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209 Cards in this Set
- Front
- Back
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What is structural Intracranial Disease?
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disorders that result in macro or microscopic neuropath lesions in the brain
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What is functional intracranial disease?
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brain parenchymal tissue functinal disorders
-+/- neuropath lesions |
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What are the CS to pontomedullary Disease?
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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) |
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What are CS to cerebellar Disease?
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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 |
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When would you see central vestibular dysfunction with cerebellar disease?
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-if caudal cerebellar peduncle or flocculonodular lobe is affected
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What are the CS to mesencephalic disease?
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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 |
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Why do you get mydriasis with mesencephalic disease?
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internal ophthalmoparesis/plegia from deficit of parasympathetic portion of CN 3
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What body posture is seen with mesencephalic disease?
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decerebrate
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Why do you get abnormal extraocular muscle movement with mesencephalic disease?
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external ophthalmoparesis/plegia from deficits of CN 3 and 4
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What are the CS of diencephalic Disease?
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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 |
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Why is there an abnormal PLR with diencephalic disease?
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CN II injury
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What are CS of telencephalic disease?
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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 |
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What is extracranial disease?
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systemic organ disease that results in secondary CS of brain dysfunction
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What are the 4 general pathophysiological reasons for extracranial disease?
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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 |
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What are the 3 most general categories of extracranial disase?
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1- metabolic
2 - toxic 3 - nutritional |
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What are CS of extracranial disease typically reflective of?
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bilateral, symmetric forebrain disease
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What are the causes of hepatic encephalopathy?
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1 - congenital portovascular anomalies
2 - end stage, chronic acquired hepatopathy (cirrhosis) 3 - anything that causes liver failure |
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What are CS of hepatic encephalopathy?
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-behavior change
- dementia -thalamocortical blindness -ptyalism -seizures -post-prandial exacerbation of signs |
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How do you diagnose hepatic encephalopathy?
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1 - CS
2 - physical 3 - plasma biochem (increased ammonia) 4 - liver function tests 5 - liver imaging 6 - liver biopsy |
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Does normal ammonia rule out hepatic encephalopathy?
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no
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What does neuropath look like with hepatic encephalopathy?
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- polymicrocavitations of white matter (spongy change)
-Alzheimer's Type II astrocytes (clear, swollen nuclei) |
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What vitamin is a necessary cofactor for brain carbohydrate metabolism?
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thiamine (B1)
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Is thiamine def. common in cats?
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uncommon in cats
rare in dogs |
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What are 4 possible reasons for thiamine def.?
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1 - eating thiaminase containing fish (white fish)
2 - destruction from overcooking meals 3 - consumption of sulfur dioxide preserved food 4 - severe intestinal malabsorptive disease |
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What are CS to thiamine deficiency?
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1 - vestibular ataxia
2 - vomiting 3 - cervical ventroflexion 4 - mydriasis 5 - tetraparesis 6 - late states --> seizure, coma death |
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What does the neck look like with thiamine def?
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cervical ventroflexion
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What happens in the late stages of thiamine def?
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seizures, coma, death
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What do the eyes look like with thiamine def?
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dilated because destroyes PN of CN 3
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What can you test for with thiamine def?
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reduced RBC transketolase activity
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How do you diagnose thiamine def?
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1 - history of risk factor
2 - reduced RBC transketolase activity 3 - MRI |
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What is seen on an MRI with thiamine def?
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symmetric hemorrhagic lesions in the brainstem nuclei
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What is treatment for thiamine def?
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-thiamine supplementation (every 8 hours for 3 days)
- correct underlying risk factors |
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What does neuropath look like with thiamine def? (list 5 areas)
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-hemorrhagic necrosis of:
1 - red, 2 - vestibular nuclei 3 - caudal colliculi 4 - oculomotor nuclei 5 - geniculate nuclei |
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What does lead interfere with?
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Hb synthesis
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What are CNS signs due to with lead toxicosis?
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ischemia or edema
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What animals are most affected by lead toxicosis?
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juveniles with pica
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What are CS to lead toxicosis?
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1 - dementia
2 - seizures 3- vomiting 4 - diarrhea 5 - anorexia 6 - constipation |
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What are lead sources?
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paint, batteries, cables, oil, caulks, golf balls
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What are blood lead concentrations with lead toxicosis?
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>35 ppm
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What do RBCs look like with lead toxicosis?
What else will help your diagnsois? |
basophilic stippling
-metaphyseal lead lines -lead objects -blood lead concentrations |
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What will you see on rads with lead consuption?
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-lead objects
- metaphyseal lead lines |
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What are 2 main therapies for lead toxicosis?
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1 - chelation
2 - anticonvulsants |
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What are 4 chelators that can be used for lead toxicosis?
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1 - succimer - BEST
2 - Ca EDTA 3 - D-pencillamine 4 - BAL |
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What does neuropath look like with lead toxicosis?
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1- status spongiosis (edema)
2 - capillary proliferation 3 - cerebrocortical laminal necrosis |
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Are general systemic diagnosistics such as CBC, biochem, US, rads helpful for localizing structural intracranial disease?
-What does diagnosis require? |
no
- advanced brain imaging -CSF analysis - ancillary tests -histopath of brain |
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How are most lysosomal storage diseases inherited?
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-autosomal recessive fashion (genetic)
-with juvenile onset |
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What do lysosomal storage diseases result from?
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absence of or defect in function of single catabolic enzyme
-- causes progressive accumulation of intracellular waste products in affected tissues |
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Why are neurological signs common with lysosomal storage diseases even though they affect multiple tissues in the body (both neural and extraneural)?
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common because of terminal differentiation and limited regeneration of the neurons
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What neuro signs are common with lysosomal storage disease?
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- cerebellar
-dementia -visual deficits -usually normal at birth with progressive neurological deterioration and death |
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What is the definative diagnosis for lysosomal storage disease?
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pathologic and biochemical examination of tissue
other tests include a genetic test from Penn Genn |
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What is symptomatic in the urine of an animal having lysosomal storage disease?
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-excessive urinary excretion of cellular metabolic products (proteinuria/aminoaciduria)
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What do neurons look like with lysosomal storage disease?
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dilation
-some will glow in the dark |
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What is the treatment for lysosomal storage disease?
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none
-it is a progressive and terminal disease |
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What are 3 hereditary dysmyelinating diseases?
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1 - leukodystrophies
2 - hypomyelinating diseases 3 - spongy degenerations |
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What are the common denominators of the hereditary dysmyelinating diseases?
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-oligodenroglial failure of synthesis or maintenance of myelin
-insufficient quantity of myelin -abnormal myelin |
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Clinical manifestations of hereditary dysmyelinating diseases occur shortly after birth when animal begins to walk. What are they?
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- brain manifestations
- spinal cord manifestations -diffuse CNS manifestations -diffuse, action related tremors |
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How is congenital hydrocephalus categorized?
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-internal, non-obstructive hydrocephalus without apparent cause
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What is the definition of hydrocephalus?
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increased CSF volume in the brain
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What breed is hydrocephalus common in?
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small/toy
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What are CS of hydrocephalus?
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- dome shaped head
- divergent strabismus - setting sun -open fontanelles -neuro signs |
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What neuro signs are seen with hydrocephalus?
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-seizures
-circling -developmental failure - cerebellovestibular signs |
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Where is the abnormaility with congenital hydrocephalus?
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at the level of the arachnoid villi
-this is the site of CSF absorption |
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What are the CS of hydrocephalus due to?
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1 - intracranial hypertension
2 - intraventricular hemorrhage 3 - neuronal death/dysfunction |
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Do clinical signs coorelate with ventricle signs with hydrocephalus?
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no
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What are drugs for hydrocephalus aimed at doing?
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1 - reduce CSF production
2 - facilitate CSF excretion |
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What are the drugs used to facilitate CSF excretionwith hydrocephalus?
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1 - prednisone
2 - furosemide 3 - proton pump inhibitor |
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What symptomatic treatments would you use in cases of hydrocephalus?
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anticonvulsants
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What surgical methods can you use to help hydrocephalus?
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-ventriculoperitoneal shunt
- ventriculoatrial shunt -ventriculovascular shunt |
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What is the prognosis for animals with hydrocephalus?
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hard to predict
-guarded - poor in animals with severe cortical loss |
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Is ventricular symmetry important in diagnosing hydrocephalus?
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no - often not significant
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What is lissencephaly?
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-smooth, external surface of the brain
-gyri and sulcal development failure -non-lethal defect of embyonal neuronal migration |
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What is lissencephaly associated with?
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-pachygyria (thickened cerebral cortex)
-abnormal laminar architecture |
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What breed is predisposed to lissencephaly?
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Lhasa Apso
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What are CS in juveniles of lissencephaly?
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-training problems, dullness, seizures
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How you diagnose lissencephaly?
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MRI
-diminished suli -pachygyria |
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What is symptomatic therapy for lissencephaly?
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-anticonvulsants
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What is the most common intracranial neoplasia?
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meningiomas
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What is the age of onset of meningiomas and what is the typical breed?
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> 10 years
-golden retrievers, boxers, GSD |
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What breed typically gets gliomas?
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brachycephalic breeds age 5-9
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Are menigiomas intra-axial or extra-axial?
gliomas? |
menigiomas - extra-axial
gliomas - intra-axial |
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Are primary or secondary tumors more likely to cause intracranial neoplasia?
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secondary are more common
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What are secondary tumors that are seen with intracranial neoplasia?
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-hemangiosarcoma
-carcinoma (mammary, prostate, lung) -pituitary tumor lymphoma |
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How can you localize intracranial neoplasia?
-forebrain -central vestibular |
forebrain - seizures and behavior
infratentorial tumors - central vestibular signs |
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Why might you see multifocal CS with intracranial neoplasia?
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intracranial hypertension
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What are mass related effects with intracranial neoplasia?
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invasion, compression, displacement, herniation
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What are secondary effects of intracranial neoplasia?
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-peritumoral edema
-tumor-induced encephalitis -hemorrhage -obstructive hydrocephalus |
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What is the final common denominator with intracranial neoplasia?
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elevated intracranial pressure
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What is the definative way to diagnose intracranial neoplasia?
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histopath
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What does CSF reveal with intracranial neoplasia?
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-normal
-non-specific changes - neoplastic cells exfoliate |
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What neoplastic cells exfoliate with intracranial disease?
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-choroid plexus tumors
-lymphoma -histiocytic sarcoma |
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What are 3 methods to diagnose intracranial neoplasia?
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1 - histopath
2 - CSF 3 - EEG - localizing, but not specific |
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What are the 2 methods for antemortem brain biopsy?
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-open (craniotomy) --> free or image guided
- minimally invasive (Burr hole) - image guided |
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What are the primary treatments for intracranial neoplasia?
Is there evidence that chemo works? |
-surgery and radiotherapy
no |
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Which type of tumors are more amenable to surgery?
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superficial (extra-axial) forebrain tumors
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What is the success of surgery directly related to with intracranial neoplasia removal?
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1 - surgeon experience
2 - completeness of tumor excision |
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What is the prognosis for a canine meningioma with cytoreductive surgery?
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standard resection - 7 months
facilitated resection 2-3 years |
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What is the prognosis for a feline meningioma with cytoreductive surgery?
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2-3 years
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What is the prognosis for a pituitary tumor with a hypophysectomy with cytoreductive surgery?
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2 years
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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 |
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What are palliative, symptomatic therapies for intracranial neoplasia?
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prednisone --> anti-inflammatory, anti-edema, euphoric effects
anticonvulsants for seizures nutritional support antioxidants |
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What is the survival for palliative treatment with intracranial neoplasia?
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<3-4 months
-dogs with forebrain tumors and mild signs (seizures) live significantly longer -- 7 months |
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Although histopathologically multifocal diseases, what percent of inflammatory diseases present with focal clinical signs?
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50-66%
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What is unique about CS in animals with meninigoencephalitides (ME).
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many animals with this condition don't have any systemic CS or clin path abnormalities
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What is the most common cause of ME in dogs and cats?
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non-infectious (immune mediated)
dogs - esosinophilic menigoencephalitis, GME, necrotizing encephaltities cats - feline polioencephalomyelitis |
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What are viral cause of ME in dogs and cats?
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dogs - distemper and rabies
cats - FIP and rabies |
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What are fungal causes of ME in dogs and cats?
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crypto and Blasto
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What kind of virus is canine distemper virus?
-what is the reservoir host |
single stranded RNA paramyxovirus
dog |
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What are routes of infection?
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transplacental
-aerosolized secretions from infected animals |
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When does shedding occur with canine distemper?
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within 1 week of infection - can last for several months
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How do you predict which animals will develop neuro signs with canine distemper virus?
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you don't know
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What are the clinical sequelae of CDV due to?
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1 - virulence of strain
2 - immunocompetence of host (good, intermediate, or poor response) 3 - protracted immunity to CDV following recovery |
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When can neuro signs develop with CDV?
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weeks to years after infection
-coicident with systemic diseases |
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What are the CS of CNS disease with CDV?
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-vestibular disease
-myoclonus -seizures -myelitits |
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What physical sign is associated with the neuro signs of canine Distemper Virus?
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hyperkeratosis
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What is a negative prognostic indicator with CDV?
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neurological complications
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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) |
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Does a negative PCR or IFA rule out CDV?
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no
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How you you diagnose acute, fulminant CDV in an unvaccinated puppy (12-20 weeks old)?
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-history
-CS -CDV inclusions -IFA -PCR |
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How do you diagnose chronic CDV encephalomyelitis?
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hard
-PCR (blood, CSF, urine) -IFA (brain, footpad, skin) -CSF IgM/IgG titer and C-value |
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What is the therapy for CDV?
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-supportive and symptomatic
-CDV associated seizures, myoclonus and optic neuritis can be well tolerated |
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What type of virus is rabies?
what is the route of infection? |
neurotropic RNA rhabdovirus
bite |
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What affects the incubation period of rabies?
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-age of host
-innervation of inoculation site -proximity to CNS -can be days to months |
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What are the 2 forms of rabies?
How long does each last? |
furious (1-7 days)
paralytic (1-5 days) |
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What are the CS of the furious form of rabies?
paralytic form |
furious - aggression, photophobia, hyperesthesia, bizarre behaviors
paralytic form - progressive LMN paralysis |
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How is rabies diagnosed antemortem?
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not recommended
-FA skin biopsy of maxillary vibrissae |
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How is rabies diagnosed PM?
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-direct FA test of brain
-Negri bodies in neurons |
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What is the most common infectious cause of feline neurological disease?
How is it spread? |
FIP
in feces |
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What percent of cats with effusive and dry forms of FIP develop neuro signs?
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effusive - 15%
dry - 33% |
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What age cats get FIP and what is the incubation?
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young cats less than 2 in multicat environments
-up to years |
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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 |
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What are the neuro signs of FIP?
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1 - reflect inflammation of the ependyma, meniges, or choroid plexus (vascular)
2 - central vestibular 3 - cerebellovestibular 4 - seizures |
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What does a cat in a multicat house with fever, ocular and neuro signs have until proven otherwise?
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FIP
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What type of CSF will a cat with FIP have?
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supperative pleocytosic (neutrophilic)
-elevated FeCoV titer |
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How MIGHT the globulins react with FIP?
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hyperglobulinemia (>3.5 g/dl)
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What is the prognosis for FIP?
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-fatal
-survive for less than 1 year |
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What are the therapies for FIP?
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1 - immunosuppression (pred, chlorambucil, cyclophosphamide, cyclosporine)
2 - immunomodulation - interferons |
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What 2 fungal diseases are common to see just neuro signs?
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Crypto neoformans and gatti
Blastomyces dermatitidis |
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What are concurrent signs with fungal menigoencephalitides?
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-occular
-derm -lymphatic -respiratory |
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FUngal menigoencephalitide signs are often multifocal. When can they be focal?
|
associated with a macrogranuloma
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What are 3 methods used for diagnosing fungal meningoencephalitides?
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1 - demonstrate the organsim
2 - antigen tests 3 - diagnostic imaging |
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What is seen on diagnostic imaging with fungal meningoencephalitides?
|
meningeal thickening/enhancement, multifocal parenchymal lesions
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What tissues would you look at to demonstrate fungal meningoencephalitides?
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-resp tract
-LN eyes CSF |
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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 |
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What is the prognosis for fungal menigoencephalitides?
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poor for cure, but prolonged remission is possible
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What is MUE?
|
inflammatory brain disease with no identifiable etiology
-presumed to be immune-mediated in origin |
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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 |
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What type of brain diseases are MUE?
|
diffuse
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What breeds are predisposed to MUE?
|
young-middle-ages small and toy breeds
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What signs does the following varients of MUE have?
necrotizing variants GME |
necrotizing variants - forebrain signs
GME - brainstem white matter (in diencephalon caudally) |
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What is the only way to really diagnose MUE while the animals are alive?
|
brain biopsy - perivascular, non-supperative inflammation
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What is the therapy for all types of MUE?
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1 - prednisone
2 - combination therapies -- pred + (cycloporine, CCNU, Cytosar, Leflunomide, Procarbazine) 3 - brain irradiation (helpful with GME) |
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What is the prognosis for MUE, a insidiously progressive disease, with:
-pred monotherapy -combo therapy |
-pred monotherapy = 3-6 months
- combo therapy = 12 months |
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Which type of MUE might be more benign?
|
eosinophilic variant
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What are 2 protozoa that cause meningoencephalitides?
|
neospora caninum
toxoplasma gondii |
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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. |
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Are cats naturally resistant to neosporosis?
|
yes
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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 |
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Where are clinical signs of toxoplasma meningoencephalitiedes?
|
-the same place as tachyzoite replication
-pulmonary, hepatic, ocular, neurologic, |
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Neuro signs with toxoplasma meningoencephalitides can localize anywhere, but dogs have higher incidence of what?
|
- have higher incidence of LMN signs
|
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What concurrent infections are common with toxoplasmosis meningoencephalitides?
|
-FIV, FeLV, FIP
-CDV |
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How do you diagnose neosporosis meningoencephalitides?
|
1 - serology (high IgG titer and seroconversion of IgG)
2 - ID og tachyzoites in tissues or fluids |
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What are CS of neosporosis in puppies less than 6 months?
|
-ascending paralysis
-polyradiculoneuritis and myositis |
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What are CS of neosporosis in older dogs?
-neuro signs can localize anywhere |
-multifocal CNS disease
|
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What is therapy for protozoal meningoencephalitides?
|
-clindamycin
-TMS with pyremethamine for 4 weeks -response is usaually rapid |
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What is the prognosis for protozoal meningoencephalitides?
|
-good to excellent
-contractures from polyradiculoneuritis is permanent -fulmanent disseminated disease may be fatal despite therapy |
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What is the most common tick borne pathogen associated with neurological complications?
|
Rickettsia rickettsii
-rocky mountain spotted fever |
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What are the CS of RMSF related to?
|
systemic vasculitis from endothelial infection
- fever, lethargy -lymphadenopathy -epistaxis -facial or limb edema -melena -central vestibular signs are common |
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How do you diagnose RMSF?
|
-history, CS, PE
-thrombcytopenia -elevated IgM or IgG titer -PCR assay |
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What is the therapy for RMSF?
|
-doxycycline
-enrofloxacin for 2-3 weeks -CNS signs = prednisone for 1 week -rapid response to therapy |
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What is the prognosis for RMSF?
|
good to excellent if treated before severe neuro signs develop
|
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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 -prednisone |
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What is the morphologic end result of severe vascular injury?
|
necrotic brain tissue
|
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What is a clinical hallmark of CVA?
|
peracute to acute onset of focal, non-progressive (after 24-48 hours) clinical signs
|
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What is more common - arterial or venous strokes?
|
arterial
|
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What is the therapy for cerebrovascular accidents?
|
-maintain normal MaBP
-Normal paO2 -normal perfusion -decreaseICP -screen for risk factors |
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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 |
|
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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 |
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How do you diagnose feline ischemic encephalopathy?
|
-CT or MRI evidence of territorial infarction of cerebrum
-maybe will see a parasitic migratory track |
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What vessel is most commonly affected with feline ischemic encephalopathy?
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-middle cerebral arterial territory
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What is the therapy for feline ischemic encephalopathy?
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-ivermectin SC once
-Premed with: diphenhydramine and dexamethazone -anticonvulsants prn for seizures -many cats will improve with supportive care |
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What is the prognosis for feline ischemic encephalopathy?
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-most will improve or recover
-some cats need chronic anticonvulsant therapy -some cats left with permanent undesirable behavior changes |
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What is the neuropath of feline ischemic encephalopathy?
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-laminar cerebrocortical necrosis
-energy deprivation change -evidence of larvae in neural parencyma; eosinophilic inflammatory infiltrates |
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What is the main CS of optic neuritis?
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acute onset of bilateral blindness
-mydriasis with no PLR -optic nerve swollen with indistinct margins -abnormal retinal vasculature |
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What is the etiology of optic nerve inflammation?
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usually non IDed
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What is the therapy for optic neuritis?
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-immunosuppressive doses of prednisone
-wean based on response |
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What is the prognosis for optic neuritis?
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-guarded to poor for visual recovery
-no other neurologic deficits develop |
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What are CS of trigeminal neuritis?
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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 |
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What is the treatment for trigeminal neuritis?
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-gauze or tape muzzle
-spontaneous resolution in 2-3 weeks |
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Is steroid therapy effective with dropped jaw?
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no
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What are the CS to idiopathic facial nerve paralysis?
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60% unilateral
-lip droop -absent menace -absent palpebral reflex -drooling of affected side -+/- exposure keratitis |
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-What is the treatment for idiopathic facial nerve paralysis?
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non - recover in 3-6 weeks
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What does Horner's syndrom indicate and what are the CS?
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sympathetic denervation of the head
- ptosis, miosis, enopthalmos, protrusion of nictican |
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What are common causes to Horner's Syndrome?
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-brachial plexus avulsion
- otitis media-interna -intrathoracic neoplasia -intracranial neoplasia -hypothyroidism |
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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 |
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What percent of dogs and cats have idiopathic horners?
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50%
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What is the treatment for Idiopathic Horner's?
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none
-resolves in 2-3 months |
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What are clinical manifestations of functional intracranial diseases?
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paroxysmal stereotypical behaviors or possibly seizure disorders
-breed associations common |
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What breed/sex are associated with rage syndrome?
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-springer spaniel
-golden retriever -young adult, often male |
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What breeds are predisposed to flank sucking?
wool sucking? |
flank sucking: Dobermans
wool sucking: Oriental breeds of cats |
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What is feline hyperestheisia induced by?
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petting or grooming
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What is feline hyperesthesia?
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-spontaneous "crawling" of the skin of the lumbar region
-biting, licking, otherwise traumatizing the area |
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What do severe cases of feline hyperesthesia look like?
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clonic-tonic movements, salivation, urination, defecation
-resembles a seizure |
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What are R/O for feline hyperesthesia?
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-derm
-orthopedic -lumbar spinal diseases |
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What is the therapy for feline hyperesthesis?
This is the same treatment for fly biting? |
anticonvulsants, anxiolytics
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What is the difference between narcolepsy and cataplexy?
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narcolepsy = excessive daytime somnolence
cataplexy = sudden, transient loss of muscle tone --> the most common sign of narcolepsy |
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What is the abnormality associated with narcolepsy/cataplexy?
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-abnormality in hypocretin/orexin neuron system
-this participates in maintenance of wakefulness, and preservation of muscle tone |
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What are the 2 forms of narcolepsey/cataplexy?
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1 - familial form = absent or functionally deficient hypocretin receptor
2 - sporadic = hypocretin def. |
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What are the methods to diagnose narcolepsy/cataplexy?
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- food elicited cataplexy test
-trigger induced episode -pharm induced episode (phyostigmine) -EEG -CSF -- check hypocretin concentration |
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What are the drugs to treat narcolepsy/cataplexy?
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cataplexy = TCAs (clomipramine, imipramine, desipramine)
-narcolepsy - stimulants, but RX not usally needed |
