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Neuro-subacute progressive disorders Flashcards

1
Q

What is the time course of subacute-progressive disorders

A

progresses over days to weeks

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2
Q

What are the disorders that cause subacute progressive disorders?

A
  1. inflammatory

2. neoplasia

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3
Q

What is a prominent feature of many of the same inflammatory and neoplastic conditions?

A

PAIN (some inflam conditions rarely cause neuro)

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4
Q

What are diseases that cause sub-acute progressive disorders +/- neck pain?

A
  1. diskospondylitis
  2. non-infectious inflammatory disease/meningitis
  3. infectious inflammatory disease/meningitis
  4. some neoplasms (metastatic_
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5
Q

What are non-infectious inflammatory diseases that cause subacute progressive neuro dz

A
  1. steroid responsive suppurative meningitis (aseptic mengitis)
  2. granulomatous meningoencephalitis (GME)
  3. necrotizing meningoencephalitis (NME)
  4. necrotizing leukoencephalitis (NLE)
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6
Q

What are infectious inflammatory diseases/meningitis that cause subacute progressive neuro dz?

A
  1. bacterial meningitis
  2. toxoplasma (dog, cat), neospora (dog)
  3. FIP meningitis/myelitits
  4. canine distemper menigoecenphalomyelitis
  5. rabies
  6. lyme meningitis
  7. fungal meningitis
  8. rickettsial meningitis/myelitis
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7
Q

What are the usual signs of steroid responsive suppurative meningitis? (aseptic meningitis)

A

usually just NECK PAIN and FEVER. Very rarely deficits

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8
Q

The signs of necrotizing meningoencephalitis are primarily what?

A

cortical

certain breeds

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9
Q

The signs for necrotizing leukoencephalitis are primarily what?

A

cortical and brainstem

certain breeds

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10
Q

Granulomatous meningoencephalitis primarily affects what?

A
  1. brain and or spinal cord
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11
Q

Pain in the neck is commonly associated with what?

A

compressive or inflammatory diseases of the cerbical spinal cord

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12
Q

What is the appearance of an animal with neck pain?

A

guarded horizontal neck carriage

unwilling to turn neck to side

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13
Q

What anatomic strucures can cause neck pain?

A
  1. meninges
  2. nerve roots
  3. joints
  4. bones
  5. muscles
  6. brain
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14
Q

forebrain mass lesions (intracranial disease) can cause what clinical symptom?

A

neck pain

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15
Q

What are muscular disorders that are associated with pain?

A
  1. immune mediated polymyositis
  2. masticatory myositis
  3. infectious myositis
  4. ischemic myopathy
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16
Q

What are two causes of muscle neck pain

A

myositis

muscle injury

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17
Q

What are 4 causes of bone neck pain?

A
  1. fracture/luxation
  2. diskospondylitis
  3. vertebral osteomyelitis
  4. neoplasia
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18
Q

What are 2 causes of joint neck pain

A

polyarthritis

degenerative joint dz

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19
Q

What are two causes of nerve root neck pain?

A
  1. neoplasia

2. compression

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20
Q

What are 3 causes of meninges neck pain

A
  1. neoplasia
  2. inflammation
  3. compression/traction
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21
Q

What is diskospondylitis?

A

an infection of the intervertebral disks with concurrent osteomyelitis in the adjacent end plates and vertebral bodies
Usually hematogenous

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22
Q

Who gets diskospondylitis?

A

medium to large breed dogs

german shepherd and labs may have increased prevalence M>F

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23
Q

What are the clinical features of diskospondylitis?

A
  1. SPINAL PAIN
  2. systemic signs in 30% of affected dogs
  3. reactive polyarthritis in some dogs
  4. neuro signs relatively uncommon (due to compression)
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24
Q

How is diskospondylitis diagnosed?

A
  1. physical exam

2. radiographic examination

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25
Q

What are radiographic changes of diskospondylitis?

A
  1. ventral endplate erosion
  2. focal lysis of one or both end plates
  3. collapse of disk space
  4. proliferative bony changes
  5. sclerosis at the margins of bone loss
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26
Q

Why are survey radiographs recommended with diskospondylitis?

A

common for diskospondylitis to affect more than one disk space

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27
Q

What is the most rewarding non-invasive method to isolate the organism responisble for diskospondylitis?

A

blood culture

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28
Q

What should be performed with a suspected diskospondylitis case?

A
  1. blood culture
  2. urine culture
  3. echocardiography looking for endocarditis
  4. percutaneous needle aspiration of disk if blood and urine culture unsuscessful and antibiotics not effective
  5. blastomycology in endemic areas
  6. brucella serology or PCR but low prevalence
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29
Q

What is the treatment for diskospondylitis?

A
  1. antibiotics
  2. cage rest
  3. analgesics
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30
Q

If an organism is not found for diskospondylitis, what should initial treatment be directed against?

A

staphyloccus

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31
Q

What kind of antimicrobials should be used with diskospondylitis?

A
  1. bactericidal
  2. spectrum against gram +
  3. ability to concentrate in bone
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32
Q

What antmicrobials are effective for diskispondylitis. what should be added if gram - drugs are suspected?

A
  1. cefazolin, cephalexin, amoxcillin with calvulanate

2. quinilones

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33
Q

How long is antimicrobial therapy continued for diskospondylitis?

A

8 weeks to 6 months

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34
Q

What is the most common form of meningitis diagnosed in most vet hospitals?

A

steroid-responsive suppurative meningitis (aseptic meningitis)

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35
Q

What animals are most often affected by steroid-responsive suppurative meningitis?

A

large dogs older than 2 years

beagles, bernese mountain dogs, boxers, german shorthaired points, nova scotia duck tolling retrievers

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36
Q

What are the clinical signs of steroid responsive suppurative meningitis?

A
  1. fever
  2. cervical rigidity
  3. vertebral pain
  4. neurologic deficits very uncommon
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37
Q

What are the lab findings of steroid responsive suppurative meningitis?

A
  1. peripheral neutrophilia
  2. CSF: increased protein, severe neutrophilic pleocytosis, negative culture, high IgA
  3. sometimes immune mediated polyarthritis
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38
Q

What is the treatment of steroid-responsive suppurative meningitis?

A

corticosteroids! (prednisone)

+/- azathioprine

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39
Q

How long are animals treated for steroid-responsive suppurative meningitis?

A

4-6 months

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40
Q

What are the gross and histological lesions of granulomatous meningoencephalitis?

A
  1. masses in white matter, occasionally grey matter, meninges and optic nerves
  2. histologically: perivascular cuffs of lymphocytes, macrophages, plasma cells
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41
Q

What are the 3 forms of granulomatous meningoencephalitis?

A
  1. ocular
  2. focal
  3. diffuse/disseminated
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42
Q

What is the least common form of granulomatou meningoencephalitis? What is the most common form?

A
  1. ocular

2. diffuse/disseminated

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43
Q

What are the features of ocular GME?

A

optic neuritis, acute onset of blindness, dilated pupils, hyperemic disk. often develops to disseminated

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44
Q

What are the features of focal GME?

A

neuro features similar to tumor

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45
Q

What are the feaures of disseminated/diffuse GME?

A

rapidly progressive signs of multifocal or disseminated dz affecting white matter of brainstem, cerebrum, cerebelllum, cervical spinal cord, optic nerve/mieninges
progression to death in days to 3 weeks

46
Q

What is the signalment of granulomatous meningoencephalitis? (GME)

A 
Small breeds
poodles, maltese, dachshunds, westies, chihuahuas
occasionally large breed
4-8 years usually
any dog can get it!
47
Q

What are the clinical signs of granulomatous meningoencephalitis? (GME?)

A

reflect location and nature of lesionforebrain signs, brainnstem signs etc
cervical pain–8% of dogs
a few have a fever and neutrophilia

48
Q

What are the lab changes seen with granulomatous meningoencephalitis (GME)?

A
  1. CSF: incresaed protein, mild to marked mononuclear pleocytosis. lymphoctes, monocytes, occasional plasma cells. sometimes normal. increased gamma globulins
49
Q

The CSF changes with GME are very non-specific. What should be done before making a presumptive diagnosis of GME?

A
  1. cuture, serum and CSF titers or PCR
  2. evaluate site of extraneural infection
  3. clinical trial with cindamycin for toxoplasma, neospora
  4. systemic search for neoplasia (thoracic radiographs, U/S, lymph node aspirates)
50
Q

Can GME be seen on diagnostic imaging?

A

yes might see with CT, more likely with MRI

51
Q

What is the treatment for GME?

A

corticosteroids can temporarily stop it (prednisone)

can also add cytosine arabinoside, procarbazine cyclosporine, azathioprine

52
Q

What is the signalment for necrotizing meningoencephalitis?

A
  1. PUGS
  2. maltese terriers
  3. westie, chihuahua, pekingese, shih tzu, lhaso apso
    6mo-7yrs
53
Q

What is the mechanism of necrotizing meningoencephalitis?

A

primarily cerebral cortex

necrosis and non-suppurative necrotizing meningoencephalitis and leptomeningitis

54
Q

What are the clinical signs of necrotizing meningoencephalitis?

A

cerebral cortical

seizures, circling etc

55
Q

What is the progression of necrotizing meningoencephalitis?

A

5-7 days–develop uncontrollable seizure or become recumbent

56
Q

How is necrotizing meningoencephalitis diagnosed?

A
  1. signalment
  2. clinical and clinicopathologic features
    nothing remarkable on CBC, chem
57
Q

What are the CSF findings of necrotizing meningoencephalitis?

A
  1. increased nucleated cell count. predominantly small lymphocyte
  2. mild to moderate increase in protein concentration
58
Q

What is seen on MRI with necrotizing meningoencephalitis?

A

focal cavitations, typically in cortical gray and subcortical white mater lateral to ventricles

59
Q

How is necrotizing meningoencephalitis treated?

A

NO treatment
can treat with antiepileptic doses of phenobarbitol to decrase seizures
can give corticosteroids but response variable.

60
Q

What is the prognosis for necrotizing meningoencephalitis

A

poor

61
Q

What is the signalment of necrotizing leukoencephalitis? (NLE)e

A
  1. yorkshire terries
  2. french bull dogs
    4mo-10 years
    some maltese, pugs, chihuahuas but more typically they get NME
62
Q

What does NLE effect? how does this differ from NME?

A

NLE affects cerebrum and brainstem

NME only affects cerebrum

63
Q

What are the common signs of NLE?

A

altered metnation, visual deficits, head tilt, cranial nerve abnormalities, proprioceptive deficits, seizures

64
Q

What is the progression of neuro signs with NLE (necrotizzing leukoencephalitis)

A

5-7 days

65
Q

What are the findings of the CSF in NLE?

A

moderate pleocytosis consisting mostly of mononuclear cels (macrophages, monocytes, lymphocytes, plasma cells)

66
Q

How do CSF findings of NLE/NME differ?

A

NLE–macrophages, monocytes, lymphocytes, plasma cells

NME–mostly small lymphocytes

67
Q

What is seen on MRI with NLE?

A

multiple cystic areas of necrosis etc

68
Q

What is the treatment for NLE?

A

none

69
Q

How does bacterial infection of the CNS occur?

A
  1. direct extension from middle ear, eye, sinus, nose or penetrating injury to skull
    hematogenous rare
70
Q

What are the clinical signs of bacterial infection of the CNS?

A
  1. pyrexia
  2. neck pain
  3. vomiting
  4. bradycardia
  5. neurologic abnormalities
    animals are systemically ill!!-shaock, hypotension, DIC
71
Q

What are the lab findings with bacterial meningits?

A

CSF: increased protein, neutrophils (can be severe), may be degenerate

72
Q

Every suspected bacterial meningitis should have what done?

A
  1. anaerobic and aerobic bacterial culture
  2. blood and urine bacterial cultures
  3. opthalmologic and otic exam
  4. screening radiographs of spine, skull and thorax
  5. abdominal U/S
73
Q

How is bacterial meningitis treated?

A
  1. antimicrobial treatment (ernofloxacin, third gen cephalosporines for gram -), metronidazole for anaerobic
    ampicillin and clavamox for gram +
74
Q

How should bacterial meningitis be treated if organism is unknown?

A
  1. ampicillin, cefotoxime and metronidazole

2. ampicillin, metronidazole, enrofloxacin

75
Q

What is the prognosis for bacterial meningitis?

A

guardedo, paresis, even with therapy

76
Q

What are signs in cats affected with FIP (dry form)

A

seizures, cerebellar, vestibular dyfunction
systemic signs like anorexia, weight loss
concurrent anterior uveitis etc

77
Q

Why should you palpate the abdomen with FIP?

A

may be able to detect organ distortion caused by concurrent granulomas

78
Q

What is the CBC like with FIP?

A
  1. inflammatory

2. serum globulin concentrations may be high

79
Q

What is the CSF like with FIP?

A

erneutrophilic or pyogranulomatous pleocytosis
increased protein concentration
MAY be normal

80
Q

How is FIP diagnosed?

A

coronavirus Ab in CSF

can sometimes detect coronavirus in CSF and tissue with PCR

81
Q

What is the prognosis for cats with CNS FIP?

A

very poor

82
Q

What are the definitive hosts of neospora caninum

A

dogs adn coyotes

83
Q

What are the intermediate hosts for neospora caninum?

A

deer, cattle

84
Q

What is the predominant route of transmission of neospora caninum?

A

transplacental

85
Q

What is the manifestation of neosporosis in young puppies 6 weeks to 6 months?

A
  1. weakness
    2 loss of patellar reflexes
  2. LMN paralysis of rear limbs due to inflammation of musles and nerve roots
  3. severe atrophy and contracture of affected muscles if no treatment
86
Q

What is the manifestation of neosporosis in older dogs?

A
  1. reactivation of encysted infection
  2. some dogs only have cerebellar signs, other have multipfocal signs
  3. some dogs have myositis
  4. usually systemically normal with CNS neosporosis
87
Q

What are hematologic and biochemical findings with neosporosis?

A

depends on organ involved
CK and AST elevated with muscle disease
serology may be negative

88
Q

What are CSF findings with neospora?

A

normal or mild protein, leukocyte count (monocytes, lymphocytes predominate)

89
Q

How can neospora be diagnosed?

A
  1. Immunocytochemistry on muscle biopsy

2. immunocytochemistry on muscle, CNS post mortem

90
Q

What is treatment for neospora?

A

clindamycin hydrochlordie

91
Q

What is associated with a poor prognosis with neospora?

A
  1. multifocal signs
  2. rapid progression
  3. pelvic limb rigid hyperextension
  4. delayed treatment
92
Q

What are the signs of progressive generalized infection with canine distemper virus? Who gets it?

A
  1. mild ocular/nasal discharge
  2. dry cough, becomes moist/productive as pneumonia develops
  3. depressed, inappetent, often febrile
  4. diarrhea mild or severe
  5. may get hyperkeratosis of footpads, nose

dogs 12-16 weeks usually get it

93
Q

When do neurologic signs occur with canine distemper virus?

A

1-3 weeks after dogs start to recover from systemic illness

dementia, disorientation, seizures, cerebellar or vestibular signs, ,tetraparesis, ataxia

94
Q

What is a seizure that is very characteristic for canine distemper virus?

A

chewing gum seizures

95
Q

What is old dog encephalitis?

A

dz of older animals that had prior canine distemper virus and recovered. Have neurologic abnormalities like progressive tetraparesis or vestibular disfunction without systemic signs

96
Q

How is canine distemper diagnosed?

A
  1. history (systemic d then neurosigns)
  2. physical exam
  3. lab findings
  4. anti-CDV antibodies in early stages, CDV in tonsils or lower resp tract
    later IHC on biopsy or necropsy because CDV stays for 60d in skin, footpads, CNS
    RT-PCR of blood, CSF
97
Q

What changes in the CSF does distemper meningoencephalitis usually cause?

A

increase in protein []=anti-CDV antibody
mild lymphocytic pleocytosis
CSF may be normal or may have increased neutrophils

98
Q

How is canine distemper virus meningoencephalomyelitis treated?

A

supportive

nonspecific

99
Q

How sucessful is canine distemper virus meningoencephalomyelitis treatment?

A

usually necessitates euthanasia

100
Q

What is the incubation period for rabies?

A

variable. 1 week to 8 months though usually 3-8 weeks

101
Q

How rapidly does rabies progress once neurologic signs develop?

A

7 days

102
Q

Any unvacinated animal with an acute, rapidly progressive of neurologic disease should be considered what?

A

a rabies suspect

103
Q

What are the two main types of rabies infection?

A

furious and paralytic

104
Q

Why is using biopsy from dorsal skin etc not sufficient for rabies diagnosis in all cases?

A

negative results

105
Q

How is rabies definitively diagnosed?

A

demonstration of r abies virus antigen by IHC on brain tissue

106
Q

What do most dogs with borrelia burgdorferi (lymes) get?

A

concurrent polyarthritis, lymphadenopathy, fever. neurologic signs rare

107
Q

What are the features of mycotic infections?

A

usually neurologic/ocular signs in conjunction with GI, resp or skeletal problems
CSF may have neutrophilic pleocytosis and increased protein
it is rare for systemic mycoses to only present with neuro signs

108
Q

What fungal organisms have a predilection for the CNS in the dog and cat?

A

cryptococcus neoformans

cryptococcus gatti

109
Q

How does infection with cryptococcus neoformans and cryptococcus gatti occur?

A

via extension from nose or via hematogenous

110
Q

What are the CSF changes with cryptococcal meningoencephalitis?

A

increased protein and cell counts (usually neutrophils, maybe eosinophils)
60% of time can see organisms. if not should do a culture or detect capsular antigen in CSF or serum

111
Q

How is cryptococcal meningoencephalitis treated?

A

amphotericin B, fluconazole (or itraconazole or voriconazole)

Small animal medicine (12 decks)

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