use them. some thing they 
are contraindicated. they are commonly used in the face of immune 
mediated polyrehowever you spell its; they are rarely used now in people 
where plasmapheresis and gamma globulin injections are preferred.

a 
while ago Jerry someone published a series of ten of these cases. with a 
Dr Brown from HUP they did some studies - here we see a control slide; 
they foudn that in dog serum is a heat stable product which when put onto 
the dorsal roots of rats, caused demyelinization.  so there is evidence 
for some circulating agent that can do this. 

more conventionally, here 
we see a cord section showing demyelinated ventral roots.
and here, while 
usually this is almost solely ventral motor disease, in this slide we see 
loss in the dorsal roots.

in the notes, it mentions the fact that we 
believe generalized peripheral neuropathy is associated with some 
endocrine abnormalities. the best, not powerful, evidence, is the 
neuropathy associated with hypothyroidism. this is based primarily on 
clinical correlation and response to thyroid hormone supplementation; 
there is littel understanding as to how the two are related. we see 
peripheral nerve dysfunction in the face of diabetes mellitus, perhaps 
more in cats than dogs, and plantigrade stance is common in these 
animals. this appears to be quite different from the diabetic neuropathy 
in people. in animals, esp hind leg, plantigrade stance, not obvious 
sensory disability, is associated with diabetes, and it may be reversible 
when diabetes is better controlled. in people the main sign is sensory - 
people get intense, unremitting pain, and quality of diabetic control 
isn't so related to abating the signs of neuropathy. 

paraneoplastic 
syndromes - another mysterious combination - generalized dysfunction 
coexisting with various tumors. bronchogenic carcinomas, insulinomas 
perhaps even more often, and it isn't known whether these tumors have 
immune mediated effects causing this, or if there is another noxious 
toxic component havieng a secondary effect on nerve function. 

finally, 
the two best known junctionopathies, of which you have already heard:

myasthenia gravis, acquired myasthenia which is most often associated not 
with failure to produce ACH but a postsynaptic problem in which Ab to the 
ACH receptor are created and which block synaptic transmission, 
preventing postsynaptic depolarization, because the receptor isn't 
available to normal amounts of ACH.

contrast with botulism, another 
neuromuscular failure characterized by dysfunctional release of ACH (due 
to that whole thing about SNARE proteins, failure to dock and fuse 
vesicles, etc, see bbd lectures)

video of some of these animals:

slide: 
st bernard with nerve sheath tumor - he's limping. we're looking for 
ipsilateral hind limb deficits - why? because it could indicate invasion 
into the spinal canal, producing cord compression and upper motor neuron 
deficits in the hind leg (suprasegmental). we see horner's syndrome in 
this dog too. when forelimb is affected, usually the radial nerve deficit 
is most obvious - his inability to extend the carpus. but note also that 
now we're trying to see if this dog has sensation. we pinch the foot, he 
withdraws. we're worrying about peripheral nerve lesion. well, reflex arc 
is intact, so this nerve here is ok. he probably felt the stimulus - if 
there was enough integrity to get impulse to the cord, it probably 
ascended from there. we have no idea what it felt like though. 

another 
dog with brachial plexus dz - a 10 yr old labrador with a 10 month 
progressive problem. limping, holding up left forepaw. ddx nerve sheath 
tumor, some other abnormality affecting nerves to the limb. he doesn't 
use this paw to hop on when asked. his other side is ok. his hind legs 
are both ok. but he can't use this front left leg. he can't extend it or 
support his weight on it. this limb is also fairly atonic and the 
musculature is fairly atrophied. triceps and distal limb atrophy. 
axillary mass is palpable. substantial atrophy of superficial pectorals, 
less of deep pectorals. no signs of invasion of spinal canal. 

dog with 
hind leg problem - walks weird - sometimes carries right hind - sort of 
floppy. the right hind leg muscles are very atrophied. when he advances 
the leg, his knee comes forward - he can advance his hip but not the 
distal parts of the leg. this also had gradual, long onset. dog is happy, 
nonpainful, wagging and affable. he's pretty good at hopping on the other 
side, not so good on right side. little tone in leg. can use coxofemoral 
joint but nothign else. doesn't correct when foot placed in knuckling 
position. tail wagging suggests cord is probably ok. other legs are all 
ok. atrophied gastroc, hamstring, anterior tib, quadriceps ok. weak 
anterior tib reflex, easily elicited knee jerk - looks so big b/c 
antagonist muscles do not work. stifle flexors are wiped out. he appears 
to have sensation medially but not laterally; suggesting the sciatic 
nerve isn't working, but the femoral nerve is. this is an uncommon 
presentation of nerve sheath tumor.

---break---

more videos

this next 
dog is a dog who had a brachial plexus avulasion - his right front leg is 
limp and dragging. the dog is happy and running around. he fell out of a 
moving pickup truck, is how he got injured. this dog has no sensory 
perception on the limb. in fact, he has no limb damage. he has no 
reflexes in this limb. these avulsions aren't associated with fractures 
or contusions, though. some sort of shearing or adducting force is what 
causes it. in people, getting the arm caught in some kind of industrial 
belt is the cause. the prognosis for recovery here is very poor due to 
the nature of the damage.
cutaneous trunci response - only the left side 
(contralateral to the avulsion) contracts. he obviously feels it, though. 


this dog has peripheral disease - normal extensor postural thrust (hind 
end wheelbarrow thing), but no use of front legs - is using hind legs to 
hop forward, and resting on his carpi - he's sort of like a kangaroo. 
he's wagging his tail. bilateral peripheral disease - two brachial plexus 
avulsions. his front limbs are contracted - common chronic consequence of 
denervation. 

it's not uncommon for animals with a radial nerve 
abnormality to have contracture - it's not relieved by paralysis. easier 
to prevent with splints and casts than to treat once it exists. 

this 
dog isn't the one we saw before but he has suffered injection neuropathy 
- repository stilbesterol - his right hind has abnormal postural ability, 
knuckles over - dorsum of foot is abraded. can't support weight. less 
tone on affected side.has anesthesia on lateral aspect. knee jerk is 
hyperresponsive. sciatic distribution of the abnormality is present, 
consistent with cause. 

this dog has "dancing doberman disease" - a 
peripheral neuropathy for which there is shaky evidence. some EMG 
abnormalities. the dog wants to sit. they try to make him stand in one 
place and he shifts weight side to side - sort of dancing in place as if 
standing on hot surface. but there is no skeletal or muscular abnormality 
present. this is a benign, lifelong, relatively insignificant problem.


dogs with more generalized abnormalities - not focal disorders - pay 
attention specifically to this first dog, an OES, nope, a cocker spaniel, 
the one who had the polyradiculoneuritis - he had 3 episodes, 6 mos 
apart. all characterized by the same signs. 

wait, we're back to the OES 
now. he has a widespread peripheral neuropathy. EMG and postmortem 
evidence confirmed this. note the short, choppy gait. tiny steps. his 
feet are all sort of squished together beneath him - this is lower motor 
neuron disease? typically the lower motor neuron involvement produces 
short strided disease. this dog had widespread neuritis, thought to be 
inherited. just note, however, the short steps he took. typical of dog 
with myasthenia as well - similar type of gait. 

ok, the cocker spaniel 
- paralyzed. the tail isn't paralyzed, the head isn't paralyzed. these 
dogs remain cognizant. tail is wagging. legs do not move. when you stop 
his tail, you see his respiration is mainly diaphragmatic - his limb 
nerves and his intercostals are all affected. these animals with acute 
polyradiculitis that do have trouble usually have respiratory 
problems.two weeks later, spontaneous gradual recovery. each of his three 
episodes was like this. he died eventually of unrelated disease. 


another dog with widespread peripheral dysfunction. not all turn out 
well. this dog- as a group, the widespread peripheral neuropathies can be 
terribly troubling, prognostically. we make the dx on signs, EMG, biopsy 
- here we see absence of knee jerk, weak anterior tib, weak gastrocs - 
anyhow many of these genralized neuropathies are prognostically guarded 
to poor, and idiopathic, and reported in a variety of species. this dog 
has also serious laryngeal paralysis, inability to swallow, change in 
voice. a little bit of extensor carpi reflex. obviously feels pain, 
though can't withdraw from pain. he has a sensory abnormality also though 
- he seems hyperresponsive to pain - is he hyperesthetic or 
hyperreactive? hard to say. but he acts as though he is hyperesthetic. 
nice dog, not biting anyone, but not appreciating being poked and prodded 
to the extent that he snaps. offering him a bowl of water to drink - he 
is trying to drink but he spills a lot of the water

another dog - for 
the religious among you, this is the first MG dog Dr S ever treated. he 
lived 12 yrs. here he is stiff, reluctant to walk, very weak. religious 
aspect is it is easy to tx the first one, you get suckered into thinking 
you know what is going on, then the trouble starts. but anyway. this is 
rusty. droopy face, droopy ears, bad voice, never developed a fullblown 
megaesophagus (key to survival) and a shot of anticholinesterase produces 
a dramatic response, he gets up and starts to chase a truck. it's very 
short acting. you can see his steps get shorter and shorter as it wears 
off and he starts to look more like that OES. 

Dr Vite's example of 
success - note the short, choppy gait of this akita. lower motor neuron 
dz, ventral horn cell disease, peripheral motor disease, cord disease 
affecting intumescence, lower motor neuron kinds of processes, tend to 
give this short gait. also he looks like he's working hard, wants to lie 
down. post injection, totally normal looking. this dog too was an 
uncomplicated recovery, and he outgrew his need for tx! the simplest of 
the MG cases are very satisfying. note the change in his gait post 
injection. 

here's a dog with profound weakness, sometimes you can show 
that they can't completely close their eyelids or that you can exhaust 
their eyelid with repeated stimulus. trouble breathing, bad 
megaesophagus, can't hold head up - balances on nose. can't stand. they 
stand her up - do the hopping things - she is ok and has good postural 
responses but can't support herself at all. the weakness is the problem. 
then they gave her the injection. she got up and walked away. she ran 
right down the hall and around the corner. everyone was cheering and 
yelling hooray! however, despite this transient recovery, this dog didn't 
do so well. the megaesophagus is a big complication.

this last one is an 
unusual example of a dog with neuropathy related to beta cell 
"insulinoma" with profound weakness. note the date - october 94. he's 
picking up his feet very distinctly, and sort of flipping them forward. 
he has generalized weakness, proprioceptive defects. he never had 
seizures despite frequently being hypoglycemic. his tumor was removed. 
depressed stretch reflexes present . we see evident improvement in gait 
after tumor removal. he lived several years. he improved beyond what we 
see here. metabolic or paraneoplastic? some manifestation of neuropathy 
associated with an insulinoma. 

continuing here with - how is it we 
assess peripheral nerves? this is the part we skipped before.


electrodiagnostic tests: 
what are they?
how are they done?
what are they 
supposed to do?
they are physiologic tests, done in labs for years 
experimentally. we apply them to determine the quality of function. they 
are intended to give objective evidence of peripheral nerve function. 
remember the two things to consider here are the soma - the cell body - 
the extension of which is the axon; and the myelin which surrounds the 
axon. recall each myelin segment is made by a schwann cell, b/w segments 
are nodes of ranvier with high resistance. long nerves have longer 
segments of myelin and bigger distances b/w nodes, so they have more 
rapid conductcance. unmyelinated fibers are smaller and conduct more 
slowly; larger axons have thicker myelin segments, longer myelin 
internodes, and more rapid conducting velocity.

so one feature 
interesting us as we use these tests is can we separate axonal function 
from myelin function? even though we know disturbing the myelin will 
disturb axonal function to a degree, they are still separable.

EMG: 
electromyography - we're examining the ventral horn cell, it's axon, and 
the muscle fibers it influences - the motor unit. when the axon 
depolarizes, all the muscle fibers innervated by it are depolarized, if 
the NMJ is working, so we get contraction of the fibers. in teh absence 
of a depolarization, these muscle fibers are at rest - the fibers are not 
depolarized, they are quiet. some muscles have 4000 muscle fibers per 
axon, some have 4 fibers per axon, it varies.

You take your dog, put an 
electrode into him, amplify the electrical activity recorded from muscle, 
play it through audio amplifier so you can hear it and into an 
oscilloscope so you can see it. you make the connection to animal using a 
23 ga needle, within which is a second point that is insulated from the 
outer needle. you're measuring the potential between them. when you do an 
EKG you have right arm and left arm lead. you look at electrical activity 
b/w them, coming from the heart. you look at the spontaneous electrical 
activity. here we look at a much smaller area, and are recording across 
this 1/10 of a mm distance. 

normal muscles at rest are electrically 
silent. when the axon isn't being depolarized, the muscle innervated by 
that axon should be electrically silent. so what you look for in EMG is 
spontaneous electrical activity - unexplained by axonal depolarization. 


what's going on here? why is this? remember, normally, the axon interacts 
wtih the motor end plate on the muscle, containing NT receptors. when 
axon is damaged, rapidly following distal degeneration of axon, there is 
failure of the NMJ, resulting in upregulation of receptor protein over 
the entire muscle surface. you end up with receptors all over the muscle 
fiber, causing the fiber to be hyperexcitable. typically after 5 or so 
days, this reaches a maximum point, and these denervated muscles become 
hyperexcitable and spontaneously active. slide: a normal EMG. slide: 
spontaneous electrical activity in this anesthetized dog - squiggly, 
irregular appearance - very small potentials, 20, 40, 60 microvolts. b/c 
individual fibers are being depolarized, not whole groups of them. 

slide: another manifestation of denervation - positive sharp waves - more 
regular but also spontaneous
slide: regular action potentials. this is 
0.2 volts compared to 200 microvolts in size - much bigger, more regular, 
iwth predictable shape. due to repeated depolarization of a motor unit. 
this recording is from levator nares muscle, which flares the nostril 
with each breath. this is nerve driven, not spontaneous.

so EMGs look at 
spontaneous activity, b/c we know that normally innervated muscles are 
electrically silent at rest. as you will read, we can't use this EMG 
abnormality to tell apart denervation from some other muscle abnormality 
like myositis or some myopathies which may produce spontaneous electrical 
activity. normally innervated normal muscle at rest is electrically 
silent, though.

so that's one way to asses peripheral nerve dysfunction. 

a second necessary task is to stimulate nerves and see how they respond. 


record the nerve activity as before, amplify it, show it on an 
oscilloscope. you put electrodes in the distal limb, you put in a ground, 
you stimulate at a distal site and a higher site. at higher site, the 
latency before depolarization is related to length of nerve. distal 
stimulation has the same response but shorter latency b/c it is closer to 
the muscle. the time it takes for nerve to be depolarized and then muscle 
to be depolarized is a measure of nerve conduction, terminal conducton, 
neuromuscular delay, conduction over the muscle. 
so we stimulate nerve 
and record from muscle at two points. the difference b/w the two is the 
time to go from proximal point to distal point on the nerve. this removes 
the neuromuscular delay and muscular conduction components.

recall that 
the myelin internodes are what dictate conduction velocity. if you have 
demyelination or something, conduction velocity slows. if you have axonal 
disease, you have EMG changes. 

sensory nerve conduction velocity - here 
we stimulate skin somewhere where all conduction is sensory, and record 
from nerve. no delay is present. this is more simple. 


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