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SS - Exam 2 > Immune Mediaged NS Diseases > Flashcards

Immune Mediaged NS Diseases Flashcards

1
Q

Immune mediated disease

A

Abnormal or self directed immune responses to the bodies own tissue and cells specifically in the CNS

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2
Q

Localization of inflammatory or neuro degenerative diseases

A

Often multi focal and present w multi focal signs

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3
Q

Animals with meningoencephlomyelitis

A

Often have no systemic abnormalities

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4
Q

Important tests for immune mediated neuro diseases

A

MRI, CSF analysis, serology, genetic test

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5
Q

What types of meningoencephalitis are recognized

A

Infectious
Immune-mediated* more common

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6
Q

Risk with MRI and CSF

A

Results can be normal which shouldn’t rule out presence of disesase

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7
Q

MUE

A

Meningoencephalitis of unknown etiology

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8
Q

Definitive diagnosis for MUE

A

Neuro pathologic exam
Brain biopsy

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9
Q

Presumptive antemortem diagnosis

A

Appropriate signalment /signs
Clinical neurologic dysfunction referable to brain
Compatible lesions on cross sections images
CSF analysis
Exclusion of infectious diseases w serology

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10
Q

Variations of MUE

A

Ganulomatous meingoencephalitis *most common
Necrotizing encephalitides (NME)
Eosinophilic meningoencephalitis (EME)

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11
Q

Ganulomatous meningoencephalitis (GME)

A

Giant macrophages mixed w lymphocytic inflammation
Disseminated form (typical)
Focal form (macrogranulomatous)
Ocular form (ocular neuritis)

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12
Q

Disseminated form of GME

A

multi focal neurologic presentation with multi focal lesions

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13
Q

Focal form of GME

A

Macrogranulomatous
Single mass like lesion in brain, often appears like tumor on imaging

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14
Q

Ocular form of GME

A

Presents as optic neuritis and BLINDNESS only

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15
Q

Necrotizing encephalitides

A

Necrotizing meningoencephalitis (NME) -gray matter
Necrotizing leukoencephalitis (NLE) - white matter

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16
Q

Eosinophilic meningoencephalitis

A

EME - commonly presents as eosinophilic inflammation in CNS

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17
Q

GME

A

Most common MUE variant (up to 30% )
Female, small/toy breeds - 4.5years
GME clinically presents of brainstem and SC disease (typically cervical)
Affects white matter of brain

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18
Q

NME

A

Younger age onset 2.5 yr
Predominately causes forebrain signs
95% of pugs w NME have structural epilepsy
Progresses readily

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19
Q

NME causes

A

Non-suppurative inflammation of letomeninges w extension into underlying cerebrum & asymmetric necrosis of neuropil

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20
Q

NME genetic testing

A

Susceptibility to NME in pugs is associated w DLA regions of chromosome 12
~11% of tests pugs S/S 1:8 develop NME

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21
Q

S/S pugs

A

Have 2 copies of NME susceptibility markers
13x more likely to develop NME in lifetime

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22
Q

Test results for NME

A

N/N - no copies of NME marker = low risk
N/S - one copy of NME marker = low risk
S/S - two copies of NME marker = 13x more likely

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23
Q

EME

A

Rare considering
Middle Ages large breed dogs
Can cause any signs of brain disease
More biologically benign than other MUE variants = better clinical prognosis

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24
Q

EME diagnosis

A

Inflammatory CSF with predominately eosinophils (>50%)
Differentials for eosinophilic pleocytosis
- protozoal or fungal
- parasitic migration

25
Q

Empirical therapy for MUE treatment

A

Life threatening signs of ME
Clindamycin, doxycycline, Enrofloxacin

26
Q

Outcome with no further diagnostics MUE

A

Continue antibiotics for 3 weeks
If no response or clinical decline start prednisone

27
Q

Outcome of treatment with further testing MUE

A

Brain imaging, CSF support, submit titers
CSF support ME, submit titers
Treat based on result of titers, if all negative of clinical decline occurs start MUE therapy

28
Q

MUE treatment

A

Corticosteroids are the most common and most efficacious therapy
- prednisone
Pred + cyclosporine, CCNU, Cytosar, leflunomide, procarbazine
- brain irradiation

29
Q

MUE prognosis

A

Lifelong therapy is often required
33% of dogs die within first month of diagnosis regardless of treatment
33% of dogs clinically improve but have persistent & significant neurological dysfunction
33% of dogs experience dramatic and durable clinical improvement
Difficult to predict how patients will react

30
Q

Feline MUE

A

Uncommon in cats
Infectious etiologies of meningoencephalitis is more common in cats than immune mediated
Often seen in middle aged to older cats

31
Q

Presentation of feline MUE

A

Multi focal clinical signs in 67% of cats
33% of cats w MUE have systemic signs
33% of cats w MUE present with SC disease
Diagnostic methods is similar to dogs
Prognosis is good to excellent for cats

32
Q

Steroid responsive tumor syndrome

A

Idiopathic (acute onset) steroid responsive tremors, idiopathic cerebellitis, young small breeds
“Little white shaker disease”

33
Q

treating steroid responsive tremor syndrome

A

Prednisone, taper for 1 month
Prognosis is excellent, relapse is possible

34
Q

Cranial neuropathies

A

Isolated or multiple dysfunction of cranial nerves without other neurological deficits
Idiopathic etiology is most common cause of cranial neuropathies

35
Q

Commonalities in cranial neuropathies

A

All idiopathic neuropathies have suspected immune mediated basis
Most idiopathic CN are transient and self limiting
None of the idiopathic CN are life threatening
Have been reported in multiple CNN

36
Q

Trigeminal neuropathy

A

Acute onset of mandibular nerve paralysis
Bilateral paralysis - dropped jaw
OR unilateral paralysis - masticatory muscle atrophy

37
Q

Clinical signs for bilateral trigeminal neuropathy

A

Dropped jaw, unable to close mouth, drooling, horners syndrome or facial hypalgesia

38
Q

Etiologies for bilateral trigeminal neuropathy

A

Idiopathic trigeminal neuropathy/neuritis**
Polyneuropathy
Hematopoietic neoplasia -RARE

39
Q

Diagnosing /treating idiopathic trigeminal neuropathy

A

MRI are usually not helpful for diagnosis
Treat by taping muzzle shut
Steroid therapy has no affective clinical course
Will spontaneously resolve in 2-3 weeks

40
Q

Etiology for unilateral trigeminal neuropathy

A

Nerve sheath tumor
Meningiomas
Lymphoma
Polyneuropathies

41
Q

Diagnosing unilateral trigeminal neuropathy

A

MRI of head recommended - aggressive DX
Lobular mass lesions extending into brainstem ipsilateral to muscle atrophy

42
Q

Facial paralysis etiologies

A

Idiopathic - dogs 75%, cats - rare
Otitis media/interna
Otic neoplasms
Polyneuropathy - hypothyroidism
Intracranial lesions- associated with other deficits

43
Q

clinical signs for facial paralysis

A

Acute**
Lip droop
Absent menace
Absent palpebral reflex
Drooling on affected side
Widened palpebral fissure
+/- exposure keratitis

44
Q

Idiopathic diseases for facial paralysis

A

60% initially unilateral
Rule out other etiologies
Recovery in 3-6 weeks
Contralateral signs may develop in future

45
Q

Vestibular neuropathy etiologies

A

Otitis media/interna - 50% of cases
Idiopathic
Otic neoplasms
Trauma
Polyneuropathy - hypothyroidism
Ototoxicity - rare

46
Q

PVL or CVL
Head tilt

A

PVL - ipsilateral to lesion
CVL - ipsilateral or contralateral to lesion

47
Q

PVL or CVL
Pathological nystagmus

A

PVL - usually horizontal or rotary, fast phase away from lesion
CVL - horizontal, rotary, vertical, direction changes w head position

48
Q

PVL or CVL
Postural reactions

A

PVL - normal
CVL - deficits ipsilateral to lesion

49
Q

PVL or CVL
CN deficits

A

PVL - +/- ipsilateral CN VII
CVL - +/- ipsilateral CN V-XII

50
Q

PVL or CVL
Horner syndrome

A

PVL - +/-
CVL - +/-

51
Q

PVL or CVL
Consciousness

A

PVL - normal
CVL - normal to comatose

52
Q

Clinical signs for vestibular neuritis

A

Acute peripheral vestibular signs
Head tilt, vestibular ataxia, pathological nystagmus
Signs may be bilateral in 25% of cats

53
Q

Idiopathic disease for vestibular neuritis

A

Geriatric disease in dogs (median 12 years)
Rule out other etiologies (middle ear disease)
Recovery in 2-4 weeks
May recur in the future

54
Q

Steroid responsive meningitis arteritis

A

SRMA
Systemic immune mediated disease w inflammation predominately affecting leptomeninges of cervical spinal cord & associated necrotizing fibroid arteritis

55
Q

SRMA cause

A

Most common cause of inflammatory SC disease in dogs
Affects young 6-18m, large breed dogs - beagle, boxer, Bernese, Weimaraner
No environmental, drug related, neoplastic, infectious triggers

56
Q

Acute form of SRMA

A

Acute form - signs present <1m
Lethargy, hyporexia, fever, cervical hyperpathia/ridigity, normal neuro exam

57
Q

Chronic form of SRMA

A

Clinical signs present for >1 months and be cyclic
Persistent and relapsing episodes of hyperpathia anywhere along vertebral column w ataxia or paresis or rarely a multifocal brain and SC presentation

58
Q

Diagnosing SRMA

A

NO Definitive antemortem diagnostic
Presumptive diagnosis based on clinical /lab findings
Non degenerative neutrophilia pleocytosis in CSF
Elevated serum IgA
MRI may show thickened /contrast enhancing meninges

SS - Exam 2 (18 decks)

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