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Neuro 4 > Neuroimmunology > Flashcards

Neuroimmunology Flashcards

(42 cards)

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1
Q

Behind trauma what is the leading cause of neurological disability in young ppl?

A

MS

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2
Q

Lesions of what location are most frequently the cause of noticeable disability in MS pts?

A

Spinal cord = major reason for disability in MS pts

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3
Q

How are MS attacks treated?

A

glucocorticoids- high dose given IV

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4
Q

How are severe MS attacks treated?

A

plasmaphoresis

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5
Q

What feature of exacerbation is associated w/ poor recovery and permanent disability

A

Inflammatory damage to myelin can also damage the underlying axon -axon damage is associate w/ poor recovery and permanent disability

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6
Q

What are the two most common disease modifying agents used in MS?

A

-interferon beta -glatiramer acetate -first line for most, safe/old drugs, but are injections

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7
Q

What is natalizumab?

A

Monoclonal antibody used as a disease modifying agent in MS -prevents lymphocytes from crossing the blood brain barrier -side effect = PML = progressive multifocal leukoencephalopathy

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8
Q

What is PML?

A

Progressive multifocal leukoencephalopathy = severe demyelinating CNS disease caused by reactivation of the JC virus

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9
Q

What can cause PML?

A

Duationof treatment w/ natalizumab (monoclonal anitbody for MS)

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10
Q

Besides acute treatment and disease modifying agents, what else can be done for MS pts?

A

Treat the physical, cognitive, and social disability Secondary meds to treat the fatigue, walking difficulties, ED, depression etc

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11
Q

What is the hallmark clinical finding of limbic encephalitis?

A

Short-term memory loss

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12
Q

What is limbic encephalitis?

A

inflammatory disorder of the limbic disorder

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13
Q

What is found in imaging of limbic encephalitis?

A

Hyperintensity of bilateral mesial temporal lobes

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14
Q

What are the clinical features of limbic encephalitis?

A

(recall: video of pt in Giant’s shirt who couldn’t remember Giants won the superbowl) -hallmark = short-term memory loss -psychiatric symptoms (hallucinations, delusions, psychosis, agitation), sleep disturbances, involuntary movements, autonomic dysfunction, seizures

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15
Q

What are some causes of limbic encephalitis?

A

LE divided into infectious and autoimmune causes -infectious often caused by viruses (ex: herpes simplex) -autoimmune often paraneoplastic: due to antibody production in association w/ a tumor

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16
Q

What is crucial to do when a pt is diagnosed w/ LE?

A

Limbic encephalitis- need to look for (to rule out or remove) tumor -removal of tumor can be curative -lots of LE cases can be paraneoplastic (due to antibodies produced in association w/ a tumor)

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17
Q

What is the treatment for LE?

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A

-find a remove primary tumor -immuntherapies: IVIG, plasmaphoresis, steroids, monoclonal antibodies

18
Q

What is NMO?

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A

Neuromyelitis optica = Devi’s disease -inflammatory disease presenting w/ pathology of the optic nerve/chiasm, spinal cord, or brainstem

19
Q

Differentiate the epidemiology of MS and NMO (a) gender disparity (b) racial disparity

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A

MS (multiple sclerosis) vs. NMO (neuromyelitis optica) epidemiology (a) MS: M:F is 2:1, while NMO M:F is 10:1 (so NMO much much more common in females, but both are more common in F than M) (b) MS more common in whites, NMO more common in African American

20
Q

How to diagnose NMO

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A

1st- do blood test to test serum for NMO-IgG (seropositive in 75% of cases) -other 25% of cases (who are NMO-IgG seronegative) have 1 core clinical characteristic (w/o a better explanation): optic neurtis, acute myelitis, area postrema

21
Q

What is Devic’s disease

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A

NMO = neuromyelitis optica

22
Q

What are the presenting features of Devic’s disease?

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A

Loss of vision (either color, acuity etc) and SC fxn Presentation of SC dysfxn = muscle weakness, reduced sensation, loss of bladder/bowel control Typical pt: acute and severe spastic weakness of legs w/ sensory signs and loss of bladder control

23
Q

Differentiate the MRI findings of MS and NMO

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A

MS- shows small discrete plaques on MRI NMO- massive (like 3 vertebral bodies long) inflammatory lesions (much larger lesions, not small white dots)

24
Q

Compare and contrast treatment for MS and NMO

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A

Similarities- treat both MS and NMO attacks w/ steroids (and plasmapharesis if severe) Difference: disease modifying agents (interferon beta and glatiramer acetate) work in MS, but have no role against NMO

25
What are Dawson's fingers?
Hyperintensities on FLAIR immgaging that radiate away from the ventricles = periventricular lesion indicative of MS = lines of demyelination occuring around the periventricular area -the pathologic counterpart to MS
26
What are tumefactive lesions?
Large area of demyelinations that mimic a neoplasm or abscess -atypical but possible presentation of MS - often requires biopsy before correct diagnosis (b/c mistaken for neoplasm or abscess) - so instead of the discrete small hyperintensities you have large intensities
27
Dawson's fingers -indicative of periventricular lesion of MS
28
Juxtacortical (near the cortex) MS lesion
29
Describe the irregular findings
See in the right frontal lobe- hyperintensities in the white matter = demyelinating lesion
30
Define demyelination
Loss of myelin with (relatively) intact axons
31
How to differentiate stroke and demyelination on MRI
Stroke would have an affected "territory"- follow a specific area -demyelination can come in waves but distinct plaques and doesn't follow a specific artery's territory
32
Describe thefindings
Optice neuritis - isolated: can be finding of NMO - can be findign of MS - see myelin (blue stain) completely lacking in second figure
33
Describe the finding
Shadow plaque - see in between kind of 'transition' area of thinner myelin sheath in the middle btwn a demyelinated and normally myelinated area - may be remyelination, or could be an area that is just not fully demyelinated yet (not sure)
34
What is adrenoleukodystrophy?
Genetic disorder of paroxismal fatty acid beta-oxidation =\> accumulation of very long chain fatty acids in body tissues - mostly myelin in CNS and adrenal cortex - if not treated =\> progressive demyleination and death - basically destruction of white matter/myelin
35
Describe the indication of the presence of the axonal transection in the green
So in MS pts- presence of axonal transection (slash axonal damage in general) correlates w/ chance of recovery - so see the green (axon) below is maintained, despite red (myelin) loss = demyelination. this has a good prognosis and chance of recovery bc the axon is unaffected - then the axonal transection (been green dot) is indicative of axon damage- this correlates w/ lower chance of recovery/worse prognosis
36
Describe the findings
= Balo's Concentric sclerosis- demyelination (damage to white mater) in concentric layers - considered a borderline form of MS - on MRI: see alternating hypotense and hypertense layers
37
How to differentiate the hypercellularity seen in a tumor and acute demyelination
Tumor- hypercellularity is due to excess tumor cells While in acute demyelination it's due to histiocytes and reactive astrocytes
38
What is acute disseminated encephalomyelitis ? (a) cause (b) features (c) how to differentiate from MS
Acute dissemianted encephalitis = autoimmune widespread attack of inflammation in the brain and spinal cord involving attack of myelin (a) following viral infection or post-vacciation (specifically rabies vaccine) (b) features = cerebral edema (brain swelling) and symptoms mirroring MS (c) ADEM occurs in children (MS 20-40 yoa) and is monophasic (only once not recurrent attacks), but pathologically and clinically looks like MS
39
What can result from mistreatment of a pt w/ severe hyponatremia
Cerebral Pontine myelinosis -uptitrate Na+ too quickly =\> iatrogenic =severe damage of myelin sheath specifically in the pons
40
What is progressive multifocal leukoencephalopathy?
PML = viral infection of the oligodendocytes leading to multifocal demyelination - caused by reactivation of the JC virus (opportunistic) - can be caused by MS medication Natalizumab
41
Possible danger of progressive multifocal leukoencephalopathy (PML)
The JC virus is oncogenic- can become incorporated into the host genome and cause neoplastic transformation
42
What progressive neurological demyelinating disorder can be a result of alcoholism?
Marchiava-Bignami disease = progressive neurologic disease due to alcoholism -characterized by demyelination of the corpus callosum

Neuro 4 (6 decks)

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