----start----

More of Dr Steinberg's neuro stuff

continuing with 
illustrations of focal and generalized disease of the spinal cord. 
everything necessary is in the handouts, we'll spend this hour looking at 
some neato videotapes. this should be one of the relaxing hours. just 
think about what you see. [ahhhhh.]
one more interesting focal disease of 
the cord, a bit of a misnomer, is this:

lumbosacral spinal column 
lesion. you see a myelogram here which shows that n ot only is there a 
narrowing of the space b/w L7 and the sacrum, and spondylosis, but 
something in the canal is distorting the dye column of this myelogram. 
now you really aren't affecting the cord at this level, signs are 
probably referable to impingment or distortion of cauda equina, but you 
get the point. the cauda equina is outside of the subarachnoid space, but 
you can infer there is root compression by whatever is causing the 
distortion of the dye column. disk material, proliferative ligamentous 
structures, or a tumor could do this too if it were in this place. so 
lumbosacral syndrome can have variable clinical signs depending on what 
roots are affected. may be painful, referable to the bony parts of the 
process; we see anal sphincter tone abnormalities, limp tails, gait 
disability, but it's variable b/c not all the same nerves are always 
affected.
rads, MRI good diagnostic tools

Video: dog with lumbosacral 
syndrome
GSD - this is often seen in larger dogs - tail is hanging down, 
limp. hind legs seem a bit weak, slow, a bit down on his hocks but that 
may not be a symptom, but he definitaly has tail flaccidity. his anus is 
similarly flaccid and he is fecally incontinent. because nerve roots are 
affected you can see signs of lower motor neuron disease. the roots have 
sensory and motor function; so EMG lends itself to diagnosis as well. dog 
now lying laterally recumbent. the recording electrode is in coccygeal 
muscle. there is a lot of spontaneous activity at rest, which you know is 
pathological. it's random and spontaneous small amplitude fibrillation - 
individual fibers are being depolarized - sounds like frying bacon, rain 
on the roof, that kind of thing. 

note also that EMG allows you to 
recognize the denervation of the muscles. 

slide: spinal cord with a 
bruise on it? a purple area with what looks like a glob of marmalade 
sitting on top of it. this is a tumor of dogs under age 2, which is 
always found in T10-L1 cord segment - neuroepithelioma or nephroblastoma 
or spinalblastoma. many names. it's an embryonic structure, possibly 
related to kidney, sitting on the cord - it's extramedullary but 
compresses the cord. a useful message here is that the severity of signs 
has something to do with the rate of development of insults. neural 
tissue - perhaps all tissue - is more tolerant of insults that are 
gradually applied, rather than acute. when a tumor grows slowly, neural 
deficits show up slowly. 

Dr S is having a very hard time with the video 
projector today. 

another way of looking at lumbosacral disease - a 
fluoroscopic view of a myelograph. we see L7, sacrum, dye column...we are 
moving legs back and forth, changing relationship b/w L7 and sacrum. look 
at dye column. leg is now back...leg is now down, as the joint angle 
changes, the dye is pushed cranially. disk material, ligamentous tissue, 
something's bulging up and pressing on dye column, and on cauda equina. 


now, this one year old beagle  who has the tumor we saw on the cord --- 
he has proprioceptive deficits in hind legs, but he can run around. 
deficits worse on left. but he obviously feels, has easily elicited large 
segmental reflexes in hind legs. he's incontinent - that's what brought 
him in in the first place. a lesion at T10-L1. but he ran really fast 
when they let go of him. a bit of trouble going up steps but not too 
much, is able to run up and down them without falling.

so a dog in this 
instance with a big ass tumor compressing his cord has paresis more 
evident on one side, with intact segmental reflexes that tend to be 
exaggerated, as expected with a lesion above the intumescence. this tumor 
is always in young dogs, in T10-L2. tumors growing slowly causing 
compression produce as a rule fewer intense signs and less intense signs 
than if the same degree of damage occured acutely. 

video of cat - with 
most common cat spinal cord tumor - LSA. hind end paresis. can walk but 
knuckles, sometimes drags hind limbs. knuckles hind limbs. long strided, 
ataxic gait. decreased tail tone but has sensory perception but 
diminished. easily elicited knee jerk. diminished extensor postural 
thrust. 

chest rad from cat with LSA - the disease is often multicentric 
and here there is also a mediastinal mass. the myelogram shows an 
interruption of the dye column. the gross dissection shows a spinal canal 
opened with a mass inside it, and a narrowed spinal cord in the area of 
the mass. this should remind you that most of the LSA masses are 
extradural. sometimes though they are intradural, or have a subarachnoid 
communication. this CSF has been filtered and trapped some cells for 
cytology study - we see a lot of abnormal lymphocytes. it's not rare that 
abnormal lymphocytes are found in CSF of animals with spinal LSA. when 
you fail to find it, it's because the lesion is extradural, we believe. 
LSA is probably also the most common bovine spinal cord tumor. it is also 
seen in dogs. 

a reminder - we're talking about spinal cord neoplasia; 
there is a possiblity of vertebral disease causing cord abnormalities - 
this round cell tumor has invaded the vertebrae and caused secondary cord 
compression; here is a prostatic carcinoma eating away at the dorsal 
spinous processes. so we see primary and metastatic vertebral neoplasia 
also producing cord signs.

a fairly uncommon focal sign of spinal cord 
dysfunction - this arteriogram shows us the aorta, kidneys - loss of flow 
to caudal aorta and iliacs which are occluded - producing signs of 
claudication. 
this standard poodle in the video (this condition is seen 
maybe every 2yrs) has ability to correct knuckling, is standing but sort 
of semi crouched. front legs normal. hind legs - some hyperreflexia but 
possibly within normal limits, obviously feels what is going on and 
doesn't like it, has withdrawal reflexes and sensory perception. he is 
biting someone restraining him. he can walk but his gait is stiff and 
becomes progressively more stiff - he walks a few steps and then 
crouches, and sort of quits. he acts as if it is painful to walk. 
certainly, ischemia can exist for a variety of reasons; the majority  
have always had some nephropathy - protein losing nephropathy - 
postulated mechanism is a lack of AT III.  the animals have a protein 
losing nephropathy and have low levels of AT III and they have this 
lesion; we really have no evidence for causal relationship per se but we 
see this and we think that's how it works. checking pulses are important, 
then! check the dog's pulses and also check your own :) (just my little 
joke). but you should check the limb pulses, they are important.


slide: 
among the causes offocal cord dysfunction are this - there is increased 
density of 1/2 of two vertebrae - this is discospondylitis - infection of 
vertebrae and space between. this dog may show very subtle signs - 
reluctance to move, can be very hard to dx. can be very painful and make 
animals sick, febrile, etc. so full range of signs exists. clinical 
sympatmotology can exist long before changes are seen on radiographs. we 
often suspect discospondylitis but can't prove it so easily. we saw a GSD 
here with primary complaint "not himself, reluctant to move, prefers to 
lie down, some malaise" came here 6 mos after going to Tufts where he had 
a thorough workup which included spinal rads and scintigraphy and no 
diagnosis. we took a spinal rad here and found the lesion. the only 
advantage we had was time. steroids make the dog feel better and probably 
make lesions worse. strep, staph, brucella, e.coli have all been 
isolated. radiology is most common means of dx. can be multicentric. when 
you look at CSF it is often sterile; the lesion is causing signs not by 
extension of inflammatory process but by compression due to swelling. 

a 
substantially less obvious problem here - same lesion but less extensive. 
just a little brightness to the edges of these two vertebrae. 

while 
discussing infections, here is a feline cord with FIP - most common 
infectious feline cause of spinal cord dysfunction, and you recall a 
young cat disease, dry/wet forms, granulomatous meningoencephalomyelitis. 
discrete cord signs are less common than brain signs but this can occur. 
a cat that hasn't been traumatized has LSA and FIP high on ddx list for 
focal cord signs.

rabies - we are in the most concentrated area for cat 
rabies. the number of cats in which bilateral posterior paresis and 
paralysis that was more long lasting that you would expect with rabies 
was the main clinical sign, who turned out to have rabies, is pretty 
disturbing. this outbreak has affected few if any dogs but a lot of cats 
including in the philadelphia area. 

finally, this is a spinal column 
from a lamb with osteomyelitis that spread to the cord. the vertebra 
shows septic, necrotic changes. this should emphasize to you that this 
kind of bacterial infection of the spine and nervous system is a disorder 
of herbivores. when you think of CNS infection in dogs, cats, we talk 
about viral, fungal, protozoal diseases. the occasional abscess occurs, 
sure, but on the whole, bacterial infection of CNS is a disease of 
herbivorous animals - cows, horses, pigs - uncommon in dogs, cats unless 
the CNS has been penetrated by puncture wounds, spreading infection from 
nearby, etc. 

video: diffuse cord disease - WHWT with Krabbe's globoid 
leukodystrophy - autosomal recessive dz of dog, cat, human. relates to an 
enzymatic abnormality - beta galactosesomething deficiency which causes 
those big fat macrophages to form, and produces breakdown of white 
matter. it's a generalized brain/white matter disease, but commonly 
presenting signs are hind end paresis, paralysis, tremors. 

think about 
degenerative myelopathy - we recognize but don't understand this well. 
here we see an old dog disease, most common in GSD but not limited to it. 
gradual destruction of white matter, both axons and myelin are affected, 
starts usually in thoracic cord. signs begin with slowly progressive, 
often asymmetrical degree of paresis, with postural and proprioceptive 
abnormalities, gradually causing increased weakness and ataxia with 
shuffling gait. it is painless, progressive, and for the most part spares 
bowel and bladder control, so not until the worst stages do animals 
suffer incontinence. they do not complain of pain or discomfort; they 
retain sensory perception. tone is good. segmental reflexes present, 
exaggerated. this is a disease that doesn't respond to steroids. that's a 
diagnostic test, in fact. dx of exclusion, really. 

many cord problems 
aren't diagnosed completely; lots aren't ever subjected to MRI. 
degenerative myelopathy isn't "idiopathic spinal cord dysfunction" 
though. it has definite clinical and histological characteristics.

video 
of weimeraner puppies. syringomyelia/spinodysraphia? failure of normal 
growth and development of the raphe of the midline of the spinal cord. 
when one foot is pinched, both hind legs flex. these dogs have 
characteristic symetrical hopping gait. it's a failure of normal cord 
development. it's present as soon as pups start to work. nonprogressive. 
they have a bizarre gait, lousy proprioceptive capability, stand in weird 
positions. sometimes you see abnormalities of hair swirling on dorsal 
midline. tail wags well, though :)
this very young pup already shows the 
symmetrical hopping gait.

here is a cord from one of those affected 
dogs. the syrinx, the tubular abnormality that is fluid filled, is 
immediately obvious - now, sometimes the central canal communicates with 
it - then you can call it hydromyelia or something; the issue is hard to 
resolve and probably isn't that important. 

closeup of this - this is 
existing in animals that hop around, not paralyzed animal, btw - there 
are huge tubular canals through these cords!!. these can go from lumbar 
to upper thoracic cord. usually affects just the hind legs. 
this cross 
section shows a sort of fusion of the ventral horns. might be related to 
the symmetrical gait. looks like there are cross connections b/w ventral 
horns.

this little puppy, had severe hind end and tail tremors - due to 
delay in spinal cord myelination. most have good prognosis - just takes 
time. the literature contains reports of a population of labradors with 
this.

slide: normal cord from 9 day old dog - note the blue myelin but 
poor myelinization in the area of the corticospinal tracts - that 
maturation is delayed in normal dogs. now in affected dogs - the whole 
cord is the same color, can't tell grey from white matter, b/c there is 
no myelin in the cord at all. peripheral nerves are well myelinated. as 
the animals recover, the myelin pattern comes back and it looks normal. 
not sure why delayed myelination causes the trembling. 

---break---


more videos.

vite - clinical evaluation of animals with brain disease


Neuroanatomy

as discussed before - functional divisions, etc. 
cerebral 
hemisphere and diencephalon are lumped together functionally because they 
are involved in thinking, emotions. not gait.
brainstem (pons, medulla, 
midbrain) and cerebellum are involved in gait.

neuro exam assesses 6 
broad categories of function.
when doing a neuro exam, you say "is 
neurologic disease present; if so where in NS is it; if it is present in 
that area, what can cause this dysfunction?" the last question is the 
easiest b/c you can look in a book. 
the hard part is saying if the 
disease is present, and localizing the disease. we use the neuro exam for 
this.
you have to check these six categories:

-mentation
-gait
-postural 
ability
-segmental reflexes
-sensation
-cranial nerves

ask yourself - is 
this animal normal, or not?
you have to use words to describe what you 
see. "he walks funny" isn't good. "that dog walks like he has a disk" 
isn't good. describe what you see precisely, localize it, grade it, then 
figure out what is causing it.

videos: 

one is normal, one is not. one 
has posterior paresis, ataxia, severe proprioceptive deficits in hind 
legs. mentation normal.that's what I say. 

now, Dr Vite says: abnormal 
dog alert, playful, wants to interact but doesn't stay as active and may 
be slightly depressed. gait - falling on back legs, hind legs extremely 
sloppy, can't predict where limbs will land, incoordinated in the back, 
so we'd say he's quadraparetic, incoordinated, crossing limbs so ataxic. 
his front leg gait is a bit dysmetric - lifts legs higher. severely 
paretic in hind limbs; some postural deficits in forelimbs b/c waits too 
long to initiate hop. no hop at all in hind limbs. wheelbarrow pretty 
good. no extensor postural thrust present. good tone to hind limbs, 
though. spastic hind limbs. 

quadraparetic
worse in hind limbs
ataxia in 
hind limbs
dysmetria in forelimbs
spastic hind limbs
hyperreflexia in 
hind legs
resting nystagmus (fast phase to right)
full body tremors a 
couple of days later and increased dysmetria

cerebral 
hemispheres/diencephalon:
signs we might see with damage to this area:


-mentation - altered. [depressed. disoriented. normal = bright, alert, 
responsive. stuporous (sleeps until provided with noxious stimulus), 
comatose (can't wake up at all).]. but with problems in cerebral 
hemisphere/diencephalon, you end up with altered mentation.
-gait - above 
the midbrain, damage doesn't affect gait. dogs do not require cerebrum or 
diencephalon in order to walk. people do, but not these animals we work 
with. they may circle, though
-postural ability: contralateral deficits

-sensation: contralateral deficits
-segmental reflexes: normal
-cranial 
nerves: blind, pupillary abnormalities
-other: seizures: they come from 
the yellow area :) diencephalon and cerebrum (forebrain, prosencephalon)


video: how animals walk with diseases of cerebral 
hemispheres/diencephalon; neuro exam of them. animals often circle toward 
the side of the lesion. 
loss of menace reflex - contralateral to side of 
defect. here we see loss of menace on right, and circling to left. 

this 
cat is depressed, disoriented, dull, not that responsive. no menace 
response on left; some on right. normal gait. seems to not have good 
sensation on the left. remember, if you have trigeminal dysfunction 
(sensation to face) it will be ipsilateral - but you'd expect other 
brainstem signs. so the problem hereisn't loss of cranial dysfunction, 
but a problem with input from the brainstem up to the cerebrum. the nerve 
is ok. the perception is lost. 

Midbrain: green area. all gait generated 
here in cats/dogs.
damage here in this part of the brainstem causes:

mentation: altered
gait: ataxia; spastic tetraparesis/paralysis
postural 
ability: contralateral or ipsilateral defects depending on site of lesion

sensation: decreased caudal to lesion
segmental reflexes: contralateral 
hyperreflexia
cranial nerves: pupillary abnormalities, strabismus


pons/medulla disease:
mentation altered
gait: ataxia, spastic 
tetraparesis/paralysis
postural ability: ipsilateral deficits
sensation: 
decreased caudal to the lesion
segmental reflexes: ipsilateral 
hyperreflexia
CN: V, VI, VII, VIII, IX, X, XI, XII deficits

videos...


tetraparesis, ataxia, balance problems, poor postural ability...looks 
similar to cervical cord disease except is off balance and has some 
depression, not expected with cord disease. add in some other cranial 
nerve deficits and it looks like pons/medulla disease. 

cerebellum - no 
primary function here. it's integrative/modulating. defects here cause:


mentation - normal
gait - ataxia, dysmetria "goose stepping" "bouncing" 
"prancing"
postural ability - ipsilateral defects
sensation - normal

segmental reflexes - normal
cranial nerves - none
menace deficits, 
intention tremor

remember signs do not have to come as a set. presence 
of a menace reflex doesn't rule out cerebellar disease.

MRI is great - 
really shows you what is going on in there. beautiful pictures that look 
like gross sections.

lissencephaly - smooth cerebrum. no wrinkles, no 
worries ;)

hydrocephalus - cure? if born with it, often can't. if high 
pressure/obstruction to flow, surgical drainage may help. 

tumors - 
space occupying masses within brain - meningiomas in cats very treatable 
via surgical resection; also in people; in dogs, not so amenable to sx, 
need radiation/chemo. tumors can be outside or inside brain. glioma - 
tumor of glial cells - surgery alone not curative. radiation therapy of 
brain can be damaging. brain radiation is not benign. radiating a whole 
brain will decrease the IQ 10-20 points...

inflammatory disease - bright 
areas on MRI
list of encephalitides in notes



---end----