Exam 2 - Intracranial Disease 1 Flashcards

1
Q

what is the cerebellum important for?

A

controlling & coordinating motor function - but no initiation of motor function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the forebrain important for?

A

seat of consciousness, behavior, & motor planning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the importance of the brainstem?

A

normal motor function & normal gait (all LMN of cn 3-12) & vestibular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the layers of the meninges?

A
  1. dura mater - outer
  2. arachnoid membrane & subarachnoid space - middle (where CSF is)
  3. pia mater - inner layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

when recognizing forebrain disease, what are you looking for changes in?

A

changes in conscious responses to sensory stimuli

vision, proprioception, touch/pain sensation, & hearing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is most commonly tested for recognizing forebrain disease?

A

vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

one-sided changes in a patient is consistent with what kind of forebrain disease?

A

unilateral forebrain disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F: circling is not always vestibular in nature

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does hemi-inattention in unilateral forebrain disease manifest?

A

animal is circling toward the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T/F: seizures are also a sign of forebrain disease

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

global changes are consistent with what kind of forebrain lesions?

A

diffuse or midline lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

global changes (diffuse or midline lesions) can cause what kind of clinical signs?

A

decreased responsiveness to all stimuli or inappropriate responses to stimuli such as fear, aggression, & affection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what all does the brainstem contain?

A
  1. ascending reticular activating system (ARAS)
  2. central vestibular apparatus
  3. nuclei for CN III-XII
  4. UMN for gait
  5. tracts carrying proprioceptive information from the limbs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why is the brainstem similar to the C1-C5 spinal cord?

A

both contain UMN for gait & tracts carrying proprioceptive information from the limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T/F: central vestibular disease is a form of brainstem disease

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F: the ARAS has connections with conscious perception

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what clues should you use from onset & progression in intracranial disease?

A

rapid vs. slow development

gets better, gets worse, stays the same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is MUO?

A

meningoencephalitis - either infectious of immune-mediated intracranial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the onset of meningoencephalitis?

A

fairly rapid in development - week to 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the progression of signs of meningoencephalitis?

A

signs will worsen over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

is there pain associated with meningoencephalitis?

A

yes - inflammatory disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what areas of the CNS does meningoencephalitis affect?

A

affects more than one neuroanatomical region - multifocal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ventral nystagmus is associated with central or peripheral vestibular disease?

A

central

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how can you differentiate between immune-mediated & infectious causes of meningoencephalitis?

A

immune-mediated is typically confined to the nervous system

infectious may affect other organs - consider viral, protozoal, rickettsial, bacterial, & fungal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is required for a definitive diagnosis of cause of meningoencephalitis?

A

histopathology - brain biopsy or necropsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what animals are typically affected by immune-mediated meningoencephalitis?

A

small-breed, middle-aged, dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what animals are typically affected by infectious meningoencephalitis?

A

cats, large-breed dogs, puppies, geriatric animals, & immunosuppressed animals!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what diagnostics can be used for diagnosing meningoencephalitis?

A

CT, MRI, & CSF evaluation

also rule in or out infectious causes - use ultrasound, antigen/antibody testing & aspirates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what would you expect to see in the CSF of an animal with meningoencephalitis?

A

> 5 nucleated cells/uL!!!! increased cell count confirms meningitis but doesn’t tell you the cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/F: normal cell counts in CSF doesn’t exclude meningitis

A

true - it’s just less likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what would you expect to see in the CT/MRI of an animal with meningoencephlitis?

A

multifocal, internal, contrast enhancing lesions

may be solitary

up to 25% don’t contrast enhance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

if there is a predominant cell type of small lymphocytes in CSF fluid, what are your prioritized differentials?

A

immune-mediated, viral in dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

if there is a predominant cell type of small neutrophils in CSF fluid, what are your prioritized differentials?

A

SRMA, non-rickettsial bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

if there is a predominant cell type of small eosinophils in CSF fluid, what are your prioritized differentials?

A

fungal disease, aberrant parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

if there is a predominant cell type of small macrophages/mixed cells in CSF fluid, what are your prioritized differentials?

A

can be any - especially if chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what virus can cause meningoencephalitis with respiratory & gi signs & often affects young dogs?

A

canine distemper virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the prognosis for meningoencephalitis caused by canine distemper virus?

A

can recover but probably won’t be neurologically appropriate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how is meningoencephalitis caused by canine distemper diagnosed?

A

PCR testing on epithelial cells - urothelial & conjunctival cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what disease causing meningoencephalitis often affects young cats from multi-cat households?

A

feline infectious peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what form of FIP often has CNS signs?

A

the dry form - no fluid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

T/F: FIP is often a presumptive diagnosis

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

if the effusive form of FIP is present, what would you expect to see in the exudates of body cavities?

A

high protein, cell-poor, & non-septic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the prognosis of FIP?

A

very poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how is rabies diagnosed?

A

IFA testing on brain tissue by a state lab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

when rabies virus is being shed, how long until the animal dies?

A

10 days

46
Q

T/F: rabies is an uncommon cause of meningoencephalitis, but is still important to remember

A

true

47
Q

what are two common protozoal causes of meningoencephalitis?

A

toxoplasmosis & neosporosis

48
Q

what animals are affected by toxoplasma?

A

dogs & cats

49
Q

how do animals become affected by toxoplasma?

A

oral exposure - eating contaminated rats or cat feces

50
Q

what animals are affected by neosporosis?

A

clinically affects only dogs - especially puppies

51
Q

what clinical signs are seen with neosporosis?

A

flaccid hindlimb paresis - contractures

can also cause neuritis & myositis (skeletal & cardiac)

52
Q

what diagnostics are used for diagnosing protozoal causes of meningoencephalitis?

A

CSF & imaging consistent with MUO

PCR antigen - specific but less sensitive
Ab - sensitive but less specific, paired titers to look for an increase (IgM or IgG)

53
Q

how is protozoal MUO treated?

A

clindamycin 25-30mg/kg/day for 28 days

54
Q

what is the pathogenesis of neurological signs of rickettsial MUO?

A

neuro signs due to vasculitis!!!!

55
Q

what are the clinical signs of rickettsial MUO?

A

thrombocytopenia, mild anemia, hypoalbuminemia, peripheral edema, fever, & lymphadenopathy

56
Q

what are the main organisms of concern when it comes to rickettsial MUO?

A

rocky mountain spotted fever - r. rickettsii

ehrlichia/anaplasma

57
Q

enrofloxacin works for treating what two rickettsial diseases?

A

rocky mountain & anaplasma

but not ehrlichia!!

58
Q

how is rickettsial MUO treated?

A

doxycycline for a minimum of 4 weeks

59
Q

how is rickettsial MUO controlled?

A

prevention!!!! communicate with the client!!

60
Q

T/F: exposure to rickettsial diseases is very common & CNS often occurs

A

false - exposure is common but CNS signs are very rare

61
Q

how is rickettsial MUO diagnosed?

A

paired titers with a 4X increase over 4 weeks

62
Q

if you have a neutrophilic CSF sample, what is that consistent with?

A

bacterial meningoencephalitis

63
Q

how is bacterial MUO spread?

A

intracranial abscess causing local spread - or bacteremia

64
Q

why not use empirical antifungals in suspect cases of fungal MUO?

A

unless clinical suspicion is high because of adverse effects & high cost

65
Q

when diagnosing fungal MUO, what is of most importance?

A

knowing your common local fungi!!!

66
Q

what is the most common fungal encephalitis?

A

cryptococcus

67
Q

what is the key point of treatment for meningoencephalitis if immune-mediated?

A

long-term immunosuppressive therapy will likely be needed - if longer than 4 months, may be life long

transition from steroids to other immunosuppressives with a gradual dose reduction

68
Q

what is the general treatment for meningoencephalitis?

A

immunomodulation + empirical antimicrobial therapy

use steroids, safe antibiotics, & maybe anti-protozoals

69
Q

when managing chronically immunosuppressed patients, what should be done with vaccines, exposure, & routine screening?

A

no vaccines they don’t need - with rabies, vx. vs. titer owner’s choice

limit dog parks, groomers, boarding, etc

routine screening typically not done but not wrong to do

70
Q

what is the prognosis of meningoencephalitis?

A

extremely variable!

subset of dogs won’t respond to therapy - euthanasia within first 1-2 months of treatment

71
Q

with intracranial neoplasia, how is it in regards to onset?

A

slow typically

72
Q

with intracranial neoplasia, how is it in regards to progression?

A

over time - progressive

73
Q

with intracranial neoplasia, how is it in regards to pain?

A

not initially - will become painful over time

74
Q

T/F: in 50% of cases, intracranial neoplasia is typically a single mass

A

true

75
Q

what are 3 common intracranial neoplasias?

A

meningioma, glioma, & pituitary tumors

76
Q

what two neoplasias will present as metastatic/multicentric problems with multiple masses & involve other organs?

A

lymphoma & hemangiosarcoma - 30% of cases

77
Q

what primary diagnostics can be used for intracranial neoplasia?

A

CT, MRI, CSF evaluation

78
Q

if you have multicentric/metastatic intracranial neoplasia, what diagnostics can you use?

A

ultrasound, rads 3 view, & FNA/biopsy

hemangiosarcoma - liver & spleen
lymphoma - lymph nodes & check everywhere

79
Q

what is the CT/MRI appearance of meningiomas?

A

on the edge & outside of the blood brain barrier

tends to enhance well

80
Q

what is the MRI appearance of gliomas?

A

in the middle & inside the blood brain barrier

use an MRI because it won’t show up well on CT

81
Q

what is the CT/MRI appearance of pituitary tumors?

A

outside of the blood brain barrier & arise from the pituitary

82
Q

what is the CT/MRI appearance of lymphoma?

A

single or multiple lesions that can be on the edge, middle, or both

increased vascular permeability = contrast enhancement

83
Q

what is the CT/MRI appearance of hemangiosarcomas?

A

typically multiple lesions & in the middle

hemorrhagic - dark on T2

84
Q

what intracranial neoplasia won’t exfoliate in the CSF?

A

primary brain tumors (meningiomas, gliomas, pituitary tumors) & hemangiosarcomas

85
Q

what intracranial neoplasia exfoliates in the CSF? what others may?

A

lymphoma

histiocytic sarcoma & choroid plexus carcinoma

86
Q

what other differential should be ruled out from intracranial neoplasia?

A

meningoencephalitis

87
Q

T/F: the majority of pituitary macrotumors are thought to be functional

A

true

88
Q

what functional testing should be used for a pituitary tumor?

A
  1. clinical picture
  2. functional testing to differentiate hyperadrenocorticism by using a LDDST
  3. differentiating test to determine if you have pituitary dependent hyperadrenocorticism or an adrenal tumor - HDDT, ultrasound, & advanced imaging
89
Q

T/F: in cats with pituitary tumors, treatment is dependent on size

A

false - independent of size

90
Q

why is functionality of pituitary tumors in cats different?

A

excess growth hormone is released causing acromegaly

difficult to control in diabetic cats

91
Q

in general, what are the 4 options for treatment of intracranial neoplasia?

A

palliative care

surgical cytoreduction

radiation therapy

chemo

92
Q

when choosing a treatment plan for intracranial neoplasia, what do you need to know?

A

where is the neoplasia - all locations

what neoplasia it is

patient needs & owner wishes

93
Q

what is included in palliative treatment for intracranial neoplasia?

A

reduce cerebral edema

short term (emergency) - mannitol

long term - steroids, diuretics, omeprazole

control seizures

94
Q

what is the median survival time for intracranial neoplasia using palliative treatment alone?

A

<6 months

even less for cerebellum/brainstem masses

95
Q

what is the median survival time for extra-axial masses, predominantly meningiomas?

A

dogs - 1-1.5 years MST with surgery or RT alone

cats - ~3 years with surgery alone

96
Q

what is the median survival time for intra-axial masses?

A

glioma - MST with surgery alone is poor

RT or chemo with alkylating agents may extend it but still <1 year

97
Q

what are the 2 forms of cerebrovascular events?

A

ischemic & hemorrhagic

98
Q

what animals are typically affected by cerebrovascular events?

A

older dogs with a peracute onset

99
Q

what may cause an ischemic cerebrovascular event?

A

thromboembolic disease

100
Q

what is the course of disease in regards to an ischemic cerebrovascular event?

A

static to improving

101
Q

what is the course of disease in regards to an hemorrhagic cerebrovascular event?

A

progressive, then static to improving

102
Q

is an ischemic cerebrovascular event painful to the animal?

A

non-painful

103
Q

is a hemorrhagic cerebrovascular event painful to the animal?

A

painful during the progressive phase

104
Q

what may cause an hemorrhagic cerebrovascular event?

A

complication of an ischemic event or coagulopathy

105
Q

T/F: ~50% of cerebrovascular events have the underlying cause identified

A

true

106
Q

what are some examples of a hypercoagulable state leading to a cerebrovascular event?

A

hyperadrenocorticism or protein losing nephropathy

107
Q

what are some examples of vessel disease leading to a cerebrovascular event?

A

hypertension & hypothyroidism

108
Q

what is the major differential for an cerebrovascular event?

A

old dog vestibular disease

109
Q

how is a diagnosis made of a cerebrovascular event?

A

presumptive diagnosis via MRI

restricted diffusion - major differential is intra-axial neoplasia (glioma)

110
Q

what is the prognosis for a cerebrovascular event?

A

good

111
Q

what is the treatment for a cerebrovascular event?

A

treat the potential underlying cause

112
Q

which is more common in cerebrovascular events, ischemic stroke or hemorrhagic stroke?

A

ischemic stroke