Neuro V- Spring 3Rd Year

Front 1

What does GME stand for?

Back 1

granulomatous meningoencephalomyelitis

Front 2

what is GME?

Back 2

inflammation of brain, meninges and spinal cord

Front 3

GME is a well-recognized idiopathic disease of the ___________ and appears to be _________ ________.

Back 3

CNS
immune mediated

Front 4

What is the age range for GME?

Back 4

6 months-11 years (but really any age and sex can be affected)

Front 5

T or F
Cats and humans get GME.

Back 5

False!
Cats and humans do NOT get this disease.

Front 6

What is the etiology of GME?

Back 6

unknown but autoimmunity is the most scientifically supported theory at this time

Front 7

What type of hypersensitivity reaction is GME?

Back 7

MHC class II and CD3 antigen + lymphocytes suggesting a T cell mediated delayed type

Front 8

Why does GME involve the brain?

Back 8

because it is close to blood vessels

Front 9

Regarding the histopathology of GME:
You get a massive _____________ reaction that starts in space between _________ _______ and ________ _________. Produces more inflammation and eventually _________.

Back 9

granulomatous; blood vessel; brain parenchyma;
granulomas

Front 10

What can the granuloma in GME look similar to?

Back 10

a brain tumor due to the mass effect it causes

Front 11

Can you have diffuse disease in the brain with GME? Focal?

Back 11

Yes, can be diffuse or one solid mass when these areas of inflammatory cells combine

Front 12

What are three types of GME?

Back 12

focal
disseminated/multifocal
ocular

Front 13

what are areas that can be involved in GME?

Back 13

1) optic nerves
2) cerebellum
3) vestibular system
4) cervical spinal cord
5) cerebral cortex

Front 14

what are the three most common areas affected by GME?

Back 14

1) cerebellum
2) vestibular system
3) cervical spinal cord

Front 15

With GME:
Clinical signs reflect the _______ and ________ of the lesion.

Back 15

location; nature

Front 16

what are some common clinical sign combinations?

Back 16

1) cervical pain +/- lateralizing hemiparesis
2) nystagmus, head tilt, ataxia, tigh circling
3) blindness with absent or decreased PLRs
4) seizure, pacing, wide circling, behavior change, head pressing

Front 17

If you have a patient with hemiparesis, what is another differential other than GME?

Back 17

disc rupture

Front 18

What will you see in your CSF analysis:
a) what type of reaction?
b) increased or decreased protein?
c) plasma cells
d) cell counts

Back 18

a) granulomatous type reaction
b) increased protein
c) occasional plasma cells
d) high cell counts (like in the thousands)

Front 19

If you have a CSF that has greater than 50% neutrophils, is this likely GME?

Back 19

No. anything > 50% neuts is most likely not GME

Front 20

Will you see neuts in CSF with GME?

Back 20

yes. 2/3 cases up to 18-20%

Front 21

When will you have GME with normal CSF?

Back 21

1. when it is confined to the optic nerve
2. can also be normal if it's confined to one white matter area of the spinal cord

Front 22

Since there is no test for GME, what are 2 other diseases you should consider if you see these lymphocytic pleiocytosis?

Back 22

1) lymphoma
2) distemper

Front 23

If you see a mixed cell granulomatous reaction, what are your differentials? Which ones have changes that look most like GME?

Back 23

1) ehrlicia
2) fungal disease
3) toxoplasma (look most like GME)
4) neospora (look most like GME)

Front 24

How do you treat GME?

Back 24

1) croticosteriod therapy
2) cytosine arabinoside (cytarabine injection)
3) procarbazine HCl (Matulane)

Front 25

T or F
Corticosteroid therapy has to be life long for GME.

Back 25

True

Front 26

T or F
You should rapidly decrease pred dose when treating a pt for GME.

Back 26

False
VERY SLOWLY decrease dosage.

Front 27

when are you going to start to decrease Pred dose in a pt with GME?

Back 27

until clinical signs disappear

Front 28

When treating GME, what drug are you going to initially combine with cytosine arabinoside?

Back 28

pred

Front 29

what are the side effects of cytosine arabinoside?

Back 29

1) PRIMARY MYELOSUPPRESSION (nadir 5-7 days)
2) anorexia/emesis/diarrhea
3) hepatotoxicity
4) fever
5) conjunctivitis
6) ORAL ULCERATION

Front 30

what is an alkalating agent that can be given orally for GME?

Back 30

procarbazine HCl

Front 31

what is a big problem (side effect) of procarbazine?

Back 31

myelosuppression

Front 32

when a patient is on Procarbazine, how often should you monitor CBC?

Back 32

weekly for the first month then on a monthly basis

Front 33

what is a bilateral and asymmetric sporadic necrotizing meningoencepahlitis?

Back 33

pug necrotizing meningoencephalitis

Front 34

what area of the brain is primarily affected in pug necrotizing meningoencephalitis?

Back 34

cerebral hemispheres

Front 35

Is there a gender presdisposition for pug necrotizing meinigoencephalitis?

Back 35

No

Front 36

What is the age range for pug necrotizing meningoencephalitis?

Back 36

6 mo to 7 years
(6 mos to 2 yrs is the classic time frame)

Front 37

What is the disease course of pug necrotizing meningoencephalitis?

Back 37

usually a few days up to several weeks (rarely up to 6 mos)

Front 38

T or F
pug necrotizing meningoencephalitis is fatal.

Back 38

True

Front 39

What will you see preceeding death in pug necrotizing meningoencephalitis?

Back 39

1) generalized seizures
2) decreased mentation/head pressing (coma preceeds death)

Front 40

What are some other cx for pug necrotizing meningoencephalitis?

Back 40

1) circling
2) cortical blindness
3) stabismus
4) cervical rigidity
5) opisthotonus
6) intermittent screaming (I think I have this)
7) +/- nystagmus

Front 41

what will your CSF analysis be with pug necrotizing...?

Back 41

1) moderate to marked mononuclear pleocytosis
2) moderate increase in protein

Front 42

what will you see on hematologic and biochemical parameters in pug necrot blah blah blah?

Back 42

WNL

Front 43

T or F
in pug necrotizing blah blah blah, seizures are never refractory to anticonvulsant medication.

Back 43

False!
Seizures are OFTEN refractory to anticonvulsant medication.

Front 44

In pug necrotizing blah blah blah, corticosteroid therapy is usually ___________.

Back 44

ineffective

Front 45

what is the prognosis for pug necrotizing blah blah?

Back 45

Very poor to hopeless

Front 46

Which of the following meningoencephalitis are NLE or NME:
a) yorkshire terrier meningoencephalitis
b) maltese terrier meningoencephalitis
c) chihuahua meningoencepahlitis

Back 46

a) yorkies is NLE
b) maltese is NME
c) chihuahua is NLE

Front 47

what tends to be worse, NME or NLE?

Back 47

NME

Front 48

what does NME mean? what does NLE mean?

Back 48

NME=necrotizing meningoencephalitis
NLE= necrotizing leukoencephalomyelitis

Front 49

what breed is the second most likely for menigoencephalitis?

Back 49

yorkies

Front 50

If you see a patient with fever and severe cervical pain, what are you going to think?

Back 50

I'm going to think, huh, I have no idea what I'm doing. But I should think steroid responsive suppurative meningitis.

Front 51

what is the signalment for steroid responsive suppurative meningitis?

Back 51

most commonly seen in < 2 year old medium to large breed dogs.

Front 52

T or F
There is no apparent breed nor sex predilection for steroid responsive suppurative meningitis.

Back 52

True

Front 53

what is the most likely etiopathogenesis for steroid responsive suppurative meningitis?

Back 53

immune-mediated

Front 54

what else might you see in conjunction with steroid responsive suppurative meningitis?

Back 54

immune-mediated nonerosive polyarthritis

Front 55

what are the cx of steroid responsive suppurative meningitis?

Back 55

fever
CERVICAL RIGIDITY
vertebral pain

Front 56

T or F
neurologic deficits are common in steroid responsive suppurative meningitis.

Back 56

FALSE!
neurologic deficits are UNCOMMON

Front 57

With steroid responsive suppurative meningitis, you will often see peripheral ____________.

Back 57

neutrophilia

Front 58

what might you see in CSF analysis with SRSM?

Back 58

increase in protein (mild to moderate)
may be normal in the early course of the dz

Front 59

Lets say you have marked neutrophilic pleocytosis (>75-80%) (in CSF?), is this more likely GME or SRSM?

Back 59

SRSM
GME will ever have that many neuts

Front 60

what is a DDx for SRSM?

Back 60

bacterial meningitis

Front 61

For SRSM, you can consistently and rapidly alleviate it with _________________ ____________.

Back 61

corticosteroid immunosuppression

Front 62

what is the steroid of choice for SRSM?

Back 62

pred

Front 63

Can you eventually wean patients with SRSM off of steroids?

Back 63

Yes

Front 64

If pred fail in SRSM, what drug can you add?

Back 64

cytosine arabinoside

Front 65

What is the prognosis for SRSM?

Back 65

very good to excellent

Front 66

what can cause severe necrotizing form of aseptic meningitis and polyarthritis?

Back 66

necrotizing vasculitis

Front 67

In necrotized vasculitis, what may lead to ischemia.

Back 67

thrombi

Front 68

In necrotizing vasculitis, ________ necrosis of vessel walls and meningeal and cardiac _________/_________.

Back 68

fibrinoid; periarteritis/leptomeningitis

Front 69

what are the breeds associated with necrotizing vasculitis?

Back 69

1) BEAGLES
2) BERNESE MT DOGS
3) BOXERS
4) german short-haired pointers
5) irish wolfhounds

Front 70

AAAAAAHHHHHHHHHHHHH!!!!!! What am I and what do I have? And what is a ddx?

Back 70

I'm a Beagle and I'm screaming because I have necrotizing vasculitis.
Ddx: disc protrusion

Front 71

necrotizing vasculitis is most common in ___________ dogs. (usually < ______ mos)

Back 71

young
< 12 mos

Front 72

what do dogs with necrotizing vasculitis often look like?

Back 72

GME

Front 73

How can you differentiate GME from necrotizing vasculitis?

Back 73

with a spinal tap and look at neutrophil numbers

Front 74

if you have a pt with the following, what is a ddx:
recurring fever
cervical rigidity
anorexia
progression to tetraparesis, seizures
brainstem signs and blindness (common)

Back 74

necrotizing vasculitis

Front 75

T or F
In necrotizing vasculitis, peripheral neutropenia is common.

Back 75

False
NEUTROPHILIA is common

Front 76

what are your treatment choices for necrotizing vasculitis?

Back 76

1) immunosuppressive corticosteroid (Pred)
(only effective in some dogs)
2) cytosine

Front 77

how long will you have tx for necrotizing vasculitis?

Back 77

long term
may be able to wean them off meds in a year or two

Front 78

what is the prognosis of necrotizing vasculitis?

Back 78

guarded to poor

Front 79

if you saw a dog with the following cx, what is a differential?
severe, RAPIDLY PROGRESSIVE neuro signs
followed by muscle rigidity, lameness, hyperesthesia, fever

Back 79

BACTERIAL meningitis

Front 80

what is the difference between the signs for BACTERIAL meningitis and ASEPTIC meningitis?

Back 80

aseptic does not progress as rapidly and rarely sho as severe neuro dysfunction as BACTERIAL (septic) meningitis

Front 81

Is secondary brainstem and cerebral involvement more common with bacterial meningitis or aseptic meningitis?

Back 81

BACTERIAL meningitis

Front 82

Are extramural signs more consistently seen in BACTERIAL meningitis or ASEPTIC meningitis?

Back 82

BACTERIAL meningitis

Front 83

Can you differentiate between BACTERIAL meningitis and ASEPTIC meningitis with CSF analysis?

Back 83

No. both dz's demonstrate an identical picture on CSF analysis. (High protein and a neutrophilic pleocytosis, > 80%)

Front 84

T or F
Toxic neutrophils and intracellular bacteria are NOT consistently seen in CSF in BACTERIAL meningitis.

Back 84

True

Front 85

Treatment for BACTERIAL meningitis consists of (long or short) term (high or low) dose abx therapy, and has a (good or poor) prognosis with (frequent or infrequent) relapses.

Back 85

Treatment for bacterial meningitis consists of LONG-term, HIGH dose abx therapy, and has a POOR prognosis with FREQUENT relapses.

Front 86

What is VERY BENEFICIAL in the initial treatment of BACTERIAL meningitis?

Back 86

High potent steroid therapy