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209 Cards in this Set

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  • Back
What is structural Intracranial Disease?
disorders that result in macro or microscopic neuropath lesions in the brain
What is functional intracranial disease?
brain parenchymal tissue functinal disorders
-+/- neuropath lesions
What are the CS to pontomedullary Disease?
1 - hemiparesis to paralysis, ipsilateral to the lesion
2 - deficits in CN 5-12
3 - abnormalities in head or body posture if vestibular system is affected
4 - abnormalities in consciousness (stupor to coma)
5 - abnormalities in vital vegetative functions (cardiac or respiratory rate and rhythm)
What are CS to cerebellar Disease?
1 - cerebellar ataxia
2 - central vestibular dysfunction if caudal cerebellar peduncle or flocculonodular lobe affected
3 - diminished or absent menace response
4 - decerebellate body posture
When would you see central vestibular dysfunction with cerebellar disease?
-if caudal cerebellar peduncle or flocculonodular lobe is affected
What are the CS to mesencephalic disease?
1 - hemiparesis that may be ipsilateral OR contralateral to the lesion
2 - abnormal extraocular muscle movement
3- mydriatic pupil with abnormal PLR
4 - head tilt/turn and tendency to walk in circles
5 - decerebrate body posture
6 - depressed level of conciousness
Why do you get mydriasis with mesencephalic disease?
internal ophthalmoparesis/plegia from deficit of parasympathetic portion of CN 3
What body posture is seen with mesencephalic disease?
Why do you get abnormal extraocular muscle movement with mesencephalic disease?
external ophthalmoparesis/plegia from deficits of CN 3 and 4
What are the CS of diencephalic Disease?
1 - contralateral hemiparesis
2 - contralateral sensory dysfunction
3 - abnormal PLR due to CN II injury
4 - head turn and circling towards side of lesion
5 - behavioral changes, autonomic dysfunction, endocrine dysfunction
6 - seizures
7 - depressed level of conciousness
Why is there an abnormal PLR with diencephalic disease?
CN II injury
What are CS of telencephalic disease?
1 - seizures and behavioral changes
2 - depressed level of consciousness
3 - normal to mild gait with contralateral postural reaction deficits
4 - head turn and tendency to circle towards the side of the lesion
5 - aimless wandering
6 - contralateral sensory deficits
What is extracranial disease?
systemic organ disease that results in secondary CS of brain dysfunction
What are the 4 general pathophysiological reasons for extracranial disease?
1 - failure of delivery or utilization of CNS metabolic substrates (Hypoglycemia/thiamine def)
2 - interference with or interruption of normal neurotransmission (hepatoencephalopathy)
3 - failure to remove endogenously generated toxins (renal failure/hepatoencephalopathy)
4 - exposure to toxic compounds
What are the 3 most general categories of extracranial disase?
1- metabolic
2 - toxic
3 - nutritional
What are CS of extracranial disease typically reflective of?
bilateral, symmetric forebrain disease
What are the causes of hepatic encephalopathy?
1 - congenital portovascular anomalies
2 - end stage, chronic acquired hepatopathy (cirrhosis)
3 - anything that causes liver failure
What are CS of hepatic encephalopathy?
-behavior change
- dementia
-thalamocortical blindness
-post-prandial exacerbation of signs
How do you diagnose hepatic encephalopathy?
1 - CS
2 - physical
3 - plasma biochem (increased ammonia)
4 - liver function tests
5 - liver imaging
6 - liver biopsy
Does normal ammonia rule out hepatic encephalopathy?
What does neuropath look like with hepatic encephalopathy?
- polymicrocavitations of white matter (spongy change)
-Alzheimer's Type II astrocytes (clear, swollen nuclei)
What vitamin is a necessary cofactor for brain carbohydrate metabolism?
thiamine (B1)
Is thiamine def. common in cats?
uncommon in cats
rare in dogs
What are 4 possible reasons for thiamine def.?
1 - eating thiaminase containing fish (white fish)
2 - destruction from overcooking meals
3 - consumption of sulfur dioxide preserved food
4 - severe intestinal malabsorptive disease
What are CS to thiamine deficiency?
1 - vestibular ataxia
2 - vomiting
3 - cervical ventroflexion
4 - mydriasis
5 - tetraparesis
6 - late states --> seizure, coma death
What does the neck look like with thiamine def?
cervical ventroflexion
What happens in the late stages of thiamine def?
seizures, coma, death
What do the eyes look like with thiamine def?
dilated because destroyes PN of CN 3
What can you test for with thiamine def?
reduced RBC transketolase activity
How do you diagnose thiamine def?
1 - history of risk factor
2 - reduced RBC transketolase activity
3 - MRI
What is seen on an MRI with thiamine def?
symmetric hemorrhagic lesions in the brainstem nuclei
What is treatment for thiamine def?
-thiamine supplementation (every 8 hours for 3 days)
- correct underlying risk factors
What does neuropath look like with thiamine def? (list 5 areas)
-hemorrhagic necrosis of:
1 - red,
2 - vestibular nuclei
3 - caudal colliculi
4 - oculomotor nuclei
5 - geniculate nuclei
What does lead interfere with?
Hb synthesis
What are CNS signs due to with lead toxicosis?
ischemia or edema
What animals are most affected by lead toxicosis?
juveniles with pica
What are CS to lead toxicosis?
1 - dementia
2 - seizures
3- vomiting
4 - diarrhea
5 - anorexia
6 - constipation
What are lead sources?
paint, batteries, cables, oil, caulks, golf balls
What are blood lead concentrations with lead toxicosis?
>35 ppm
What do RBCs look like with lead toxicosis?

What else will help your diagnsois?
basophilic stippling

-metaphyseal lead lines
-lead objects
-blood lead concentrations
What will you see on rads with lead consuption?
-lead objects
- metaphyseal lead lines
What are 2 main therapies for lead toxicosis?
1 - chelation
2 - anticonvulsants
What are 4 chelators that can be used for lead toxicosis?
1 - succimer - BEST
2 - Ca EDTA
3 - D-pencillamine
4 - BAL
What does neuropath look like with lead toxicosis?
1- status spongiosis (edema)
2 - capillary proliferation
3 - cerebrocortical laminal necrosis
Are general systemic diagnosistics such as CBC, biochem, US, rads helpful for localizing structural intracranial disease?

-What does diagnosis require?

- advanced brain imaging
-CSF analysis
- ancillary tests
-histopath of brain
How are most lysosomal storage diseases inherited?
-autosomal recessive fashion (genetic)
-with juvenile onset
What do lysosomal storage diseases result from?
absence of or defect in function of single catabolic enzyme

-- causes progressive accumulation of intracellular waste products in affected tissues
Why are neurological signs common with lysosomal storage diseases even though they affect multiple tissues in the body (both neural and extraneural)?
common because of terminal differentiation and limited regeneration of the neurons
What neuro signs are common with lysosomal storage disease?
- cerebellar
-visual deficits

-usually normal at birth with progressive neurological deterioration and death
What is the definative diagnosis for lysosomal storage disease?
pathologic and biochemical examination of tissue

other tests include a genetic test from Penn Genn
What is symptomatic in the urine of an animal having lysosomal storage disease?
-excessive urinary excretion of cellular metabolic products (proteinuria/aminoaciduria)
What do neurons look like with lysosomal storage disease?
-some will glow in the dark
What is the treatment for lysosomal storage disease?
-it is a progressive and terminal disease
What are 3 hereditary dysmyelinating diseases?
1 - leukodystrophies
2 - hypomyelinating diseases
3 - spongy degenerations
What are the common denominators of the hereditary dysmyelinating diseases?
-oligodenroglial failure of synthesis or maintenance of myelin
-insufficient quantity of myelin
-abnormal myelin
Clinical manifestations of hereditary dysmyelinating diseases occur shortly after birth when animal begins to walk. What are they?
- brain manifestations
- spinal cord manifestations
-diffuse CNS manifestations
-diffuse, action related tremors
How is congenital hydrocephalus categorized?
-internal, non-obstructive hydrocephalus without apparent cause
What is the definition of hydrocephalus?
increased CSF volume in the brain
What breed is hydrocephalus common in?
What are CS of hydrocephalus?
- dome shaped head
- divergent strabismus - setting sun
-open fontanelles
-neuro signs
What neuro signs are seen with hydrocephalus?
-developmental failure
- cerebellovestibular signs
Where is the abnormaility with congenital hydrocephalus?
at the level of the arachnoid villi
-this is the site of CSF absorption
What are the CS of hydrocephalus due to?
1 - intracranial hypertension
2 - intraventricular hemorrhage
3 - neuronal death/dysfunction
Do clinical signs coorelate with ventricle signs with hydrocephalus?
What are drugs for hydrocephalus aimed at doing?
1 - reduce CSF production
2 - facilitate CSF excretion
What are the drugs used to facilitate CSF excretionwith hydrocephalus?
1 - prednisone
2 - furosemide
3 - proton pump inhibitor
What symptomatic treatments would you use in cases of hydrocephalus?
What surgical methods can you use to help hydrocephalus?
-ventriculoperitoneal shunt
- ventriculoatrial shunt
-ventriculovascular shunt
What is the prognosis for animals with hydrocephalus?
hard to predict
-guarded - poor in animals with severe cortical loss
Is ventricular symmetry important in diagnosing hydrocephalus?
no - often not significant
What is lissencephaly?
-smooth, external surface of the brain
-gyri and sulcal development failure
-non-lethal defect of embyonal neuronal migration
What is lissencephaly associated with?
-pachygyria (thickened cerebral cortex)
-abnormal laminar architecture
What breed is predisposed to lissencephaly?
Lhasa Apso
What are CS in juveniles of lissencephaly?
-training problems, dullness, seizures
How you diagnose lissencephaly?
-diminished suli
What is symptomatic therapy for lissencephaly?
What is the most common intracranial neoplasia?
What is the age of onset of meningiomas and what is the typical breed?
> 10 years
-golden retrievers, boxers, GSD
What breed typically gets gliomas?
brachycephalic breeds age 5-9
Are menigiomas intra-axial or extra-axial?

menigiomas - extra-axial

gliomas - intra-axial
Are primary or secondary tumors more likely to cause intracranial neoplasia?
secondary are more common
What are secondary tumors that are seen with intracranial neoplasia?
-carcinoma (mammary, prostate, lung)
-pituitary tumor
How can you localize intracranial neoplasia?

-central vestibular
forebrain - seizures and behavior
infratentorial tumors - central vestibular signs
Why might you see multifocal CS with intracranial neoplasia?
intracranial hypertension
What are mass related effects with intracranial neoplasia?
invasion, compression, displacement, herniation
What are secondary effects of intracranial neoplasia?
-peritumoral edema
-tumor-induced encephalitis
-obstructive hydrocephalus
What is the final common denominator with intracranial neoplasia?
elevated intracranial pressure
What is the definative way to diagnose intracranial neoplasia?
What does CSF reveal with intracranial neoplasia?
-non-specific changes
- neoplastic cells exfoliate
What neoplastic cells exfoliate with intracranial disease?
-choroid plexus tumors
-histiocytic sarcoma
What are 3 methods to diagnose intracranial neoplasia?
1 - histopath
2 - CSF
3 - EEG - localizing, but not specific
What are the 2 methods for antemortem brain biopsy?
-open (craniotomy) --> free or image guided

- minimally invasive (Burr hole) - image guided
What are the primary treatments for intracranial neoplasia?

Is there evidence that chemo works?
-surgery and radiotherapy

Which type of tumors are more amenable to surgery?
superficial (extra-axial) forebrain tumors
What is the success of surgery directly related to with intracranial neoplasia removal?
1 - surgeon experience
2 - completeness of tumor excision
What is the prognosis for a canine meningioma with cytoreductive surgery?
standard resection - 7 months
facilitated resection 2-3 years
What is the prognosis for a feline meningioma with cytoreductive surgery?
2-3 years
What is the prognosis for a pituitary tumor with a hypophysectomy with cytoreductive surgery?
2 years
When radiation therapy is used as the sole modality for intracranial neoplasia, what is the survival time. When is this typically done?

what about when used as an adjuct therapy?
1-2 years
-on inoperable lesions

adjunct therapy doubles survival
What are palliative, symptomatic therapies for intracranial neoplasia?
prednisone --> anti-inflammatory, anti-edema, euphoric effects

anticonvulsants for seizures

nutritional support

What is the survival for palliative treatment with intracranial neoplasia?
<3-4 months

-dogs with forebrain tumors and mild signs (seizures) live significantly longer -- 7 months
Although histopathologically multifocal diseases, what percent of inflammatory diseases present with focal clinical signs?
What is unique about CS in animals with meninigoencephalitides (ME).
many animals with this condition don't have any systemic CS or clin path abnormalities
What is the most common cause of ME in dogs and cats?
non-infectious (immune mediated)

dogs - esosinophilic menigoencephalitis, GME, necrotizing encephaltities

cats - feline polioencephalomyelitis
What are viral cause of ME in dogs and cats?
dogs - distemper and rabies

cats - FIP and rabies
What are fungal causes of ME in dogs and cats?
crypto and Blasto
What kind of virus is canine distemper virus?

-what is the reservoir host
single stranded RNA paramyxovirus

What are routes of infection?
-aerosolized secretions from infected animals
When does shedding occur with canine distemper?
within 1 week of infection - can last for several months
How do you predict which animals will develop neuro signs with canine distemper virus?
you don't know
What are the clinical sequelae of CDV due to?
1 - virulence of strain
2 - immunocompetence of host (good, intermediate, or poor response)
3 - protracted immunity to CDV following recovery
When can neuro signs develop with CDV?
weeks to years after infection
-coicident with systemic diseases
What are the CS of CNS disease with CDV?
-vestibular disease
What physical sign is associated with the neuro signs of canine Distemper Virus?
What is a negative prognostic indicator with CDV?
neurological complications
What type of CDV do neonates or immunocompromised dogs get?

other dogs?
neonates/immuno-compromised = acute CDV encephalitis (demyelinating)

other = chronic CDV encephalitis (waxing and waning, static, or progressive course)
Does a negative PCR or IFA rule out CDV?
How you you diagnose acute, fulminant CDV in an unvaccinated puppy (12-20 weeks old)?
-CDV inclusions
How do you diagnose chronic CDV encephalomyelitis?
-PCR (blood, CSF, urine)
-IFA (brain, footpad, skin)
-CSF IgM/IgG titer and C-value
What is the therapy for CDV?
-supportive and symptomatic
-CDV associated seizures, myoclonus and optic neuritis can be well tolerated
What type of virus is rabies?

what is the route of infection?
neurotropic RNA rhabdovirus

What affects the incubation period of rabies?
-age of host
-innervation of inoculation site
-proximity to CNS

-can be days to months
What are the 2 forms of rabies?
How long does each last?
furious (1-7 days)
paralytic (1-5 days)
What are the CS of the furious form of rabies?

paralytic form
furious - aggression, photophobia, hyperesthesia, bizarre behaviors

paralytic form - progressive LMN paralysis
How is rabies diagnosed antemortem?
not recommended
-FA skin biopsy of maxillary vibrissae
How is rabies diagnosed PM?
-direct FA test of brain
-Negri bodies in neurons
What is the most common infectious cause of feline neurological disease?

How is it spread?

in feces
What percent of cats with effusive and dry forms of FIP develop neuro signs?
effusive - 15%
dry - 33%
What age cats get FIP and what is the incubation?
young cats less than 2 in multicat environments

-up to years
What may CS of FIP be preceeded by?

-What are systemic sings?
stress, surgery, illness

-waxing and waning fever and anorexia
-ocular signs (iritis, chorioretinitis)
-irregular kidney palpation, abdominal lymphadenopathy
-neuro signs
What are the neuro signs of FIP?
1 - reflect inflammation of the ependyma, meniges, or choroid plexus (vascular)
2 - central vestibular
3 - cerebellovestibular
4 - seizures
What does a cat in a multicat house with fever, ocular and neuro signs have until proven otherwise?
What type of CSF will a cat with FIP have?
supperative pleocytosic (neutrophilic)
-elevated FeCoV titer
How MIGHT the globulins react with FIP?
hyperglobulinemia (>3.5 g/dl)
What is the prognosis for FIP?
-survive for less than 1 year
What are the therapies for FIP?
1 - immunosuppression (pred, chlorambucil, cyclophosphamide, cyclosporine)
2 - immunomodulation - interferons
What 2 fungal diseases are common to see just neuro signs?
Crypto neoformans and gatti
Blastomyces dermatitidis
What are concurrent signs with fungal menigoencephalitides?
FUngal menigoencephalitide signs are often multifocal. When can they be focal?
associated with a macrogranuloma
What are 3 methods used for diagnosing fungal meningoencephalitides?
1 - demonstrate the organsim
2 - antigen tests
3 - diagnostic imaging
What is seen on diagnostic imaging with fungal meningoencephalitides?
meningeal thickening/enhancement, multifocal parenchymal lesions
What tissues would you look at to demonstrate fungal meningoencephalitides?
-resp tract
What therapies would you use to treat fungal meningoencephalitides?

How long do you treat?
-amphotericin B + (fluconazole/flucytosine/new gneration azole)

-treat until antigen titers aare zero or at least for 6 months
What is the prognosis for fungal menigoencephalitides?
poor for cure, but prolonged remission is possible
What is MUE?
inflammatory brain disease with no identifiable etiology

-presumed to be immune-mediated in origin
What are the specifically named diseases associated with MUE?

* they are all TREATED THE SAME
1 - granulomatous meningoencephalitis (GME)
2 - breed specific encephalitides (Pug/Maltese encephalitis)
3 - Necrotizing meningoencephalitides (Necrotizing leukoencephalitis (NLE) OR necrotizing meningoencephalitis (NME)
4 - esosinophilic meningoencephalitis
What type of brain diseases are MUE?
What breeds are predisposed to MUE?
young-middle-ages small and toy breeds
What signs does the following varients of MUE have?

necrotizing variants
necrotizing variants - forebrain signs

GME - brainstem white matter (in diencephalon caudally)
What is the only way to really diagnose MUE while the animals are alive?
brain biopsy - perivascular, non-supperative inflammation
What is the therapy for all types of MUE?
1 - prednisone
2 - combination therapies -- pred + (cycloporine, CCNU, Cytosar, Leflunomide, Procarbazine)
3 - brain irradiation (helpful with GME)
What is the prognosis for MUE, a insidiously progressive disease, with:

-pred monotherapy
-combo therapy
-pred monotherapy = 3-6 months
- combo therapy = 12 months
Which type of MUE might be more benign?
eosinophilic variant
What are 2 protozoa that cause meningoencephalitides?
neospora caninum
toxoplasma gondii
What stage of host is toxo in cats?

Neospora in dogs?
Toxo is definitive host in cats.

Neospora is the intermediate host in dogs.

Both toxo and neospora are obligate intracellular parasites.
Are cats naturally resistant to neosporosis?
How do you diagnose toxoplasma meningoencephalitides?
1 - serology = high IgM titer; seroconversion of IgG
2 - ID of tachyzoites in tissues or fluids
3 - PCR = will not distinguish active disease from latent infection
Where are clinical signs of toxoplasma meningoencephalitiedes?
-the same place as tachyzoite replication

-pulmonary, hepatic, ocular, neurologic,
Neuro signs with toxoplasma meningoencephalitides can localize anywhere, but dogs have higher incidence of what?
- have higher incidence of LMN signs
What concurrent infections are common with toxoplasmosis meningoencephalitides?
How do you diagnose neosporosis meningoencephalitides?
1 - serology (high IgG titer and seroconversion of IgG)
2 - ID og tachyzoites in tissues or fluids
What are CS of neosporosis in puppies less than 6 months?
-ascending paralysis
-polyradiculoneuritis and myositis
What are CS of neosporosis in older dogs?

-neuro signs can localize anywhere
-multifocal CNS disease
What is therapy for protozoal meningoencephalitides?
-TMS with pyremethamine for 4 weeks

-response is usaually rapid
What is the prognosis for protozoal meningoencephalitides?
-good to excellent

-contractures from polyradiculoneuritis is permanent
-fulmanent disseminated disease may be fatal despite therapy
What is the most common tick borne pathogen associated with neurological complications?
Rickettsia rickettsii
-rocky mountain spotted fever
What are the CS of RMSF related to?
systemic vasculitis from endothelial infection

- fever, lethargy
-facial or limb edema
-central vestibular signs are common
How do you diagnose RMSF?
-history, CS, PE
-elevated IgM or IgG titer
-PCR assay
What is the therapy for RMSF?
-enrofloxacin for 2-3 weeks
-CNS signs = prednisone for 1 week

-rapid response to therapy
What is the prognosis for RMSF?
good to excellent if treated before severe neuro signs develop
If there are life threatening signs of ME, what three antibiotics would you pull off the shelf first as practical empirical therapy?

If further diagnostics are not performed and the after 3 weeks there is not response, what should you try?
1 - clindamycin
2 - doxycycline
3 - enrofloxacin

What is the morphologic end result of severe vascular injury?
necrotic brain tissue
What is a clinical hallmark of CVA?
peracute to acute onset of focal, non-progressive (after 24-48 hours) clinical signs
What is more common - arterial or venous strokes?
What is the therapy for cerebrovascular accidents?
-maintain normal MaBP
-Normal paO2
-normal perfusion
-screen for risk factors
What is the likely cause of feline ischemic encephalopathy and when is the highest incidence?
-aberrant migration of Cuterebra larva through the brain
-highest incidence in late summer to early fall
What are the CS of feline ischemic encephalopathy?
-acute, non-progressive unilateral forebrain dysfunction = circling, personality changes, dementia, seizures, blindness

-may be preceded by mild upper respiratory signs
How do you diagnose feline ischemic encephalopathy?
-CT or MRI evidence of territorial infarction of cerebrum
-maybe will see a parasitic migratory track
What vessel is most commonly affected with feline ischemic encephalopathy?
-middle cerebral arterial territory
What is the therapy for feline ischemic encephalopathy?
-ivermectin SC once
-Premed with: diphenhydramine and dexamethazone
-anticonvulsants prn for seizures
-many cats will improve with supportive care
What is the prognosis for feline ischemic encephalopathy?
-most will improve or recover
-some cats need chronic anticonvulsant therapy
-some cats left with permanent undesirable behavior changes
What is the neuropath of feline ischemic encephalopathy?
-laminar cerebrocortical necrosis
-energy deprivation change
-evidence of larvae in neural parencyma; eosinophilic inflammatory infiltrates
What is the main CS of optic neuritis?
acute onset of bilateral blindness
-mydriasis with no PLR
-optic nerve swollen with indistinct margins
-abnormal retinal vasculature
What is the etiology of optic nerve inflammation?
usually non IDed
What is the therapy for optic neuritis?
-immunosuppressive doses of prednisone
-wean based on response
What is the prognosis for optic neuritis?
-guarded to poor for visual recovery
-no other neurologic deficits develop
What are CS of trigeminal neuritis?
acute to subacute onset of bilateral mandibular paralysis
-dropped jaw
-cant close mouth
-drooling, prehensile problems
-may have diminished facial sensation or Horner's syndrome
What is the treatment for trigeminal neuritis?
-gauze or tape muzzle
-spontaneous resolution in 2-3 weeks
Is steroid therapy effective with dropped jaw?
What are the CS to idiopathic facial nerve paralysis?
60% unilateral
-lip droop
-absent menace
-absent palpebral reflex
-drooling of affected side
-+/- exposure keratitis
-What is the treatment for idiopathic facial nerve paralysis?
non - recover in 3-6 weeks
What does Horner's syndrom indicate and what are the CS?
sympathetic denervation of the head

- ptosis, miosis, enopthalmos, protrusion of nictican
What are common causes to Horner's Syndrome?
-brachial plexus avulsion
- otitis media-interna
-intrathoracic neoplasia
-intracranial neoplasia
How is Horner's syndrome classified?

How do you tell the difference?
pre or post gangilionic

-use the topical 10% phenylephrine test --> if there is rapid improvement (in less than 20 minutes), or temporary resolution of HOrner's syndrome, then it is post ganglionic and lesion is rostral to the cranial cervical ganglion
What percent of dogs and cats have idiopathic horners?
What is the treatment for Idiopathic Horner's?
-resolves in 2-3 months
What are clinical manifestations of functional intracranial diseases?
paroxysmal stereotypical behaviors or possibly seizure disorders

-breed associations common
What breed/sex are associated with rage syndrome?
-springer spaniel
-golden retriever
-young adult, often male
What breeds are predisposed to flank sucking?

wool sucking?
flank sucking: Dobermans
wool sucking: Oriental breeds of cats
What is feline hyperestheisia induced by?
petting or grooming
What is feline hyperesthesia?
-spontaneous "crawling" of the skin of the lumbar region
-biting, licking, otherwise traumatizing the area
What do severe cases of feline hyperesthesia look like?
clonic-tonic movements, salivation, urination, defecation

-resembles a seizure
What are R/O for feline hyperesthesia?
-lumbar spinal diseases
What is the therapy for feline hyperesthesis?

This is the same treatment for fly biting?
anticonvulsants, anxiolytics
What is the difference between narcolepsy and cataplexy?
narcolepsy = excessive daytime somnolence
cataplexy = sudden, transient loss of muscle tone --> the most common sign of narcolepsy
What is the abnormality associated with narcolepsy/cataplexy?
-abnormality in hypocretin/orexin neuron system
-this participates in maintenance of wakefulness, and preservation of muscle tone
What are the 2 forms of narcolepsey/cataplexy?
1 - familial form = absent or functionally deficient hypocretin receptor
2 - sporadic = hypocretin def.
What are the methods to diagnose narcolepsy/cataplexy?
- food elicited cataplexy test
-trigger induced episode
-pharm induced episode (phyostigmine)
-CSF -- check hypocretin concentration
What are the drugs to treat narcolepsy/cataplexy?
cataplexy = TCAs (clomipramine, imipramine, desipramine)
-narcolepsy - stimulants, but RX not usally needed