Neuro - 5 Q's Flashcards
what to differentiate when evaluating neuro dz
central from peripheral
what to avoid with misdiagnosis
rabid animal
how to localize
evaluate central nervous signs
what to associate neurological signs with
clinical scenarios
four types of cerebral lesions
vestibular
frontal lobe
brain stem
cortex
vestibular signs
circling and head tilt
frontal lobe signs
propulsive movement
brainstem signs
disturbed sensorium
blind
seizures
cortex signs
consciousness
what is the occipital lobe responsible for
visual reception and interpretation
what is the basal ganglia and what does it do
processing link
initiates and directs voluntary movement
cerebellar signs
spastic ataxia
dysmetria
tremors
brain stem controls what
neurological function necessary for survival
what are the functions of the brain stem
breathing digestion heart rate blood pressure awake and alert
where do most cranial nerves arise from
brain stem
brain stem cranial nerves are pathways for what
pathway for all neuro tracks to the highest parts of the brain
two types of defecits with a brain stem lesion
gait
cranial nerve
three parts of the brain stem
midbrain
pons
medulla oblongata
type of abnormalities seen with spinal cord lesion
bilateral gait abnormalities
normal mentation
what does Upper Motor Neuron initiate, maintain, and control
initiates voluntary motor activity
maintains muscle tone and posture - anti gravity
controls muscular activity assoc. with visceral fxn
what is the efferent neuron of the PNS
LMN
what does LMN connect
CNS with muscle
where is the function of the CNS manifested
through the LMN
what controls spinal reflexes
LMN
spasticity, stiffness, hypertonia
UMN
loss of inhibition of myotactic reflexes
UMN
spinal reflexes in tact and/or exaggerated
UMN
loss of voluntary motor function - paresis or paralysis
UMN
hypotonia, hyporeflexia
LMN
muscle weakness - paresis or paralysis
LMN
loss of spinal reflexes
LMN
muscle atrophy
LMN
loss of motor innervation
LMN
2 causes of hydrocephalus
blue tongue
akabane
what does vitamin A deficiency interfere with
absorption of CSF at arachnoid villi
what happens when CSF pressure elevates from vitamin A deficiency
results in blindness first, followed by seizures
papillidema at the optic chiasm
what is an autosomal recessive trait of herefords and shorthorns
cerebellar abiotrophy
BVD in relation to cerebellar abiotrophy
can cause it between 100-200 days gestation
folial degeneration
cavitation of cerebellum
45-day-old holstein fresian female with cerebellar abiotrophy
recumbent and blind
45-day-old holstein fresian female with cerebellar abiotrophy and BVD-MD positive, what to do
virus neutralization
another time you can see BVD
in utero
21-day-old holstein on the slide
BVD brain lesions
ocular lesions seen in both spontaneous and experimental studies of BVD
retinal atrophy
micro-opthalmia
find out rest of the CS, covered with pic on slide
3 reasons for malformed vertebral canal
myelin disorder of charolais
neuraxial edema of herefords
hereditary hypomyelinogenesis of jerseys
myelin disorder of charolais etiology
probable familial etiology
what is neuraxial edema of herefords
autosomal recessive of polled breed
what do we see with hereditary hypomyelinogenesis of jerseys
spastic dysmetric gait if they can walk
what is the organism for tetanus
clostridium tetani
is c. tetani gram neg or gram positive
positive
c. tetani aerobic or anaerobic?
anaerobic
what does c. tetani form
spore forming rod
how long does c. tetani remain viable
years
what does c. tetani produce and release
toxins - neurotoxin and tetanolysin
what is TeNT
neurotoxin
what does TeNT cause
signs called tetanospasmin
what type of effect does tetanolysin have
tissue necrotizing effect
decreased tissue oxygenation
facilitates bacterial proliferation
what does TeNT bind to and what happens
binds to nerve cell
taken up by endocytosis
moves retrograde up the axon
what kind of interneurons is TeNT internalized into
ones that regulate motor neuron activity
what does TeNT inhibit
action of inhibitory neurons
prevents release of glycine and GABA
what are the inhibitory neurons
glycine and GABA
how does neurotoxin bind
irreversibly
recovery after neurotoxin
only with the growth of new nerve terminals - can be days to weeks
how is tetanus acquired
wound infection - tail docking, castration, puncture wounds, retained placenta
CS of tetanus
stiff gait mild bloat difficulty rising 'pump-handle' tail loss of rumenation erect ears pulled back to poll - sardonic grin prolapsed third eyelid - spasm of retractor oculi mm.. spasm of masseter mm. - lock jaw loss of swallowing spastic paralysis
death via tetanus
respiratory paralysis
diagnosing tetanus
CS - muscle spasms and hyperesthesia
treating tetanus
elimination of infection neutralization of free TeNT relief of muscle spasms provision of good nursing care - need time for toxin to decay prevention
how to eliminate infection of tetanus
wound debridement
gram pos spectrum abx - PPG 24,000IU/kg BID 2-3d
how to neutralize free TeNT
can only do this before uptake into nerve
tetanus antitoxin - 1500-100,000U per animal per day for 3-5 days
how to relieve muscle spasms with tetanus
tranquilization - acepromazine
muscle relaxation - diazepam
components of good nursing care when treating tetanus
minimize stimulation from environment
quiet, dark, well-padded stall, cotton in ears
keep sternal to prevent bloating
rumen fistula
prevention of tetanus
routine vaccine with tetanus toxoid
booster pregnant ewes/does in late gestation to protect lambs and kids
tetanus antitoxin when docking and castrating
what is the routine tetanus toxoid usually combined with
other clostridium bacterins - C and D
dose of tetanus antitoxin when docking and castrating
150-200 IU per animal
when to start the tetanus vaccine and how often to give
start around 6 weeks of age - decline of maternal antibodies
give at least twice at 2-4 week intervals
booster at 8-10 weeks
how long is the duration of protection from the tetanus vx
unknown but the vx is inexpensive and it works
where to get botulism
decaying vegetation, carrion
what happens with botulism
exotoxin blocks Ach release, causes flaccid paralysis
see inability to eat, limberneck
what usually happens with botulism
usually affects multiple animals in the heard
how quickly after the first signs of botulism have cows died
80 were dead within 8 hours of first CS
what did the TMR of botulism herd have
rotten oat hay and a dead cat
what did the botulism cat carcass have
type C botulinum toxin in the carcass
no botulinum toxin was found in the milk or sera
prevention of botulism
no vaccine in the US
treatment via antitoxin - not commercially available
what type of dz is tick paralysis
ascending LMN
what does tick saliva contain
neurotoxin
how quickly do tick paralysis signs progress
24 hours
treatment for tick paralysis
remove tick
prognosis for tick paralysis
fair if dx quickly
two ticks that can cause paralysis
ixodes holycyclus
dermacentor spp.
three phases of rabies
prodromal
furious
paralytic
when is infection of the limbic system in rabies
furious stage
when is infection of the neocortex in rabies
paralytic stage
should you vx all livestock for rabies
no, not recommended
vx valuable animals is suggested
what is the rabies vx
Imrab 3 - Merial
what organism causes listeriosis
listeria monocytogenes
describe L. monocytogenes organism
small gram positive non-spore forming diphtheritic rod bacteria
where to find listeria monocytogenes
spread in feces of many mammals, birds, and fish
how long can L. monocytogenes survive in the environment
months to years
is listeriosis zoonotic
yes
what are the serotypes of listeriosis and what do they cause
1/2a and 4b
encephalitic listeriosis
which animals is listeriosis more common in
more common in sheep than in cattle
sources of contamination for listeriosis
silage
fecal contamination
chronic intramammary infection
poultry litter used for bedding
what ph of silage inhibits growth for listeriosis
ph less than 5.5
other infectious dz of the brain from listeriosis
generalized disease with abnormal behavior
circling, dysphagia
do carrier animals of listeriosis exist
yes, small gram positive rod
pathogenesis of listeriosis, commonly associated with what
environmental and nutritional stress
what does listeriosis require for entry
wound
common types of wounds that obtain listeriosis
rough browse/hay
erupting teeth
ages of patients seen with listeriosis
1 month or older
hallmark sign of listeriosis
multiple unilateral cranial nerve defecits
circling, head tilt, facial paralysis
anorexia, dysphagia
when do we see fever with listeriosis
early
what is silage eye from listeriosis
uveitis
conjunctivitis
keratitis
what are the late signs of listeriosis
recumbent
opisthotonos
paddling
pathogenesis / path of listeriosis
rootlet trigeminal -> intra-axonal migration -> brainstem
what type of movement does listeriosis have and what does this accomplish
cell to cell movement
evades phagocytosis
treatment of listeriosis
difficult
listeria monocytogenes bacteria found where
decaying organic matter
found on many areas of the farm
must have a ph above 5.5 for proliferation
listeria bacteria binds to the cell via what
surface proteins
after listeria bacteria binds to the surface proteins, how does it enter the cytoplasm
via hemolysin - listeriolysin O
after listeria enters via listeriolysin O (hemolysin), what happens
multiplies, presses on internal surface cell membrane
forms listeriopods that invaginate into adjacent cell
gross lesions with listeriosis
absent or minimal
CSF with listeriosis
turbid
medulla oblongata with listeriosis
softened
fetus with listeriosis
autolyzed
what type of transmission of listeria is possible
venereal
how do humans become contaminated with listeria
via processed foods - soft cheeses, deli cold cuts, sliced cheese, ice cream
how many organisms can be infective with listeria
less than 1000
how to treat listeria
penicillin 44,000U/kg BID for 7 days
reduce to 22,000U/kg for 14 days
OTC 10mg/kg BID
what do we see on chemistry with listeriosis
stress leukogram
evidence of dehydration
what do we see in CSF with listeriosis
increased protein - more than 20mg/dL
high number of mononuclear cells - more than 10/uL
do we see limb paralysis with listeriosis
not usually
definitive diagnosis for listeriosis
post mortem
multi-focal to coalescing areas of necrosis
severe infiltration of macrophages/neutrophils
axonal swelling and degeneration
lesions most severe in pons and medulla
where are the lesions most severe with listeriosis
pons and medulla
culture?
usual outcome of treatment for listeriosis
unrewarding
when does mortality approach 100% with listeria
if recumbent
when is the best chance at successful treatment for listeriosis
at the onset of signs
what is supportive treatment for listeriosis
NSAIDs
fluids
vitamins
what antibiotics used for listeria
penicillin - 22,000-44,000IU/kg IV q6 or IM q12
or
tetracycline - 10mg/kg IV q 12
success rate for treatment of listeria
0-62%
what is TEME
thromboembolic meningoencephalitis
main component in TEME
histophilus somni
is H. somni gram pos or neg
negative
does H. somni form spores
no
what type of bacteria is H. somni
non spore forming coccobacillus
what does TEME cause
pneumonia arthritis UTI abortion myocarditis neurologic disease
in which animals does TEME have a very high case fatality rate
feedlot cattle
signs and death when it comes to TEME
signs develop rapidly
death within 36 hours
TEME commensal bacteria in many mammals is where
URT and urogenital tract
TEME is an obligate microbe of what
mucosal surfaces
when does TEME dissemination occur
as a result of other pathogen or compromised host immune system
where does TEME migrate and what does it cause
through unprotected epithelial cells to meet brain epithelial cells and cause cytoskeletal rearrangement
what does TEME’s migration and rearrangement result in
drastic influx of albumin
reduced transendothelial electrical resistance
end result is increased paracellular permeability of vascular endothelial cells - neuro signs
death from TEME’s pathogenesis
subsequent endothelial cell apoptosis
if multiple animals are affected with TEME, what is the only sign that may be noticed
sudden death
what do we initially see with TEME
ataxia and weakness
as TEME progresses, what might we see
lateral recumbency profound depression opisthotonos convulsions closed or partially closed eyelids
what is sleeper syndrome
closed or partially closed eyelids - sometimes seen with TEME
TEME diagnosis
history and physical exam
CBC is nonspecific
cellular changes on CSF are reflective of a bacterial infection with hemorrhage
how do we confirm TEME
necropsy
when to attempt treatment of TEME
only attempt early in the disease
what antibiotics for TEME
gram negative spectrum
what do we do with down animals suffering from TEME
euthanize
treatment is unrewarding
how to prevent TEME
vaccine
H. somni - wyoming calves with disease syndrome
lethargy, fever, death
november-january each year
what is the appreciable source of death loss with H. somni
focal myocarditis
gross lesions detected with h. somni
in affected hearts
what types of deaths do we see with acute, subacute, and chronic fatal forms of h. somni
single deaths over time rather than heavy death loss in a short period
when are h. somni cardiac lesions missed
when hearts are not opened
specifically when cranial and caudal papillary muscles of the left ventricular myocardium are not incised
what is most often the cause of brain and pituitary abscesses
trueperella pyogenes
brain abscesses in cattle
relatively rare
lesions with t. pyogenes brain & pituitary abscesses
asymmetric
signs of brain & pituitary abscesses
vision loss in contralateral eye depression mania head pressing circling with head tilt toward lesion
treatment of brain & pituitary abscess
difficult with grave prognosis
origin of pituitary abscess
hematogenous - rete mirabile, cavernous sinus
dehorning complication
head butting
rete mirabile
mesh of capillary beds covering the pituitary
cavernous sinus
valveless venous system that bathes pituitary
signs of pituitary abscess
blindness pupillary dysfunction nystagmus dysphagia facial paralysis circling head tilt
polioencephalomalacia
swelling and softening of gray matter
what dysfunction contributes to polio
Na-K-ATP pump
what promotes water into the cell
intracellular Na
what is the cofactor in neuronal ATP production
thiamine
what do we need for thiamine production
rumen microbes
what do non-ruminants rely on for thiamine production
diet
where do thiaminases come from in regards to polio
bacterial and plant
what are sulfur and sulfates metabolized to with polio
toxic sulfide ions
what do grain diets promote with polio
h2s gas - absorbed or inhaled post eructation
what does sulfur (S) interfere with
oxidative processes of mitochondria leading to depletion of ATP
why does h2s like the brain
because of the high lipid content
where is h2s found
drinking water molasses forage urine acidifiers mineral supplements some plants - Brassica
how quickly do polio signs develop
rapidly
what are the signs of polio
central blindness ataxia proprioceptive deficits head pressing hyperexcitability - occasionally
what do these polio signs lead to
recumbency opisthotonus seizures coma death
what ages are affected by polio
all ages, most common in growing animals
what type of strabismus do we see with polio
dorsomedial
what is the polio diagnosis based on
clinical signs and response to treatment
bloodwork and CSF are unrewarding
what other test must we do in the face of polio
test food and water for h2s
how many ppm of h2s in water, diet, and rumen gas to indicate toxic levels
> 1000ppm in water
4000ppm in diet
1000ppm in rumen gas
thiamine for polio treatment
10mg/kg q6hrs IV or IM until improvement
then q12 hrs for 48 hours
dexmethasone tx for polio
1-2mg/kg q 24h ?
when treating polio, what should we increase and add to the diet
increase forage and add glucogenic precursors
what is nervous ketosis
multifactorial metabolic derangement
functional metabolic encephalopathy
what do we frequently see with nervous ketosis and what is less common
frequently see anorexia and milk drop
less commonly see wandering, head pressing, and compulsive licking
what type of necrosis is transpiring in nervous ketosis and what does that result in
diffuse cerebrocortical neuronal necrosis
this causes bilateral blindness with in tact pupillary function
also see cerebellar purkinje cell necrosis
what type of nystagmus with nervous ketosis
vertical
main isolate of otitis media/interna
mycoplasma bovis
what is meningitis usually associated with
gram negative septicemia in calves
chronic sinusitis
what type of problem is lead toxicosis
worldwide problem
where is lead toxicosis most common and why
pastured cattle in US
because it’s highly palatable to some animals
sources of lead
grease oil old paint lead-headed nails batteries* linoleum smelter discharges
what does the form of lead affect
absorption
what type of leads are poorly absorbed
metallic/sulfide forms
what type of leads are readily absorbed
lead salts - acetate, phosphate, carbonate, hydroxide
what do lead salts bind to
erythrocytes, tissues, bone
how long does lead remain in the system
long time
what do the signs of lead toxicosis resemble
polio
what signs do we see with lead toxicosis
sudden death central blindness tremors chewing fits seizures bellowing occasional aggression
diagnosis of lead toxicosis
basophilic stippling
normocytic normochromic anemia
blood lead measurement
heparanized blood - no chelation
treatment and prognosis of lead toxicosis
usually die before treatment or in spite of treatment
what to do immediately with lead tox
remove from source
what to provide with lead tox
intermittent CaEDTA to chelate from bone
66-110mg/kg/d divided into several doses
for 3-5 days then stop 2-3 days
what to provide early in the disease with lead tox
thiamine 10mg/kg q6h
or 25mg/kg q12 along with the CaEDTA
two types of spinal cord diseases
congenital or inherited
types of acquired spinal cord diseases
infectious
traumatic
metabolic/nutritional
toxic or neoplastic
signs of spinal cord disease
vary with location of the lesion
lesion to c1-c5
UMN to front limbs and hind limbs
lesion to c6-t2
LMN to front
UMN to hind
t3-L3
UMN to hind
lesion to sacral intumesence
LMN to hind limbs, anus, bladder
lesion to coccygeal nerves
LMN to tail and spinal area
what is sway back considered
enzootic ataxia
what type of deficiency leads to sway back
copper deficiency during prenatal/perinatal period
what type of does or ewes birth sway backs
cu deficient does and ewes
what type of myelin degeneration with sway back
bilateral symmetrical myelin degredation in dorsolateral spinal cord tracts
+/- cavitations in cerebral white matter
what is myelin degeneration secondary to
oxidative degeneration
clinical signs of sway back
rear limb ataxia
muscle atrophy
paresis
tetraparesis seen at birth
when do we usually see signs of sway back
usually at birth but may take up to 3 months
signs of sway back in neonates
static
signs of sway back in older animals
progressive paresis
definitive dx of sway back
necropsy
where do we measure cu when dealing with sway back
in the body tissue
plasma copper status - blood copper will increase with stress
also assess dietary copper
what is irreversible in regards to sway back
hypomyelinogenesis and demyelination
how to prevent more cases of sway back
supplement copper
copper to molybdenum ratio
6:1
progressive ataxia is a recessive defect in what animals
pure/mixed breed charolais calves 6-36 months
what type of paresis seen with progressive ataxia
posterior paresis and recumbency by 2 years
major lesion with progressive ataxia
eosinophilic plaques on white matter in the brain/spinal cord
stiff neck, dragging rear toes, stumbling, proprioceptive deficits
when do these signs in progressive ataxia worsen
with exercise
what happens with urinating with progressive ataxia
difficulty maintaining posture during urination, we see pulsatile micturition
what is weaver syndrome
progressive degenerative myeloencephalopathy
weaving gait
common to see weaver syndrome in what animals
inherited in brown swiss calves and angler cattle
what do we see in animals with weaver syndrome
paraparesis ataxia dysmetria of pelvic limbs insidious progression muscle wasting over hind quarters
onset of weaver syndrome
5-12 months
recumbent by 2 years
lesions in weaver syndrome
white matter of spinal cord
axonal swelling, degeneration, vacuolation
ways to get organophosphate toxicity
ingestion
inhalation
percutanous
what are the substances in OP tox
OP based insecticides or anthelmintics
what happens in OP tox
bind with acetylcholinesterase – increased Ach
what two categories of effects from OP toc
muscarinic
nicotinic
which effects are sympathetic NS
nicotinic
which effects are parasympathetic
muscarinic
what are the muscarinic effects of OP tox
dyspnea hypersalivation diarrhea bradycardia pupillary constriction
what are the nicotinic effects of OP tox
muscle tremors
tetany
recumbency
opisthotonus
what does the treatment of OP tox depend on
route and severity of intoxication
what to use in cattle and sheep with OP tox to reduce muscarinic signs
atropine 0.25mg/kg IM
what else to administer in OP tox
oral activated charcoal
oximes (2-pyridine aldoxime methiodide)
what are the oximes for in OP tox treatment
to break the bond of OP and ACHase within the first 24 hours
what can cervical fractures look similar to
meningitis
characteristics of cervical fractures
painful, may refuse to lower head to eat
pain on palpation, may be recumbent
resist passive flexion
BAR
what might we see in a c1-c4 lesion in regards to cervical fracture
may refuse to lift head
which animals most commonly have vertebral osteomyelitis/spinal abscess
calves
lambs
fawns
what is present with vertebral osteomyelitis/spinal abscess
bacteremia with localization in vertebral veins
pulmonary/umbilical infections (tail docking)
clinical signs vary with location of lesion
what are the two common organisms present with vertebral osteomyelitis/spinal abscess
trueperella pyogenes
fusobacterium necrophorum
how to diagnose vertebral osteomyelitis/spinal abscess
acute signs after pathologic fracture, vertebral collapse and/or spinal cord compression
what other dx for vertebral osteo/spinal abscess
malaise fever stiffness proprioceptive deficits paresis and/or recumbency history and CS
what imaging for vertebral osteo/spinal abscess
plain rads - look for proliferation, lysis, sclerosis, and soft tissue swelling (2-8 weeks after onset of signs)
organisms in epidural abscess
trueperella (archanobacter) pyogenes
cornyebacteria spp.
treatment for epidural abscess
surgical curettage, drainage, lavage
long-term abx
how to prevent epidural abscess
adequate colostrum
what is often associated with poor prognosis in epidural abscesses
subsequent meningitis
what are two broad causes for spinal cord fracture
trauma
osteodystrophy
what types of trauma can cause spinal cord fractures
squeeze chutes
other animals
AL and atlantoaxial joints in pygmy goats from restraint
TL fractures from extraction during dystocia
LS fractures in adult cattle from slipping on cement floors
in which animals do we commonly see spinal cord fractures
3-6 month old ruminants due to nutritional deficiencies - vitamin D, calcium, copper
CS with degenerative myeloencephalopathy
pelvic limb paresis and ataxia
recumbency
usually remain BAR
non-responsive to therapy
where have we seen degenerative myeloencephalopathy
reports in two non-related adult llamas
degenerative myeloencephalopathy - lesions in where
spinal cord white matter
marked axonal degeneration
loss of axons and myelin, and status spongiosus
hepatic encephalopathy is usually related to what
liver disease of some type
history of abnormal behavior - poor doers
where is hypoderma bovis found
NW united states and canada
life cycle / events of hypoderma bovis
deposit eggs on legs
hatch and burrow into skin
1st instar larvae migrate subcutaneously to spinal canal
dormancy for 2-3 months in epidural fat thru winter
what is spinal hypodermosis
neurologic signs associated with death of larvae near spinal cord when treated with OPs and ivermectins
what is released by the hypoderma larvae when they die
toxins released
severe host inflammatory reaction
what do we see with spinal hypodermosis
rear limb paresis and ataxia, recumbency
signs can resolve within a week of onset
in severe cases - prolonged recumbency, euthanasia
treatment of spinal hypodermosis
NSAIDs:
flunixin meglumine 1.1mg/kg BID or
dexmethasone 0.1-0.25mg/kg
want to deworm with ivermectins before larvae reach spinal cord - varies with geographical location
in north america, when do hypoderma flies appear and when do the larvae end up near the spinal cord
flies appear in may and the larvae are near spinal cord in november
when to deworm for hypodermosis
august/september in warmer climates
october in colder areas
what are the peripheral nerves of the pelvic limb
saphenous nerve common peroneal nerve cutaneous branches of the pudendal nerve tibial nerve cranial clunial nerves middle clunial nerves lateral cutaneous femoral nerve caudal cutaneous femoral nerve caudal coccygeal nerves
what types of nerve damage with pictures on the slides can we often see
sciatic femoral tibial peroneal obturator radial nerve paralysis
what will we see with radial nerve paralysis
dropped elbow will support weight if foot is placed
