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
2
Q
what is the forebrain important for?
A
seat of consciousness, behavior, & motor planning
3
Q
what is the importance of the brainstem?
A
normal motor function & normal gait (all LMN of cn 3-12) & vestibular function
4
Q
what are the layers of the meninges?
A
- dura mater - outer
- arachnoid membrane & subarachnoid space - middle (where CSF is)
- pia mater - inner layer
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
6
Q
what is most commonly tested for recognizing forebrain disease?
A
vision
7
Q
one-sided changes in a patient is consistent with what kind of forebrain disease?
A
unilateral forebrain disease
8
Q
T/F: circling is not always vestibular in nature
A
true
9
Q
how does hemi-inattention in unilateral forebrain disease manifest?
A
animal is circling toward the lesion
10
Q
T/F: seizures are also a sign of forebrain disease
A
true
11
Q
global changes are consistent with what kind of forebrain lesions?
A
diffuse or midline lesions
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
13
Q
what all does the brainstem contain?
A
- ascending reticular activating system (ARAS)
- central vestibular apparatus
- nuclei for CN III-XII
- UMN for gait
- tracts carrying proprioceptive information from the limbs
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
15
Q
T/F: central vestibular disease is a form of brainstem disease
A
true
16
Q
T/F: the ARAS has connections with conscious perception
A
true
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
18
Q
what is MUO?
A
meningoencephalitis - either infectious of immune-mediated intracranial disease
19
Q
what is the onset of meningoencephalitis?
A
fairly rapid in development - week to 2 weeks
20
Q
what is the progression of signs of meningoencephalitis?
A
signs will worsen over time
21
Q
is there pain associated with meningoencephalitis?
A
yes - inflammatory disease
22
Q
what areas of the CNS does meningoencephalitis affect?
A
affects more than one neuroanatomical region - multifocal
23
Q
ventral nystagmus is associated with central or peripheral vestibular disease?
A
central
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
25
what is required for a definitive diagnosis of cause of meningoencephalitis?
histopathology - brain biopsy or necropsy
26
what animals are typically affected by immune-mediated meningoencephalitis?
small-breed, middle-aged, dogs
27
what animals are typically affected by infectious meningoencephalitis?
cats, large-breed dogs, puppies, geriatric animals, & immunosuppressed animals!!!
28
what diagnostics can be used for diagnosing meningoencephalitis?
CT, MRI, & CSF evaluation
also rule in or out infectious causes - use ultrasound, antigen/antibody testing & aspirates
29
what would you expect to see in the CSF of an animal with meningoencephalitis?
> 5 nucleated cells/uL!!!! increased cell count confirms meningitis but doesn't tell you the cause
30
T/F: normal cell counts in CSF doesn't exclude meningitis
true - it's just less likely
31
what would you expect to see in the CT/MRI of an animal with meningoencephlitis?
multifocal, internal, contrast enhancing lesions
may be solitary
up to 25% don't contrast enhance
32
if there is a predominant cell type of small lymphocytes in CSF fluid, what are your prioritized differentials?
immune-mediated, viral in dogs
33
if there is a predominant cell type of small neutrophils in CSF fluid, what are your prioritized differentials?
SRMA, non-rickettsial bacteria
34
if there is a predominant cell type of small eosinophils in CSF fluid, what are your prioritized differentials?
fungal disease, aberrant parasites
35
if there is a predominant cell type of small macrophages/mixed cells in CSF fluid, what are your prioritized differentials?
can be any - especially if chronic
36
what virus can cause meningoencephalitis with respiratory & gi signs & often affects young dogs?
canine distemper virus
37
what is the prognosis for meningoencephalitis caused by canine distemper virus?
can recover but probably won't be neurologically appropriate
38
how is meningoencephalitis caused by canine distemper diagnosed?
PCR testing on epithelial cells - urothelial & conjunctival cells
39
what disease causing meningoencephalitis often affects young cats from multi-cat households?
feline infectious peritonitis
40
what form of FIP often has CNS signs?
the dry form - no fluid accumulation
41
T/F: FIP is often a presumptive diagnosis
true
42
if the effusive form of FIP is present, what would you expect to see in the exudates of body cavities?
high protein, cell-poor, & non-septic
43
what is the prognosis of FIP?
very poor
44
how is rabies diagnosed?
IFA testing on brain tissue by a state lab
45
when rabies virus is being shed, how long until the animal dies?
10 days
46
T/F: rabies is an uncommon cause of meningoencephalitis, but is still important to remember
true
47
what are two common protozoal causes of meningoencephalitis?
toxoplasmosis & neosporosis
48
what animals are affected by toxoplasma?
dogs & cats
49
how do animals become affected by toxoplasma?
oral exposure - eating contaminated rats or cat feces
50
what animals are affected by neosporosis?
clinically affects only dogs - especially puppies
51
what clinical signs are seen with neosporosis?
flaccid hindlimb paresis - contractures
can also cause neuritis & myositis (skeletal & cardiac)
52
what diagnostics are used for diagnosing protozoal causes of meningoencephalitis?
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
how is protozoal MUO treated?
clindamycin 25-30mg/kg/day for 28 days
54
what is the pathogenesis of neurological signs of rickettsial MUO?
neuro signs due to vasculitis!!!!
55
what are the clinical signs of rickettsial MUO?
thrombocytopenia, mild anemia, hypoalbuminemia, peripheral edema, fever, & lymphadenopathy
56
what are the main organisms of concern when it comes to rickettsial MUO?
rocky mountain spotted fever - r. rickettsii
ehrlichia/anaplasma
57
enrofloxacin works for treating what two rickettsial diseases?
rocky mountain & anaplasma
but not ehrlichia!!
58
how is rickettsial MUO treated?
doxycycline for a minimum of 4 weeks
59
how is rickettsial MUO controlled?
prevention!!!! communicate with the client!!
60
T/F: exposure to rickettsial diseases is very common & CNS often occurs
false - exposure is common but CNS signs are very rare
61
how is rickettsial MUO diagnosed?
paired titers with a 4X increase over 4 weeks
62
if you have a neutrophilic CSF sample, what is that consistent with?
bacterial meningoencephalitis
63
how is bacterial MUO spread?
intracranial abscess causing local spread - or bacteremia
64
why not use empirical antifungals in suspect cases of fungal MUO?
unless clinical suspicion is high because of adverse effects & high cost
65
when diagnosing fungal MUO, what is of most importance?
knowing your common local fungi!!!
66
what is the most common fungal encephalitis?
cryptococcus
67
what is the key point of treatment for meningoencephalitis if immune-mediated?
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
what is the general treatment for meningoencephalitis?
immunomodulation + empirical antimicrobial therapy
use steroids, safe antibiotics, & maybe anti-protozoals
69
when managing chronically immunosuppressed patients, what should be done with vaccines, exposure, & routine screening?
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
what is the prognosis of meningoencephalitis?
extremely variable!
subset of dogs won't respond to therapy - euthanasia within first 1-2 months of treatment
71
with intracranial neoplasia, how is it in regards to onset?
slow typically
72
with intracranial neoplasia, how is it in regards to progression?
over time - progressive
73
with intracranial neoplasia, how is it in regards to pain?
not initially - will become painful over time
74
T/F: in 50% of cases, intracranial neoplasia is typically a single mass
true
75
what are 3 common intracranial neoplasias?
meningioma, glioma, & pituitary tumors
76
what two neoplasias will present as metastatic/multicentric problems with multiple masses & involve other organs?
lymphoma & hemangiosarcoma - 30% of cases
77
what primary diagnostics can be used for intracranial neoplasia?
CT, MRI, CSF evaluation
78
if you have multicentric/metastatic intracranial neoplasia, what diagnostics can you use?
ultrasound, rads 3 view, & FNA/biopsy
hemangiosarcoma - liver & spleen
lymphoma - lymph nodes & check everywhere
79
what is the CT/MRI appearance of meningiomas?
on the edge & outside of the blood brain barrier
tends to enhance well
80
what is the MRI appearance of gliomas?
in the middle & inside the blood brain barrier
use an MRI because it won't show up well on CT
81
what is the CT/MRI appearance of pituitary tumors?
outside of the blood brain barrier & arise from the pituitary
82
what is the CT/MRI appearance of lymphoma?
single or multiple lesions that can be on the edge, middle, or both
increased vascular permeability = contrast enhancement
83
what is the CT/MRI appearance of hemangiosarcomas?
typically multiple lesions & in the middle
hemorrhagic - dark on T2
84
what intracranial neoplasia won't exfoliate in the CSF?
primary brain tumors (meningiomas, gliomas, pituitary tumors) & hemangiosarcomas
85
what intracranial neoplasia exfoliates in the CSF? what others may?
lymphoma
histiocytic sarcoma & choroid plexus carcinoma
86
what other differential should be ruled out from intracranial neoplasia?
meningoencephalitis
87
T/F: the majority of pituitary macrotumors are thought to be functional
true
88
what functional testing should be used for a pituitary tumor?
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
T/F: in cats with pituitary tumors, treatment is dependent on size
false - independent of size
90
why is functionality of pituitary tumors in cats different?
excess growth hormone is released causing acromegaly
difficult to control in diabetic cats
91
in general, what are the 4 options for treatment of intracranial neoplasia?
palliative care
surgical cytoreduction
radiation therapy
chemo
92
when choosing a treatment plan for intracranial neoplasia, what do you need to know?
where is the neoplasia - all locations
what neoplasia it is
patient needs & owner wishes
93
what is included in palliative treatment for intracranial neoplasia?
reduce cerebral edema
short term (emergency) - mannitol
long term - steroids, diuretics, omeprazole
control seizures
94
what is the median survival time for intracranial neoplasia using palliative treatment alone?
<6 months
even less for cerebellum/brainstem masses
95
what is the median survival time for extra-axial masses, predominantly meningiomas?
dogs - 1-1.5 years MST with surgery or RT alone
cats - ~3 years with surgery alone
96
what is the median survival time for intra-axial masses?
glioma - MST with surgery alone is poor
RT or chemo with alkylating agents may extend it but still <1 year
97
what are the 2 forms of cerebrovascular events?
ischemic & hemorrhagic
98
what animals are typically affected by cerebrovascular events?
older dogs with a peracute onset
99
what may cause an ischemic cerebrovascular event?
thromboembolic disease
100
what is the course of disease in regards to an ischemic cerebrovascular event?
static to improving
101
what is the course of disease in regards to an hemorrhagic cerebrovascular event?
progressive, then static to improving
102
is an ischemic cerebrovascular event painful to the animal?
non-painful
103
is a hemorrhagic cerebrovascular event painful to the animal?
painful during the progressive phase
104
what may cause an hemorrhagic cerebrovascular event?
complication of an ischemic event or coagulopathy
105
T/F: ~50% of cerebrovascular events have the underlying cause identified
true
106
what are some examples of a hypercoagulable state leading to a cerebrovascular event?
hyperadrenocorticism or protein losing nephropathy
107
what are some examples of vessel disease leading to a cerebrovascular event?
hypertension & hypothyroidism
108
what is the major differential for an cerebrovascular event?
old dog vestibular disease
109
how is a diagnosis made of a cerebrovascular event?
presumptive diagnosis via MRI
restricted diffusion - major differential is intra-axial neoplasia (glioma)
110
what is the prognosis for a cerebrovascular event?
good
111
what is the treatment for a cerebrovascular event?
treat the potential underlying cause
112
which is more common in cerebrovascular events, ischemic stroke or hemorrhagic stroke?
ischemic stroke
