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Immune Mediaged NS Diseases Flashcards

(58 cards)

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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

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A

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

25
Empirical therapy for MUE treatment
Life threatening signs of ME Clindamycin, doxycycline, Enrofloxacin
26
Outcome with no further diagnostics MUE
Continue antibiotics for 3 weeks If no response or clinical decline start prednisone
27
Outcome of treatment with further testing MUE
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
MUE treatment
Corticosteroids are the most common and most efficacious therapy - prednisone Pred + cyclosporine, CCNU, Cytosar, leflunomide, procarbazine - brain irradiation
29
MUE prognosis
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
Feline MUE
Uncommon in cats Infectious etiologies of meningoencephalitis is more common in cats than immune mediated Often seen in middle aged to older cats
31
Presentation of feline MUE
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
Steroid responsive tumor syndrome
Idiopathic (acute onset) steroid responsive tremors, idiopathic cerebellitis, young small breeds “Little white shaker disease”
33
treating steroid responsive tremor syndrome
Prednisone, taper for 1 month Prognosis is excellent, relapse is possible
34
Cranial neuropathies
Isolated or multiple dysfunction of cranial nerves without other neurological deficits Idiopathic etiology is most common cause of cranial neuropathies
35
Commonalities in cranial neuropathies
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
Trigeminal neuropathy
Acute onset of mandibular nerve paralysis Bilateral paralysis - dropped jaw OR unilateral paralysis - masticatory muscle atrophy
37
Clinical signs for bilateral trigeminal neuropathy
Dropped jaw, unable to close mouth, drooling, horners syndrome or facial hypalgesia
38
Etiologies for bilateral trigeminal neuropathy
Idiopathic trigeminal neuropathy/neuritis** Polyneuropathy Hematopoietic neoplasia -RARE
39
Diagnosing /treating idiopathic trigeminal neuropathy
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
Etiology for unilateral trigeminal neuropathy
Nerve sheath tumor Meningiomas Lymphoma Polyneuropathies
41
Diagnosing unilateral trigeminal neuropathy
MRI of head recommended - aggressive DX Lobular mass lesions extending into brainstem ipsilateral to muscle atrophy
42
Facial paralysis etiologies
Idiopathic - dogs 75%, cats - rare Otitis media/interna Otic neoplasms Polyneuropathy - hypothyroidism Intracranial lesions- associated with other deficits
43
clinical signs for facial paralysis
Acute** Lip droop Absent menace Absent palpebral reflex Drooling on affected side Widened palpebral fissure +/- exposure keratitis
44
Idiopathic diseases for facial paralysis
60% initially unilateral Rule out other etiologies Recovery in 3-6 weeks Contralateral signs may develop in future
45
Vestibular neuropathy etiologies
Otitis media/interna - 50% of cases Idiopathic Otic neoplasms Trauma Polyneuropathy - hypothyroidism Ototoxicity - rare
46
PVL or CVL Head tilt
PVL - ipsilateral to lesion CVL - ipsilateral or contralateral to lesion
47
PVL or CVL Pathological nystagmus
PVL - usually horizontal or rotary, fast phase away from lesion CVL - horizontal, rotary, vertical, direction changes w head position
48
PVL or CVL Postural reactions
PVL - normal CVL - deficits ipsilateral to lesion
49
PVL or CVL CN deficits
PVL - +/- ipsilateral CN VII CVL - +/- ipsilateral CN V-XII
50
PVL or CVL Horner syndrome
PVL - +/- CVL - +/-
51
PVL or CVL Consciousness
PVL - normal CVL - normal to comatose
52
Clinical signs for vestibular neuritis
Acute peripheral vestibular signs Head tilt, vestibular ataxia, pathological nystagmus Signs may be bilateral in 25% of cats
53
Idiopathic disease for vestibular neuritis
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
Steroid responsive meningitis arteritis
SRMA Systemic immune mediated disease w inflammation predominately affecting leptomeninges of cervical spinal cord & associated necrotizing fibroid arteritis
55
SRMA cause
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
Acute form of SRMA
Acute form - signs present <1m Lethargy, hyporexia, fever, cervical hyperpathia/ridigity, normal neuro exam
57
Chronic form of SRMA
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
Diagnosing SRMA
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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