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Rumi Neuro

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sihirlifil's version from 2018-04-06 16:08

Cortical Disease

Question Answer
CS of cortical dzAtaxia
CP deficits
Altered mentation (aggressive or depressed)
CN deficits
Opisthotonus
Stargazing, opisthotonos, splayed legs
Polioencephalomalacia (PEM) = Necrosis of cortical gray matter
COMMON!
PEM: in who?SR > Cattle > Camelids
PEM: etiologyInitiated by thiamine (Vit B1) metabolism problems
PEM: mechanismsDecreased thiamine production (rapid incr of grain, high concentrates)
Increased thiaminase activity (Bracken fern, levamisole)
Increased thiamine analogs
Dietary deficiency (rare, in preruminants)
Increased sulfur (diet or water) --> ruminal production of hydrogen sulfide gas (NOT responsive to thiamine supplementation!)
PEM: what is the role of thiamine?Cofactor for transketolase (rate-limiting in pentose phosphate pathway in RBCs & brain) & pyruvate dehydrogenase (enzymes in Krebs cycle)
PEM: PathophysDecrease of ATP-dependent Na/H2O transport in neurons --> neuronal swelling --> laminar cortical necrosis
PEM: CSAnorexia, D+
Muscle tremors
Head pressing, star gazing, depression, abnormal behavior (aggressive/depressed), seizures, coma, death
Ocular signs (sudden blindness, dorsomedial strabismus, nystagmus)
PEM: what do eye signs tell us?Absent menace response (CN II)
Functional PLRs! (CN II, III) (reflex is within brainstem)
Dorsomedial strabismus (loss of CN IV: innervation of dorsal oblique)
Visual pathway: where is vision perceived?Contralateral cerebral hemisphere
Visual pathway: eye & optic nerve lesions cause what?Ipsilateral blindness
Visual pathway: optic tracts & lateral geniculate lesions cause what?Contralateral blindness with normal PLRs
What is the pupillary light pathway?Optic nerve --> crosses chiasm to optic tracts on contralateral side --> midbrain --> MOTOR response: nuvlei to CN3 --> ciliary ganglia to constrict pupils
Pupillary light pathway: reflex is where? why do we care?Reflex is within brainstem and not affected by lesions in the cerebral visual cortex!
PEM: where does the dorsomedial strabismus come from?Not a true nerve paralysis! Due to cerebral edema involving nerve pathways. Nerve is not paralyzed, so eye will move with head movement
PEM: cortical blindness = Lack of menace
Normal PLR
Dorsomedial strabismus
PEM: DiansosisPresumptive: Hx, CS, response to therapy
Necropsy, histopath
PEM: How does PEM look on necropsy?Edema, laminar necrosis
May fluoresce w/ UV (Pb & Na tox also will though)
PEM: TxThiamine (Vit B1, not complex)
Dexamethasone or NSAID if pregnant
Supportive (diazepam if seizing, rumen transfaunation, IV/PO fluids)
PEM: PrognosisDepends on severity & duration
PEM: preventionThiamine supplementation
Adapt slowly to high-grain diets & prevent free-choice access
Limit dietary sulfur
PEM: Common DdxSalt poisoning (water deprivation)
Lead poisoning
Vit A deficiency
(Rabies, enterotox type D in sheep)
Salt poisoning: EtiologyHigh salt intake or H2O deprivation --> rapid H2O intake
Salt poisoning: how can it happen?Frozen/nonfunctional waterers
Mixing errors (milk replacer, feed mixes, e-lyte mixes)
Water deprivation
Salt poisoning: pathophysNa+ accumulates in neurons & CSF --> hyperosmolarity causes decrease in energy-dependent Na+ transport --> Inefficient cell Na+ removal
Thirst receptors are triggered --> H2O consumption --> moves to ECF, the ICF --> CNS edema, increase ICP, acute encephalopathy
Salt poisoning: what happens with chronic hypernatremia?Brain cells generate idiogenic osmoles to help retain intracellular water & prevent cell shrinkage
Rapid rehydration --> rapid reduction in ECF osmolarity --> Cerebral edema
Salt poisoning: DxHx & CS
Clin path: serum/CSF Na+ >160mmol/L, CSF osmolality >300mOsm/L
Feed analysis
Necropsy/histopath
Salt poisoning: TxSlowly decrease serum Na+ lvls
Steroids, thiamine, supportive
Salt poisoning: PrognosisPoor :(
Lead poisoning: common sourcesBatteris, lead shot, motor oil, roofing, paoint...
Most common intoxicant of cattleLead
Lead poisoning: more common in who?Calves>cattle>>>>>everyone else (indiscriminate eaters & drinkers)
Lead poisoning: PathophysGIT/respiratory entry --> sequestered in bone matrix --> inhibits enzymes at Cu, Zn, Fe binding sites, inhibits heme synthesis & decrease RBC lifespan, capillary dysfxn (CNS hge, edema)
Lead poisoning: DxHx & CS (walk pasture)
Rads: reticulum & CrV rumen
BLood/Urine Pb lvls (if chronic, pre & post-EDTA)
Basophilic stippling on RBCs
Whats going on with this rad?
Pb poisoning
What's this?
Basophilic stippling (indication of Pb poisoning)
Lead poisoning: TxRemove source from environment
Ca-EDTA chelation
Thiamine, steroids, cathartics, supportive
(Rumenotomy)
Lead poisoning: what's the ethical issue?Intended use: Pb is found in milk, meat, bones
Must inform owner of risks; recommend not using for food or milk (t1/2 in blood is 48-2507d)
Rabies: who, what, how?Most warm-blooded animals caused by neurotropic RNA Rhabdovirus, assoc with bite of infected animal. Incubation 3w-6m. Virus shed in saliva & milk, nursing offspring can be affected
Rabies: CSDumb form: depression
Paralytic form: flaccid paralysis (most common in cattle)
Furious form: Hyperexcitable, fear, rage
Vocalization, pruritis, ataxia, lameness, dysphagia
Recumbency w/in 2-5d, death w/in 10d
Rabies: DxHx, CS, suspicion
Postmortem (DFA on brain tissue)
What is this?
Negri body (pathognomonic for rabies)
Rabies: TxNone... post-exposure management based on state bet/public health depts
Rabies: how are cattle treated post-exposure if vaccinated? If not?Vax'd: re-vax & observe for 45d
Unvax: slaughter immediately or quarantine 6m
Rabies: which species can be vax'd?Killed vax labeled for cattle & sheep
Goats, camelids, swine: Off-label, state may still req quarantine or slaughter
Pseudorabies: aka? agent?Mad Itch, Aujesky's dz
Alpha-herpesvirus
Pseudorabies: what is it? who gets it?Acute, fatal encephalitis of domestic & wild rumis. Definitive host is pig, adults may experience asymptomatic infx & be long-term carriers (still in feral pig populations in USA)
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Transmissible Spongiform Encephalopathies

Question Answer
Spongiform encephalopathies: who can get?7 types of spongiform encephalopathies affecting various species (including humans!)
BSE: aka? affects who?Mad Cow Dz
Affects ruminants (& humans, other animals)
Scrapie: who gets it?Sheep & goats only!
BSE & Scrapie: agent? what happens?Prion disease! Abnormal form of normal protein found in all cell mb (esp neurons), protease-resistant
Induces conformational changes (peer pressure lol), disrupts normal cellular fxns
BSE: TransmissionFeeding rendered animal proteins from infected animals
Spontaneous mutation
Scrapie: TransmissionClassical: horizonal & vertical (IN PLACENTA! NOT IN UTERO!). Suceptibility is heritable (not the disease). Requires suceptible genotype AND exposure
Atypical: spontaneous mutation
BSE: CSBehavior changes
Ptyalism, licking
Reluctance to be milked
Fasiculations, abnormal gait
CP deficits
Scrapie: CSBehavior changes
Weight loss, abnormal gait, ataxia
Pruritis
Biting, licking, grinding teeth
Cannibalism
BSE/Scrapie: age affected?Long incubation period! BSE = 4-6y, Scrapie = 2-4y
BSE: DxHistopath for lesions, western blot. No antemortem tests (not with semen sample)
Scrapie: Dx(Variable btw sheep & goats)
3rd eyelid/rectal mucosal biopsy (ID in lymphatic tissue)
Histopath specific areas of brain
Scrapie: USDA-approved antemortem tests?Rectal mucosal biopsy, 3rd eyelid biopsy (pic)
Tonsilectomy, LN biopsy, blood test under development
BSE/Scrapie: ControlPrevention is key! (Genetic testing for resistance for classical scrapie in sheep) No tx :( progressive to death
No feeding ruminant-derived protein
NOTIFIABLE IN USA
Scrapie genetic testing: how is prion protein defined? comprised of?Defined by single pair of genes, one from each parent. Comprised of 254 codons, which defines an amino acid
Scrapie genetic testing: which codons do we care about?171: arginine, glutamine, histadine, lysine
136: valine, alanine, threonine
(154 not used for testing)
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Brainstem & Cranial Nerves

Question Answer
What's wrong with this guy
Strabismus
Which CN comes to mind with this guy?
8
Which CNs are responsible for motor & sensory to larynx & pharynx? CS result? think what?Glossopharyngeal & vagus --> unable to swallow or drink. THINK RABIES!
Brainstem consists of?Diencephalon, mesencephalon, pons, medulla
Brainstem responsible for?(Similar to cortical signs) Basal life fxns, cranial nerves
Brain stem/cranial nerve CS?CP deficits
Circling, head tilt
Coma, depression, convulsions
CN deficits: blindness, anisocoria, mydriasis, miosis, ptosis, strabismus, nystagmus; flaccid tongue; facial paralysis
Listeriosis: agent? Found where?Listeria monocytogenes G(+)
Grows in improperly stored sliage/forage (pH >5.4), soil, GIT
Listeriosis: pathophysBacteria --> brain --> multifocal microabscesses --> Diffuse meningoencephalitis, asymmetrical lesions
Listeriosis: manifestationsNeuro
Abortion
Septicemia
Listeriosis (Neuro): CS?Fever (early), anorexia, depression, ataxia, head pressing
CN deficits from V-XII, especially V & VII
Listeriosis (Neuro): CN V =Drooped jaw, drooling, facial analgesia
Listeriosis (Neuro): CN VI =Strabismus, ptosis
Listeriosis (Neuro): CN VII =No menace, drooped ear/lips/nose, no palpebral reflex
Listeriosis (Neuro): CN VIII =Nystagmus, head tilt, circling
Listeriosis (Neuro): CN IX, X =Stertor, dysphagia
Listeriosis (Neuro): CN XII =Tongue protrusion, weakness
Listeriosis: Dx
CS (facial nerve paralysis), access to silage/grass clippings/moldy feed
CSF: incr mononuclear cells, cloudy, pleocytosis (Do culture)
Necropsy, histopath, IHC of brain (+/- brain tissue culture)
Listeriosis: Tx/ Prevention/ controlAntibx: long term, IV at first if possible
Supportive
Flock/herd tx w/ long acting oxytetracycline, or in feed (VFD!!!)
REMOVE SOURCE, prevent contamination
Listeriosis: super important to rememberZoonotic
Can be transmitted in milk & milk products... PASTEURIZE for human or animal consumptin. Carriers can shed the bact for a long time
Thromboembolic meningoencephailits: aka? agent?TEME. Histophilus somni, gram(-)
TEME: pathophysSepticemia from respiratory dz --> brain stem microthrombi & micronecrosis
Endothelial cell death --> expose subendothelial collagen --> clotting cascade, thrombosis
Activation of immune system --> inflamm process
TEME: CSFEVER!
Asymmetrical signs in brainstem & any CNs
Retinal hge, hyphema, hypopyon
Other syndromes: RESPIRATORY & POLYARTHRITIS, repro, ocular, ears, udder
TEME: DxHx, CS
CSF analysis: incr protein, neutrophilia, hge & xanthochromia
CBC: septicemia
Necropsy w/ histopath & culture
TEME: what does it look like on necropsy?Suppurative meningitis aka pus in the brain... never good
Necrotic meningoencephalitis (also never good)
TEME: TxAntibx (Oxytet based on sensitivity; penicillin, ceftiofur, florfenicol...). Fair prognosis if caught early
TEME: PreventionVax, but efficacy iffy
Paralaphostrongylus tenuis aka? who affected?Meningeal worm (of white-tailed deer). Affects sheep, goats, camelids, and is REGIONAL! (east USA)
P. tenuis: Dx?(R/o other causes)
CS: posterior paresis, proprioceptive deficits, ataxia
Location
CSF analysis: +/- eosinophilia
P. tenuis: TxFenbendazole, supportive
P. tenuis: preventionIvermectin, monthly injxns
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