30 Medical neuro dz

Question 1

ddx scheme for spinal cord disorders

Answer 1

DAMNIT Vdegenerativeanomalous metabolicneoplastic , nutritionalinfectious, inflammatorytraumatic, toxinsvascular disorders**most common

Question 2

neurodegenerative disorders clinical presentation

Answer 2

slow, insidious onset, progressive(exception IVDD can present peracute thru chronic)familial, hereditarySYMMETRIC (ex. DM)

Question 3

neuro anomaly disorders clinical presentation

Answer 3

nonprogressive or slowly progressive; symmetricseen early in life (exception vertebral malformations may take time and instability to worsen condition)may be incidental finding (ie. hemivertebra)

Question 4

metabolic disorders clinical presentation

Answer 4

any age, acute or chronic presentationdiffuse, symmetric nonspecific signs (wax and wane)ex. lysosomal storage disorders

Question 5

neoplasia and clinical presentation

Answer 5

any age, chronic, progressive with acute deterioration possibleasymmetric (focal–more common) or symmetric

Question 6

nutritional neuro dz and clinical presentation

Answer 6

raresymmetrical , slowly progressivediffuse or multifocalex. thiamine deficiency, secondary HyperPTH

Question 7

infxn/inflm neuro dz clinical presentation

Answer 7

acute or chronicasymmetric (more common) or symmetric progressive (but may wax/wane)

Question 8

traumatic neuro dz and clinical presentation

Answer 8

acute non progressive (may stay static or improve with time)symmetric or asymmetric depending on lesion

Question 9

vascular neurologic disorders and clinical presentation

Answer 9

acute non progressive (or improvement with time)focal and asymmetric

Question 10

CSF fluid collection

Answer 10

sensitive but not specific for disease; collecting fluid from subarachnoid spacecerebellomedullary cistern (atlanto-occipital space) vs lumbar cistern (L5-6 dog, L6-7 cats)–collect close to lesioncollect NO MORE THAN 1 ml CSF per 5 kgcytology, culture, virology, immunologic studies

Question 11

level of spinal cord taper

Answer 11

L5-6 dogL6-7 cat (may be able to do LS in cats)conus medullaris (taper portion) surrounded by nerve roots (caudal equina)subarachnoid space rarely extends to LS in dogs

Question 12

what is xanthochromic CSF

Answer 12

CSF with yellow or straw-tinged colorsuggests previous subarachnoid hemorrhage (in the absence of hyperbilirubinemia)

Question 13

normal vs abN CSF cell counts and TP

Answer 13

normal 0-5 WBC x 10^6; 5 WBC x 10^6

Question 14

Antibody titer testing in CNS for what diseases

Answer 14

Toxoplasma gondiiNeospora canisEhrlichia sppRickettsia sppCoccidiodes immitisreflect direct exposure but does not confirm active infection (may need serial titers)IgM—acuteIgG–chronic

Question 15

Antigen testing in CNS for what disease

Answer 15

Cryptococcus

Question 16

high IgA in CSF and serum may indicate what disease process

Answer 16

steroid responsive meningitismost likely secondary to dysregulation of the immune system (TH2 and B cells)**other biomarkers: C reactive protein!

Question 17

stain used to detect myelin

Answer 17

Luxol fast bluepost mortem staining of spinal cord for diagnosis of degenerative myelopathy

Question 18

degenerative myelopathy pathophysiology

Answer 18

primary affects spinal cordcharacterized by diffuse axonopathy w necrosis lateral and ventral funiculi of TL spine (T3-L3 progressive UMN paresis and proprioceptive ataxia)demyelination and astrogliosisslowly progressive–no txGSD, Pembroke Welsh Corgi, Boxer, Ridgeback, Huskie

Question 19

T/FDegenerative myelopathy is a UMN disease

Answer 19

TRUEDM is an UMN disease (T3-L3)10-20% may present with absent patellar reflexeslater in disease fecal and urinary incontinence

Question 20

genetic risk factor for pembroke welsh corgis and degenerative myelopathy

Answer 20

homozygous missense mutation in superoxide dismutase (SOD1) geneSOD 1 is a gene that converts free radicals to H202 and oxygen to prevent damageabsence of it’s function leads to damage of axons and myelin

Question 21

most frequently recognized infectious and noninfectious cause of menigomyelitis

Answer 21

infectious–canine distemper virus, protozoanoninfectious–steroid responsive meningitis

Question 22

T/Fidiopathic/autoimmune meningomyelitides predominate in dog; infectious meningoencephalomyelitis predominate in cats

Answer 22

TRUEidiopathic/autoimmune meningomyelitides — doginfectious meningoencephalomyelitis — cats

Question 23

idiopathic steroid responsive meningitis-arteritis pathophysiology

Answer 23

systemic immune dz characterized by inflammatory lesions of leptomeninges and associated arteries (occasionally associated with IM polyarthritis)typically respond to GCC (tx over 6 month)acute or chronic presentation; may relapseIMPORTANT DDX FOR CERVICAL SPINAL CORD DZ

Question 24

CSF fluid in dogs with steroid responsive meningitis

Answer 24

acute: nontoxic PMNchronic: mononuclear cells

Question 25

monitor treatment success of steroid responsive meningitis with what biomarker?

Answer 25

C reactive protein!IgA may never decrease despite remission

Question 26

3 forms described for granulomatous meningoencephalomyelitis

Answer 26

1. disseminated (most common): acute, rapidly progressive (poor px 8 d)2. multifocal3. focal: slowly progressive, like space occupying mass; may survive longer (114 d)

Question 27

inflammatory characteristics of GME/MUE

Answer 27

angiocentricnonsupperativemixed lymphoidWHITE MATTER

Question 28

most common MRI findings of disseminated GME

Answer 28

multiple hyper intensities on T2W or FLAIRscattered throughout CNS WHITE MATTER

Question 29

characteristics of canine distemper virus menigoencephalomyelitis

Answer 29

unvx dogs; Paramyxoviridae virus family; affects all epithelial tissues (GI, resp, ocular, skin)FLEXOR spasms of limbs,neck, masticatory musclesusually puppies 2-6 mo of ageGRAY matter disease–die within 1 week; nonsupperative inflammationWHITE matter disease–most common demyelination; noninflammatory; die within 4-5 weeksmay progress to necrotizing inflammation

Question 30

FIP meningitis

Answer 30

mutated form of nonpathogenic feline enteric coronavirusCNS meningitis is with NONeffusive or dry form (less common 30%)–perivascular, pyogranulomatous CNS infiltration

Question 31

2 clinical syndromes of Toxoplasma and Neospora meningoencephalomyelitis

Answer 31

1. meningoencephalomyelitis: cerebellitis, multifocal signs2. myositis-polyradiculoneuritis: LMN deficits; severe muscle atrophy with secondary limb contracture and arthrogryposis in young growing animals

Question 32

potential sources of bacterial meningomyelitis and spinal cord empyema

Answer 32

–blood from other infectious foci (urine)–direct inoculation (wounds, needles)–direct extension from other parts of body (ocular, ears, cribiform plate)*systemic signs, focal pain, acute, progressive

Question 33

treatment of bacterial meningomyelitis and spinal cord empyema

Answer 33

ideally culture/sensitivity; tx 1-4 months after clinical signs resolvemetronidazolefluoroquinolonechloramphenicol TMS3rd generation cephalosporins(CCFMS)

Question 34

Discospondylitis background

Answer 34

bacterial and/or fungalyoung males predominatevariable presentation (pain–>paralysis)spread via hematogenous, lymphatic, directly (rare)may be due to rich vascular supply in end plates and “dead end” capillary loops

Question 35

most common concurrent condition in dogs with Discospondylitis

Answer 35

UTI

Question 36

organisms most commonly isolated from Discospondylitis patients

Answer 36

Staph EcoliBrucellaStrepKlebsiella Candida, Aspergillus

Question 37

Combined blood and urine cultures ID organism in how many Discospondylitis cases

Answer 37

> 40%Burkert et al JAVMA 2005

Question 38

initial Ab therapy while pending cultures for discospondylitis

Answer 38

selected based on Staph spp BUT 17% staph may be resistant to first generation cephalosporins(consider clavamox, TMS)

Question 39

T/FFCE may show signs of clinical progression for the first few up to 24 hours after onset

Answer 39

TRUEmay progress initially but then usually static and improve with time

Question 40

locations of FCE

Answer 40

43-47% LS30-33% cervicothoracicother study says 37-42% T3-L3

Question 41

theories of how FCE occurs

Answer 41

1. nucleus pulpous directly penetrates vessel2. remnant vessel within nucleus pulpous exists3. herniation of nucleus pulpous into bone marrow of vertebral body goes into sinuses4. neovascularization of a degenerated disc

Question 42

T/FGray matter is more affected than white matter with an FCE

Answer 42

TRUEGray&raquo_space; whitelikely due to higher metabolic demand in gray matter

Question 43

gold standard dx of FCE

Answer 43

MRIshows focal sharply delineated hyper intensity on T2W Fast spin echo or hypo intense on T1Wischemic lesion to length ratio: compared to length of C6 or T2 body21% MRI of FCE had no detectable lesions

Question 44

prognosis of FCE after 2 weeks

Answer 44

if no improvement seen in 2 weeks, considered to have a worse prognosis

Question 45

FCE recovery time until motor, ambulation, and max recovery

Answer 45

motor 6 daysambulation 11 daysmax recovery 3.75 monthsdeRisio et al JVIM 2007 (per TJ page 409)

Question 46

ischemic lesion length to C6 or T2 length ratiofor predicting outcome in dogs with FCE (Per TJ page 409)

Answer 46

with lesion: length rations >2 60% had unsuccessful outcome< 2 100% had a successful outcome