---start---
chronic diarrhea in horses
frustrating - often never dx, 
can't fix.

definition of chronic diarrhea:

diarrhea lasting > 1 month 
(acute diarrhea lasts < 1 month, usually 2-3 wks)
cow like feces
watery 
feces
diarrhea varies with stress
usually we put these horses in our 
isolation unit, which cures them, until they go home - it varies with 
stress. you put them back in home environment and start training and it 
comes back.

patient profile:
more males than females, probably not a big 
deal
any age
sucklings, weanlings. can start at foal heat and last. can 
be young race horse - common - but can be any age. 
often in good 
condition ** maybe some mild weight loss, but most in good condition. 

most common in standardbreds - this may be a real or artificial finding. 
if you're training a stb you have a lot invested in fixing it b/c you sit 
behind it when training.
can occur in any breed. 

history:
duration >1 
month
maybe years - not uncommon to last years
frequently since weaning - 
commonly starts at foal heat or weaning and lasts
usually sporadic, 
sometimes occurs as an outbreak.

back in the 1970s, the big standardbred 
farms were gearing up, and a vet at one farm found that sometimes they 
shipped yearlings from one farm to another and a yearling would come in 
with diarrhea after which 12 others in contact with him developed chronic 
diarrhea. he thought it was a contagious problem and got a grant to study 
it. Purdue U did a study to see what was going on, and found a virus in 
these yearlings that were having the diarrhea. there are many enteric 
viruses. they took that virus, and didn't really have much money but they 
vaccinated a horse with that virus to make him hyperimmune, then they 
gave the serum orally to the affected yearlings and the diarrhea stopped. 
then they gave it to some other horses with other types of diarrhea and 
their diarrhea stopped. 5-6 yrs later they got some more money and they 
couldn't find the stored virus. (not sure if someoen took it, or it 
disappeared out of the sample, he was unclear)

onset:
can be associated 
with dietary changes or weaning
may be after acute enteritis
it's not 
that unusual for a horse to have acute enteritis, totally recover in 
every way except continue to have diarrhea. on some farms where outbreaks 
of salmonellosis occur, often a lot of those animals have diarrhea for a 
couple of years or so after that. if you take those horses and do 
necropsy, youwon't find salmonella
happens after abx tx
happens after 
shipping or other stress

PE  - need a full PE
TPR, MM, hydration normal

abdomen may be normal, tucked up, or distended - if distended, try to 
find out why, it's trying to tell you something.
borborygmal sounds may 
be loud - heard outside stall! listen for quiet areas you might hear.


rectal exam:
masses - LSA, granulomatous enteritis?
LNs - usually you 
don't feel them, but you might
thickened bowel? infiltrative dz
displaced 
bowel?
rectal biopsy usually unrewarding in these situations. 

Chronic 
diarrhea - lab findings
often low WBC, < 5000, not sure of significance 
of this. it might be due to imbalance of flora causing more absorbance of 
endotoxin or something, might be some other reason. if there is 
leukocytosis, look for abscess or something.
serum protein - often there 
is normal TP
if TP is < 5.5 mg/dl or lower than you think it shoudl be, 
look for cause of protein losing enteropathy, check kidneys, liver. but 
usually normal.
if TP high, look for abscess
electrophoretic patterns 
with increases in alpha and beta area may be signs of parasites.


electrolytes - 90% of the time are abnormal. Na+ a bit low, Cl, K, bicarb 
all a bit low...but the horse is used to it, this is a chronic problem, 
and they are at a steady state. if you watch carefully, these horses 
probably are drinking more and taking more salt. they are losing some 
'lytes, but are in steady state, so don't go rushing in to correct this 
stuff. could offer an electrolyte beverage. 
abdominocentesis - often 
nice thing to do; usually normal though
might find peritonitis or 
eosinophils associated with parasites. probably a good idea to do it to 
rule out some unusual problems

fecal exam: helps direct tx
protozoa - at 
least 48 spp live in large intestine of horse, if you take fresh 
colonic/cecal contents it looks like rumen fluid. anyway 20 spp can 
appear in feces; but when you look at it (squeeze feces so fluid gets on 
slide) in normal horse, you might see 8-10 protozoa - very few. in the 
diarrhea cases when you look at fecal water you see hundreds of them. or, 
in others, you look at many slides and see zero protozoa. so it can be 
increased or decreased number. this helps you decide how to tx. 
gram 
stain: normally > 90% of the stuff in there is gram neg, except in 
nursing foals where it is 50:50 +/-
if you see predominantly one species 
that might be a problem - look for fungi
if you have lots of fungal 
elements you could have fungal enteritis (some fungus is normal). you're 
looking for hundreds of them, not a few.
diff-quick for fecal leukocytes. 
finding WBC in fecal water means inflammatory dz of GI tract, mucosal 
inflammation. again, almost always in these cases you do NOT find this. 
you usually see it in acute enteritis types of cases.

fecal cultures: we 
dno't know what to culture for. routinely, salmonella. other bacteria? 
most of the time others aren't important in chronic diarrhea state, 
except overall balance. viral isolation? well, we're not sure - Purdue 
study wasn't followed up. fecal egg count is a good idea probably to do 
just to check pasture management, deworming program, see how effective 
that is. you can have parasitism with no fecal eggs, or high counts with 
unrelated disease present.

usually we can't dx this. it's idiopathic 
diarrhea. "open" dx, imbalance of flora is probable cause per Dr. Palmer; 
some indication on VFA profiles suggest this is true. probably 90% of 
these cases are idiopathic. 
Larval Cyathostomiasis can cause chronic 
diarrhea esp in younger horses, or older horses with poor immunity. so 
it's worthwhile to try to tx that to see if it helps.
chronic salmonella, 
other less common causes.

so for this idiopathic form:
most cases are 
this.
mild weight loss but *in good body condition* <-- remember!

persistent diarrhea - may be sl intermittent
fecal output 2-3x normal but 
drinking more water, taking more salt
change in protozoal numbers


increased protozoa: can give drug to suppress flora a bit - best is 
iodochlorhydroxyquin (Reaform is old trade name - a drug that seems to 
work best on these horses with many protozoa - but company stopped making 
it. you can buy it from compounding companies but they can't call it 
Reaform so you have to remember the name iodochlorhydroxyquin. this was 
originally used to tx tropical protozoal dzs in humans). 
other possible 
tx: metronidazole, clioquinol - efficacy of these ??? metronidazole has 
caused some dramatic responses, but not sure if better when many protozoa 
are there or not. also clioquinol has had some success but dr p hasn't 
used it yet so won't vouch for it.
tx for at least 5-7 days; if no 
response, discontinue - it's not like an antibiotic you have to tx for 
10-14 days....
note one side effect of reaform is diarrhea, another is 
colic. so it's hard to tell whats going on. comes in 10 g boluses, you 
give it SID, and if it works at that dose good, if not you could try 20 g 
but not more. that's in typical 1200 lb  horse. sometimes it works at 10 
g and can decrease dose gradually and d/c after a few weeks; some need 
the drug the rest of their lives. sometimes can get down to 5 g every 2nd 
or 3rd day. it's not one of those things that will start to work in 3 
weeks though. if not by 5-7 days, give up.

decreased protozoa - another 
approach is used. it was found that horses with diarrhea when turned out 
with normal horses would eat the normal feces, and cure themselves.
"self 
cure"
"fecal cocktail"
transfaunation: colonic/cecal liquor 5-6 L; sieved 
ingesta - repeat several times. this is more effective than using the 
fresh feces of a normal horse, however you need to be at a university or 
obtain the liquor from a horse killer or something. bleah. 

the presence 
or absence of the protozoa reflects the GI flora balance. if they aren't 
present, the bacteria are probably not right either. transfaunation puts 
everything back. it doesn't always work. sometimes you have to repeat it. 
it may pay to find out where horses are slaughtered in your area, so you 
have a source. sometimes this therapy backfires - more often it backfires 
if you try it with an acute enteritis. there is the possibility that the 
source horse had salmonella or something. so warn the owner it could 
backfire. 

Other Treatments:

probiotics (lactobacillus, cultured 
yogurt, Probios) - these are a good idea but flora are so complicated 
that these don't return it to normal. you need to find a flora to 
displace what is there now, but that can be displaced by normal flora. 
like, in chickens, in first 2 weeks of life, there are 12 sets of flora, 
one replacing the other, but they need to be in order or it won't work. 
but, this sometimes helps, gives owner something to do, isn't costly...


bismuth subsalicylate or loperamide may give symptomatic relief - can 
try, often don't work, sometimes cure though.
phenoxybenzamine is good 
antidiarrheal but also a hypotensive - when you stop the drug, diarrhea 
comes back, too. also, was an investigational drug but caused a lot of 
vasodilation and death...
oral serum - only positive responses were in 
the Perdue study - people still sometimes try it but it doesn't work. 

immune modulation - sometimes people think floral imbalance is due to 
reduced IgA - if you look at these horses some do have lower IgA 
levels...but immune modulation doesn't seem to work
some people give 
large doses of mineral oil, occasionally works, no idea why
barium enema 
also sometimes works to fix the problem without finding the cause. 
it 
will constipate them, you have to be careful. sometimes diarrhea doesn't 
come back.

In general: **The best treatment is NO TREATMENT*
most tx 
don't work
reaform or transfaunation ok
yogurt ok
but often, the more you 
do, the more you screw things up. the problem often is that the owner is 
more upset and worried about it than the horse. horse is in good body 
condition, doing fine, sort of messy, but not upset about it. 
standardbreds can still race well, just messy. best thing then is to do 
nothing. but clients will get pissed off. you may have to do something 
but the less you do is probably the better.
*do nothing*
*do nothing*
*do 
nothing*
*these horses are in good body condition.*

ok, that's the story 
with 90-95% of chronic diarrhea in adult horses.

Larval cyathostomiasis 
- 
associated with some chronic diarrhea
changes in motility - occur with 
few lumenal parasites; soluble toxins from the parasites. enteritis can 
occur with encysted larvae breaking out of cysts.
history of parasite 
control program important - may be poor program, often a good control 
program is in place though.
onset is in spring or late winter or fall; 
recurrent colic; peritoneal fluid eosinophils; cowlike to watery 
diarrhea; dermatitis - patchy alopecia, scaling. electrophoretic pattern 
of serum proteins
note: we see dz in late winter, early spring; in south 
in late summer, early fall, b/c hypobiosis in south is in summer to 
protect from heat, here is in winter to protect from cold. 
if chronic 
diarrhea horse is sort of thin, with dermatitis - consider parasite.



tx: ivermectin (moxidectin?) q 2 weeks. not sure if moxidectin is good. 

fenbendazole q 2 weeks
daily pyrantel tartrate may prevent recurrence


Rhodococcus equi may cause chronic diarrhea: 
mostly in weanlings
look 
sick
bad haircoat, history of past respiratory dz may or may not be 
present
may be hx of rhodococcus on farm, or not
diarrhea variable - 
watery and persistent or cowlike
enlarged mesenteric LNs seen on 
ultrasound
usually have abdominal distension
abdomen pendulous, poor body 
tone
search for abscess
high white count
high fibrinogen, high TP
fecal 
culture/gram stain - unfortunately, about 1/2 of the horses whose feces 
you culture will show rhodococcus equi. finding it is just a sign that is 
consistent with dx, but isn't the dx. you can find it, and horse could be 
sick with something else. but it's of limited value. not finding it 
doesn't rule it out. 
therapy: erythromycin, rifampin - even though 
emycin is associated with diarrhea.
prognosis used to be considered poor. 
now that we find it earlier with u/s and tx more aggressively, it is less 
poor than it was a few years ago, but it still isn't good. fair? more 
likely than not that you will be unsuccessful in tx these horses. usually 
you find large LNs along GI tract at necropsy, and peyers patches that 
are almost ulcerated into abscesses. can be very dramatic, can dx 
grossly.

chronic salmonellosis: some people say it is most common cause 
of chronic diarrhea. if you look hard enough, 10% of horses are shedding 
it, so 10% of chronic diarrhea cases will be positive, but is it 
causative or an incidental finding?
10% are subclinical carriers. the 
ones that have chronic salmonellosis diarrhea are those with a history of 
full blown salmonella enteritis 
also weight loss, poor condition, 
protein losing enteropathy, may have colic, variable diarrhea. 
no magic 
therapy. diarrhea is usually there after salmonella is gone - at 
postmortem you don't find any great salmonella lesions or inflamed areas 
and sometimes you find no signs of salmonella at all...we try bacterins, 
immune stimulants, other things. prognosis is variable. depends on how 
patient the owner is. some horses will have diarrhea x 2-3 years, then 
get better. if not shedding salmonella, probably can put back with herd. 
will be in poorer condition than other chronic diarrhea horses, though. 
it's a rare thing, though.

giardiasis - identified in outbreaks of 
chronic diarrhea esp in yearlings; sporadic in adults
pathogenesis is 
unclear. 
some farms in texas have had giardia outbreaks

Globidium 
leukarti - another parasite, similar to giardia
horses and donkeys
small 
intestine parasite
heavy oocyst
role as true pathogen debated - may be 
seen in healthy animals
may depend on dose, age, condition of host. 


other causes of chronic diarrhea:
CHF
liver disease w/portal hypertension

renal dz
toxemia
stress

so on initial PE, look around carefully.


---break---

Dr. Steinberg

small animal neuro

This hour is really an 
introductory hour, to help you appreciate an approach you will be heraing 
from each of us who talk with you over the next 12-14 hrs that is pretty 
consistent. we may use different words or emphasize different things, but 
the basic way to address neuro problems is pretty consistent. the other 
things that are consistent are that we have an idea of the prior 
education you've had here. the neuro course you had is a neuroscience 
course giving a broad overview of the nervous system. consequently you've 
had very little functional neuroanatomy. and yet, that is probably the 
primary tool in clinical neurology. so, one of our missions, and the 
primary one, is to help you recognize the essential elements of 
neuroanatomy, functional neuroanatomy. 
my message is to tie together 
clinical signs, and the clincal approach. 

how many of you diagnosed a 
brain abscess last night? one. what? no idea what that was about.

the 
neurologic signs that we see are for the most part abnormalities of 
function, sensation, motor activity, behavior. signs of disease are 
either the signs the client is concerned about or that we see during an 
exam. btw, we will follow the handout closely this hour so you don't need 
to take notes. in fact, we often talk about how much more useful the 
lecture would be if you didn't write anything down. maybe for him, but 
for me, I need to write it down or I forget it all - it seems that my 
fingers have a better memory than i do. 

it's good to read ahead. 
illustrations of things that we see in clinics will be discussed. you 
will profit more from the videos if you have read ahead. we'll emphasize 
clinical signs, not necessarily postmortem material. we'll see some CT, 
MR but the thrust of this is for vets who can interpret animal dz as it 
relates to the nervous system, using heads and hands and other tools at 
your disposal. 

one message here - clinical signs tell you more about 
anatomic location of the causal lesion than about the cause. it's 
commonplace for people to come in and say "this dog is doing the same 
thing the dog's cousin did three years ago." and think it is the same dz. 
but it may be a different one in the same location. if the dentist puts a 
local into a nerve - those signs of numbness are the same signs you would 
see if he had transected the nerve. the signs reflect a failure of 
function - not necessarily physical interruption. deficit is related to 
nerve that isn't working, not to a specific pathologic process that 
caused the failure.

signs relate to site.

this requires an 
understanding of what parts of NS do. what is normal function of what 
site. how does disease influence that site to cause signs, what are the 
signs?finally, how do i examine an animal so that i can recognize those 
signs?

the effect of the lesion 		the biological behavior of the lesion
					
anatomic site
					normal function
	clinical signs					history
					
breed, age,sex
					history, PE, tests
			
					diagnosis
					clinical 
decisions

there is a relationship b/w signs and sites
lesions affect the 
anatomic site in a way that disturbs normal function to produce abnormal 
function. that is what clinical signs mean. manifistations of 
dysfunction. murmur = manifestation of valvular disfunction. limp = 
manifestation of stifle disease. not starting is a manifestation of 
electrical failure in the car. site and signs are intimately related. 
dysfunction and signs are intimately related.

in contrast, the behavior 
of the lesion, and the way it disturbs the site, are what created the 
history - was it progressive, slow, and unremitting as a degenerative dz 
might be? was it sudden onset like ischemia, trauma might be?

the 
history gives a hint to the type of process
a technique that is very 
separate from doing a PE and making a neuroanatomic dx.
the history helps 
you form a differential diagnosis - what might be the causes.
the 
physical exam and stuff help you forma  neuroanatomic diagnosis.
in 
clinics you will have to form neuroanatomic diagnoses - figure out if 
problem is in nervous system, and if so where. then after that, you will 
have to contemplate what kind of process might be going on, and then 
finally what is the cause of the pathologic process.

intro to every 
classical neuro book is what are the three diagnostic questions?
where is 
the lesion?
what process caused it?
what etiologic agent caused the 
process?

we assess the NS functionally. we don't see it or palpate it. 
we see how it works. it's by that functional assessment that we decide 
where lesions might be and pursue cause subsequently. 

please interrupt 
with questions as needed.

having made these two distinct diagnostic 
efforst - neuroanatomic and differential (and we use the same vitamin d 
or damnit list) - the necessity is to be complete in your consideration; 
then we utilize other peripheral information - signalment, which is very 
useful - we know some diseases are more common in the young or old or a 
breed or species or whatever. observations about other abnormalities that 
may be pertinent are important too - with those ideas, we look for a 
specific test to do - take a radiograph of thoracolumbar junction, do an 
MRI to see something in the brain, whatever. this leads us we hope to a 
diagnosis, and then the clinical step that gets little attention 
sometimes is clinical decision making - should we operate on the brain or 
not, for instance. 

this is a little like ministerial preaching, where 
we spend time talking about obvious truth, that on the surface sounds of 
little importance, but is really the key to life. this is really a 
fundamental clinical idea. it's not peculiar to neuro and you probably 
have heard it before but many people come to the clinics without 
appreciating the merit of dissecting the problem into manageable parts. 


if you want to approach this in order to make a neuroanatomic dx by 
knowing how normal parts function - how lesions affect normal function - 
and knowing they are the signs of diseas e- you have to know hwat each 
part of the NS does.

a while ago, he created a "hierarchy" of how to 
look at neural function and build from simple to more complex. he lost 
the english slide though, but here is the italian version. 

the Function 
of the CNS and PNS

in the PNS, PNs are excitable and they conduct. they 
conduct toward CNS (afferent) and away from CNS (efferent). that's it. 
that's all they do. if you have a lesion of the PNS, signs are what? 
disturbance of one of those functions. 

CNS - spinal cord and brain - 
there are reflexes - the cord has places where sensory and motor nerves 
form reflex arcs. the cord also integrates impulses. not every peripheral 
afferent produces a predictable response. there is some integrative 
processing of afferent info. those reflexes are modified, either by local 
activity, the nature of the peripheral input, or central activity - the 
brain affecting the reflex center. so cords are more complex, but depend 
on PNS input.

the brain - adds volition, control, learning and such. 


in the handout, a similar hierarchy is present.
role played by PNs, cord 
and brain is listed. check it out. 

during the course of this hour and 
days to come, we'll discuss function of various parts of the NS, there 
will be some repetition to help you out.

in 1850s, Hughlings Jackson was 
a clinical neurologist who contributed in great measure to how 
neurologists considered and looked at their patients. because we depend 
on functional exam in neuro, and the number of ways of examining the NS 
are limited, people were looking for the best ways to look at it. jackson 
had a great capacity for this. Jacksonian seizures were named after him. 
these are epileptic events named after him. we'll talk about them later.

this is a steinberg modification to his theories:
if we know what the 
function of parts are, can we make a general statement about how lesions 
affect normal function? the method is to divide all possible signs into 
two categories - negative and positive signs. function is diminisshed or 
function is exaggerated.

lesions/normal function --> signs of disease


negative signs --> deficiency, eg. anesthesia. cut a nerve - conduction 
fails. part innervated by nerve is anesthetic. muscle innervated by nerve 
is paralyzed. these are deficiencies as manifestation of how lesion 
affects function. you cut the wire, the light goes out. easy.
more 
indirect, but also useful, is the secondary idea of release:
negative 
signs --> release (from facilitation) eg spinal shock. nerves and cords 
have functions that are modified by many impulses - remember temporal and 
spatial summation, where multiple influences come into reflex center and 
get integrated. in general, those functions may show evidence of having 
been "released" from facilitation. what's the idea here? if you strike 
the quadriceps tendon, you evoke simple monosynaptic reflex (knee jerk). 
for that to work, there must be a level of excitability in alpha motor 
neurons to femoral nerve making nerve excitable when stimulated. is that 
motor neuron pool always ready to produce the response? no. there are 
times when the femoral nerve motor neuron pool is depressed. it's 
inexcitable. it is determined by the descending influences which maintain 
them in a ready state. if you remove the influences which maintain the 
excitability, you take away facilitatory influence, neuron pool is 
depressed, you can't depolarize it, you have failure of function. so 
there are constantly influence bombarding the system from elsewhere, 
usually in descending brain to cord direction but not always. but if you 
take away the facilitatory influence you have a new cause for failure. 
the failure is due to abscence of facilitation. this is most dramatic in 
the primate, especially people, but all primates really. in people, it is 
not rare for those who suffer significant thoracic spinal cord problem, 
to have absent hind limb reflexes. ordinarily, you'd expect with adequate 
afferent input to lumbar cord segments and adequate efferent output to 
lower area, you'd think the knee jerk would work. but people are highly 
dependent on descending facilitatory influences so they lose the 
segmental reflex, merely because of loss of facilitation. this occurs in 
lower animals also. the major difference is in the duration of the 
reliance on the excitatory influence. the term is called "spinal shock." 
absence of reflex below level of lesion due to loss of facilitation is 
"spinal shock" and we see it shortly after severe cord trauma in the 
species with which we deal, but it is most evident in higher animals. so 
we have to reasons here for function to fail. deficiency and release from 
facilitiation.

positive signs --> irritation, eg. pain. tumor growing on 
nerve is likely to excite axons and make them fire. the disc pressing on 
sciatic roots will irritate the axon, depolarize it, cause radiating pain 
down back of leg. the tumor that is associated with a seizure in the 
brain is very likely to have an irritative influence which could be 
mechanical or chemical, on the surrounding tissue, producing irritation 
and seizure. pretty easy to figure this out. lesion irritates tissue, 
causes hyperactivity.
positive signs --> release (from inhibition) very 
important in veterinary species. this is the opposite of above. 
descending inhibitory influences also act on motor neuron pools. release 
from inhibition causes hyperreflexia. spinal shock is characterized by 
hyporeflexia or areflexia. the release from inhibition causes positive 
effects - depolarization and hyperreflexia. so reflex is more easily 
elicited. when they occur they are exaggerated in a variety of ways. 


characteristics of peripheral nerve disease (PND)
1. anesthesia (absence 
of sensation)/hypesthesia (diminished sensation)
2. paralysis (loss of 
volitional motor activity) (also paresis - weakness associated with 
incomplete paralysis) --> results in muscle atrophy, EMG changes
3. 
trophic and autonomic effects (less common) - we don't think about this 
too much b/c manifestation of this is less common...recall that these 
nerves, though, contain not only somatic afferent/efferent axons, but 
autonomic fibers controlling blood vessel tone, glands, etc. so sometimes 
manifestation of PND is edema, or glassy change in skin, disease or 
dysfunction around nail beds, that kind of thing. 
when discussing PND 
clearly the signs relate to anatomic distribution of the nerve. so you 
shoudl know sensory and motor distribution of major limb nerves so you 
can recognize when ulnar nerve had been damaged, know sensory 
distribution of sciatic vs femoral nerve in hind leg, etc b/c this is how 
you localize the problem. 

characteristics of Spinal Cord Disease (SCD)

1. anesthesia
2. paralysis
3. disturbed reflexes (hyper/hypo)
deficits 
tend to be bilateral at or below the level of the lesion. there are 
exceptions. 
keep in mind - you can have paralysis and still be able to 
induce reflex activity. paralysis is the absence of volitional control. 
maybe you can't walk, but we can induce in the paralyzed legs, reflex 
activity. that shouldn't surprise you. paralysis does not mean "can't 
move," means "can't control movement". similarly, could have very active 
flexor withdrawal to pain stimulus without feeling any pain. dog can have 
anesthetic foot with exaggerated segmental reflexes. ok? withdrawal does 
not imply perception. knee jerks do not imply motor capacity. the cord 
segments function in an isolated fashion - this is why it's inhibited or 
facilitated. 
it's important to know that with SCD - focal SCD - the 
lesion produces deficits that are often bilateral but typically 
asymmetrical. consider the size of cord, it's small, so the lesion is 
very likely to produce ipsilateral deficits below the level of the 
lesion, but cord isn't big so a lesion causing right sided deficits 
probably will also affect left side. with only one or two exceptions the 
deficits are below or caudal to level of lesion. usually ipsilateral.


diseases of the brain:
cause abnormalities of 
gait
posture
sensation

metabolism
mental awareness

in a general way, we can talk about parts of 
the brain and how they might show signs of a lesion. separate and about 
five hours from now, dr vite will discuss cranial nerves and their role 
but just remember the cranial nerves and their nuclei are distributed 
along the brainstem, so one consideration with the brain is which nerves 
are functional and might that point to a level of concern. so II, III, IV 
- rostral; IX, X, XI, XII consider medulla. but grossly, 

T = 
telencephalon, cerebral cortex. first and foremost, think about people 
who have had strokes - Dr. Buchanan - someone with hemiparesis - one side 
of the body being weak in the hand and limb, the whole side of the 
body..the animals we deal with are not likely to show signs like that. 
the animals with which we deal do not have obvious postural or motor 
deficit associated with cortical lesions. experimentally, removing the 
cortex doesn't cause motor paresis. the animal can walk with normal gait 
and posture despite cerebral lesions. now, when you examine them, you 
will find postural abnormalities. but when you observe them walking, they 
have normal gait. having siad that, they may walk in circles, and they 
tend typically to walk in circles toward the side of the lesion. but they 
walk with normal gait. the telencephalon taken with the Diencephalon 
(thalamus and hypothalamus) == forebrain, prosencephalon. these are the 
structures from which seizures emanate. a lesion in one of these 
structures, or a dysfunction caused by metabolic dz elsewhere, has origin 
in prosencephalon, forebrain.
hypothalamus - eat, sleep, reproduce, 
maintain body temp
the BN basal nuclei are also worth recognizing are 
nothing like human BN. we do not see a Parkinsonian dz in animals, a dz 
characterized by the sinuous, uncontrolled jerky motions we see in 
people. mostly, the BN are invovled in motor control but we see no 
dramatic deficits from lesions here.

MES mesencephalon -part of brain 
surrounding the aqueduct, where colliculi are, where extraocular muscle 
nuclei are, where reticular activating system is that maintains the alert 
state. 

the MED medullary centers controlling ANS, respiration, 
cardiovascular system, reflexes that have to do with eating and 
swallowing. all the really essential stuff is in the brainstem. 
also 
below cerebellum in brainstem is vestibular apparatus
finally in 
cerebellum there is primary motor control

signs you see will call 
attention to one or more sites.

only after all that do you form ddx

signalment
history
PE and neuro exam
assessment: list abnormalities
then 
and only then - formulate ddx - the damnit list
list problems - order by 
importance
plan - dx tests to confirm tx plan

remember history is 
essential for creation of damnit list
history taking - boy this is really 
preaching because you're supposed to learn this four or five times in the 
curriculum, but it is really difficult so here are five minutes from Dr S 
on it.

one: history taking is kind of primary human interaction b/w 
strangers. basic intercourse b/w people, and we are not always 
sympathetic to how hard the wquestions we are asking are. there should be 
a course called sick so you have to experience illness yourself and know 
how hard it is to reconstruct events, and maybe you had a flat tire on 
the way in and you're distratcted and it's costing you a lot to be there 
and your dog has been sick a long time and you know the vet is annoyed 
you didn't come in sooner and all this stuff gets in the way and you 
should be sympathetic to that.
two: it's very hard to focus on the signs 
the owner saw, and not the conclusions the owner has made. why are you 
here today? b/c dog convulses. it is easy to forget that's a conclusion. 
the question is, what did your dog do? what did you see? owner says 
"convulsion" but maybe it wasn't? maybe someone else said that's what it 
was. a lady from Pine st brought in a cocker spaniel for seizures. back 
then, cocker spaniels often convulsed. Dr S asked her "tell me what you 
saw". she said she used to find the dog writhing on the floor, banging 
head on floor, salivating, rubbing face, and that it would go on for a 
while, but if she opened the refrigerator door the dog would stop, come 
to the kitchen, and get some butter. dog liked butter. then, sometimes he 
would go back and have another seizure. dog had a raging otitis. was 
rubbing ear on the floor, salivating for some reason (ecstasy?) but liked 
butter more than he liked scratching the hear. they took him off the 
dilantin which doesn't work. dog didn't have a seizure disorder. you have 
to make the dx. you have to get owner to share observations with you. ask 
the right questions, and listen to their answers. formulate questions 
based on their answers. 
another thing to do - make some observations 
about how your pet behaves and how you might want to check reflexes. 
we'll talk more about it monday. 


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