Inflammatory Disease Flashcards
Name 4 infectious inflammatory CNS diseases (5)
–Viral
–Bacterial
–Protozoal
–Algae
–Parasitic
Name 5 non infectious CNS inflammatory diseases (7)
–GME
–NME
–NE
–SRMA
–Cauda equina neuritis
–Pachimeningitis
–Eosinophilic
Label
A) Grey matter
B) White matter
C) Meninges
D) Ventricles
How do you diagnose:
- GME granulomatous meningoencephalomyelitis
- NME necrotising meningoencephalitis
- NLE necrotising leukoencephalitis
Histopathology
If no histopathology = MUA
What are the clinical signsof inflammatory CNS disease?
–Acute/sub-acute in onset
–Progressive in nature
–Associated with multifocal/diffuse neuroanatomical localisation
–Systemic signs rarely reported
A) What is GME?
B) What is characteristic?
A) Inflammatory (immune-mediated) disease of unknown aetiology
B)
•Characteristic granulomatose, angiocentric encephalitis
–Macrophages
–Lymphocytes
–Plasma cells
With GME is there more:
White matter and meninges OR
Grey matter?
Grey
What 3 things are seen with angeiocentric encephalitis with GME?
–Macrophages
–Lymphocytes
–Plasma cells
What is this?
Angiocentric encephalitis
What are the 2 classifications of GME?
- Clinical
- Histopathological
What are the 3 clinical forms of GME?
•Disseminated
–Most common, acute rapidly progressive multifocal signs
–Cerebrum, caudal brainstem, cerebellum, or cervical spinal cord
•Focal
–Acute or slowly progressive signs reflecting single space-occupying mass lesion
•Ocular
What are the 3 major pattern of lesion distribution with GME?
•Common disseminated form
–Spinal cord, brainstem and mid-brain (<
- Disseminated form with angiocentric expansion (multiple coalescing lesions)
- Focal form, single discrete mass lesion
–Spinal cord, brainstem and mid-brain, thalamus, optic nerves, cerebrum
What are the clinical features of GME?
•Young adult dogs (average age 4.5yrs range from 6 months to 12 years)
- Any gender
- Female, toy and terrier breeds over- represented
What do the clinical signs of GME reflect?
Lesion distribution
What are the clinical signs of GME?
–Vestibulo-cerebellar
–Cranial nerves deficits
–Visual impairment
–Paresis (tetra)
–Cervical pain
–Body turn
–Altered mentation
–Seizures
How do you diagnose GME?
–Rule out systemic dx
–Advanced imaging (MRI)
- Multiple hyperintensities on T2-weighted or (FLAIR) throughout the CNS white matter.
- Variable intensity in T1-weighted
- Variable contrast uptake on T1 post gadolinium
- Variable meningeal enhancement
–CSF
•Mononuclear mixed pleocytosis, increased TP
–Histopathology
- Angiocentric
- Mixed-lymphoid
- With matter encephalitis
- Lymphocytic meningitis
How do you treat GME?
–Supportive
•Mannitol?
–Immunomodulatory
A) What is NME?
B) Where is there pan-encephalitis?
C) Where is mainly affected?
A) Inflammatory (immune-mediated) disease of unknown aetiology
B)
–Meninges
–Grey matter
–White matter
C) Cerebral hemispheres mainly
What is this?
•Non-suppurative, necrotising ME
What are the clinical features of NME?
- Young adult dogs mean age 2Yr (6mo to 7Yr)
- No gender predisposition
- Breeds? Pug, Maltese, Pekingese…
- Rapidly progressive signs
–Seizures
–Depression
–Circling
–Visual deficits
How do you diagnose NME?
–Rule out systemic dx
–Advanced imaging (MRI)
- hyperintense on T2-weighted and FLAIR
- Isointense to slightly hypointense on T1-weighted
- Variable contrast enhancement on T1-weighted
- Loss of grey/white matter demarcation
–CSF (lymphocytic), increased TP
–Histopathology
- Lymphocytic meningitis
- Polioencephalitis
- Necrotising leukoencephalitis
How do you treat NME?
–Supportive
- Antiepileptic
- Mannitol?
–Immunomodulatory
NLE:
A) What is it?
B) What does it cause?
C) What is seen?
A) Inflammatory (immune-mediated) disease of unknown aetiology
B) Non-suppurative, necrotising encephalitis
C)Hemispheric white matter, and brainstem
•Cortex and meninges not involved
What is this?
•Non-suppurative, necrotising encephalitis
What is this?
•Hemispheric white matter, and brainstem
What are the clinical features of NLE?
- Young adult dogs mean age 4.5Yr (4mo to 10Yr)
- No gender predisposition
- Breeds? Yorkshire terrier, Pomeranian, French bulldog
What are the signs of NLE?
Rapidly progressive signs
- Depression
- Circling
- Vestibulocerebellar signs
- Visual deficits
- Seizures
How do you diagnose NLE?
–Rule out systemic dx
–Advanced imaging (MRI)
- Hyperintense on T2-weighted and FLAIR images
- Multiple cystic areas of necrosis
- Hypointense or isointense on T1-weighted images,
- Contrast enhancement is variable
–CSF monocytic, increased TP
–Histopathology
- Asymmetric, bilateral necrotising encephalitis
- Hemispheric white matter and brainstem
- Overlying cortex and meninges not involved
- Histiocyte, microglia and macrophages cell infiltrates and lymphocytic perivascular cuffing
How do you treat NLE?
–Supportive
•Mannitol?
–Immunomodulatory
How can you treat MUA?
Immunosuppression
- Corticosteroids
- Cytosine arabinoside
- Ciclosporines
- Azathioprine
How can we treat MUA with corticosteroids?
- Prednisolone, 1.5mg/kg BID then progressively reduced over 6 months to a maintenance dose of 0.5mg/kg EOD
- Dexamethasone, 0.2mg/kg SID then progressively reduced over about 6 months to a maintenance dose of 0.05mg/ kg EOD
How can you treat MUA with Cytosine Arabinoside?
- Synthetic nucleoside analog, competes for incorporation into nucleic acidsà inhibits DNA polymerase in mitotically active cells
- 50gm/m2 SC every 12 hours for two consecutive days, this protocol is repeated every 3 to 6 weeks (or longer intervals according to clinical signs)
- Monitor haematology
How can you treat MUA with ciclosporin?
- Suppressing T-lymphocyte activation and proliferation
- 6mg/kg PO every 12 hours
- Can be combined with ketoconazole
- Adverse effects:
- GI upset
- Gingival hyperplasia
- Change in coat (shedding or hirsutism)
How can you treat MUA with azathioprine?
Include the side effects
- Thiopurine, interferes with the productions of purine nucleotides = increased lymphocytes proliferation
- =Hepatic metabolism
- 2mg/kg SID
- Tapered to 0.5-1mg/kg EOD long term
Side effects:
Bone marrow suppression and GI upset
What is SRMA?
What is seen?
SRMA steroid responsive meningitis arteritis
- Inflammatory (immune-mediated) disease
- Suppurative inflammation (neutrophilc)
- Leptomeninges spinal cord
- Necrotising fibrinoid arteritis
What is the predisposition of SRMA?
- Young dogs 6-18months
- No gender predisposition
- Any breed but over represented
–Beagle
–Boxer
–Bernese mountain dog
–Weimaraner
–etc
What are the clinical features of SRMA?
- Profound cervical hyperaesthesia
- Pyrexia
- Depression
- Neutrophilia
What are the 2 forms of SRMA?
- Acute “typical”
- Chronic, due to inadequate treatment or relapses of acute disease
How do you diagnose SRMA?
–Neutrophilia
–(MRI) longus colli myositis, altered CSF signal
–CSF
- Acute: marked neutrophilic pleocytosis and raised TP
- Chronic: mixed or mononuclear pleocytosis and raised TP
- Measure IgA in serum and CSF
What is this?
SRMA steroid responsive meningitis arteritis
What does this show?
SRMA steroid responsive meningitis arteritis
How can you treat SRMA?
Immunosuppression
- Corticosteroids
- Cytosine arabinoside
- Ciclosporines
- Azathioprine
What is the prognosis of SRMA?
Fair to good
A) What is Cauda equina neuritis?
B) What is occassionally affected?
C) What is the likely origin?
D) Who is most affected?
A) Rare and sporadic disease in horses and Involves the nerves on the cauda equina
B) Occasionally affects CN, VII, VIII and rarely V
C) Likely autoimmune or post infectious origin (herpes, adenovirus)
D) Adult female mostly affected
What does cauda equina neuritis lead to?
To tail paralysis and sphincters incompetence
What makes Cauda equina neuritis lymphoplasmacytic?
•The inflammation starts in the intradural portion of the nerve root
What makes Cauda equina neuritis granulomatous?
The inflammation continues in the extradural portion forming large “mass- like” lesions
How do you diagnose Cauda equina neuritis?
•Compatible clinical signs
–Tail paralysis, incontinence, gait deficits, CN
•CSF (lumbar)
–Non-suppurative pleocytosis
–Elevated TP
•Post mortem
What is the prognosis of Cauda equina neuritis?
Poor
A) What is Eosinophilic meningoencephalitis (EME)?
B) Who is at risk?
C) What is seen?
A) Inflammatory likely immune-mediated, allergic mechanism?!?
B) Young, male Golden Retrievers and Rottweilers may be over-represented, any breed and gender can be affected
C) Severe meningitis and periventriculitis with infiltration of underlying parenchyma
How do you diagnose Eosinophilic meningoencephalitis (EME)?
- MRI multifocal changes
- CSF = eosinophilic pleocytosis
What is this?
Eosinophilic meningoencephalitis (EME)
•eosinophilic pleocytosis
What is the prognosis of Eosinophilic meningoencephalitis (EME)?
–Immunosuppressive doses of corticosteroids
–Occasionally needs additional immunosuppressive drugs such as cytosine
Pachimeningitis (hypertrophic chronic):
A) What is this?
B) Which breeds are at risk?
C) What is it chracterised by?
A) Inflammatory likely immune mediated origin
B) Greyhounds and crossed-sight hounds are over-represented
C) Charaterised by diffuse thickening of the dura mater by fibrosing inflammatory process
What do the clinical signs of Pachimeningitis (hypertrophic chronic) reflect?
Multiple CN deficits
What is the most common sign of Pachimeningitis (hypertrophic chronic)?
Dropped jaw
How do you diagnose Pachimeningitis (hypertrophic chronic)?
- MRI
- CSF may be inflammatory
How do you treat Pachimeningitis (hypertrophic chronic)?
–Immunosuppressive doses of corticosteroids
–Occasionally needs additional immunosuppressive drugs such as cytosine
What is the prognosis of Pachimeningitis (hypertrophic chronic)?
–Fair, most dogs achieve clinical remission however a cure is difficult to obtain
