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14. Consult Liaison Psychiatry > Autoimmune encephalitis + Cryptococcal Meningitis + Hepatic Encephalopathy > Flashcards

Autoimmune encephalitis + Cryptococcal Meningitis + Hepatic Encephalopathy Flashcards

1
Q

what is the usual course of autoimmune encephalitis

A

usually, but not always, SUBACUTE (timeline of sx onset usually over course of several weeks)

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2
Q

what is the incidence of all encephalitis, both infectious and autoimmune encephalitis

A

5-10 per 100 000 in high income countries

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3
Q

why is early diagnosis of autoimmune encephalitis so important

A

so therapy can begin quickly

early tx is associated with decreased seizure frequency, faster cognitive improvement and IMPROVED SURVIVAL

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4
Q

define encephalitis

A

INFLAMMATION of the brain parenchyma

assoc. with neurologic dysfunction (i.e altered mental status, behavioural changes)

can be infectious or non infectious

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5
Q

define encephalopathy

A

refers to neuro dysfunction but can be with OR WITHOUT inflammation of brain tissue

i.e wernicke encephalopathy

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6
Q

what should be considered in a patient presenting with rapidly progressive memory impairment, behavioural or psychiatric changes or seizures of unknown etiology

A

autoimmune limbic encephalitis

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7
Q

name some of the autoimmune encephalitis examples

A

autoimmune limbic encephalitis

acute disseminated encephalomyelitis

anti-NMDA receptor encephalitis

Bickerstaff’s brainstem encephalitis

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8
Q

what 3 criteria need to be met to diagnose autoimmune encephalitis

A
  1. SUBACUTE onset–> rapid progression of less than 3 months of WORKING MEMORY deficits (short term memory loss), altered mental status or psych symptoms
  2. at least 1 of:
    –new FOCAL CNS findings
    –seizures not explained by a previously known seizure disorder
    –CSF pleocytosis (WBC count more than 5 cells per mm3)
    –MRI findings suggestive of encephalitis
  3. reasonable exclusion of alternative causes
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9
Q

what number of WBCs in the CSF is considered “pleocytosis”

A

more than 5 cells per mm3

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10
Q

what would be considered MRI findings suggestive of encephalitis

A

hyperintense signal on T2 weight fluid-attenuated inversion recovery sequences highly restricted to one or both medial temporal lobes (autoimmune limbic encephalitis)

or

hyperintense signal on T2 weighted fluid-attenuated inversion recovery sequences in multifocal areas involving grey matter, white matter, or both compatible with demyelination or inflammation

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11
Q

what causes the symptoms of autoimmune limbic encephalitis

A

dysfunction in the limbic structures of the brain

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12
Q

what symptoms can be caused by autoimmune limbic encephalitis

A

ST memory impairment

behavioural changes

anxiety

depression

psychosis

seizures

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13
Q

in which population does autoimmune limbic encephalitis most commonly occur

A

middle aged adults–but can occur in all ages

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14
Q

what 4 criteria must be met to diagnose autoimmune limbic encephalitis

A
  1. subacute onset of sx suggesting involvement of limbic structures
  2. BILATERAL brain abnormalities that is HIGHLY RESTRICTED to the MEDIAL TEMPORAL LOBES on T2 weighted FLAIR MRI
  3. at least one of:
    –CSF pleocytosis
    and/or
    –EEG with epileptic or slow wave activity involving the temporal lobes
  4. reasonable exclusion of alternative causes

**if one of first 3 not met, must find antibodies against cell surface, synaptic or onconeural proteins to make the definite autoimmune limbic encephalitis diagnosis

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15
Q

what might be seen on EEG in autoimmune limbic encephalitis

A

epileptic or slow wave activity involving temporal lobes

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16
Q

what other brain imaging technique may actually be more sensitive to autoimmune limbic encephalitis

A

18F-FDG PET–> may show increased FDG uptake in otherwise normal appearing medial temporal lobes thus indicating autoimmune limbic encephalitis

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17
Q

what is acute disseminated encephalomyelitis

A

a monophasic CNS inflammatory disease

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18
Q

in what population does acute disseminated encephalomyelitis most commonly occur

A

children and adults under age 40

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19
Q

what can trigger acute disseminated encephalomyelitis

A

can be triggered by acute systemic infection or vaccination

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20
Q

list symptoms of acute disseminated encephalomyelitis

A

cranial nerve palsies

ataxia

hemiparesis

myelopathy

optic neuritis

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21
Q

what types of antibodies may be found in those with acute disseminated encephalomyelitis

A

myelin oligodendrocyte glycoprotein (MOG) antibodies

can be found in up to 50% of children with acute disseminated encephalomyelitis

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22
Q

what 5 criteria must be met to diagnose definite acute disseminated encephalomyelitis

A
  1. a first, MULTIFOCAL, clinical CNS event of presumed inflammatory demyelinating cause
  2. encephalopathy that cannot be explained by fever
  3. abnormal brain MRI
  4. NO NEW clinical or MRI findings after 3 months of symptom onset
  5. reasonable exclusion of alternative causes
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23
Q

what brain abnormalities would be seen in MRI in acute disseminated encephalomyelitis

A

DIFFUSE, poorly demarcated, LARGE (bigger than 1-2cm) LESIONS predominantely involving the CEREBRAL WHITE MATTER in T2-weighted FLAIR imaging that can be present in the supratentorial white matter, basal ganglia, brainstem, cerebellum, and spinal cord (with or without contrast enhancement)

T1-hypointense lesions in the white matter in rare cases

deep grey matter abnormalities (i.e thalamus or basal ganglia) can be present

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24
Q

what antibodies are associated with anti-NMDA receptor encephalitis

A

CSF IgG antibodies against the GluN1 subunit of the NMDA receptor

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25
Q

what symptoms characterize the presentation of anti-NMDA receptor encephalitis

A

prominent psychiatric manfestations–> can delay diagnosis and treatment

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26
Q

what 3 criteria must be met for a “probable” diagnosis of anti-NMDA receptor encephalitis

A
  1. rapid onset of at least 4 of the following 6 major groups of symptoms:
    –abnormal (psychiatric) behaviour or cognitive dysfunction
    –speech dysfunction (pressured speech, verbal reduction, mutism)
    –seizures
    –movement disorder, dyskinesias, or rigidity/abnormal postures
    –decreased level of consciousness
    –autonomic dysfunction or central hypoventilation
  2. at least 1 of the following:
    –abnormal EEG
    –CSF with pleocytosis or oligoclonal bands
  3. reasonable exclusion of alternative causes

**can also be made in the presence of 3/6 of the above symptoms clusters + presence of a SYSTEMIC TERATOMA

27
Q

what abnormalities may be seen on EEG in anti-NMDA receptor encephalitis

A

focal or diffuse slow or disorganized activity, epileptic activity or extreme delta brush

28
Q

when can a DEFINITE diagnosis of anti-NMDA receptor encephalitis be made

A

in the presence of ONE OR MORE of the 6 major groups of symptoms PLUS IgG anti-GluN1 antibodies (including CSF testing) after reasonable exclusion of other disorders

29
Q

what is the period of onset of symptoms associated with Bickerstaff’s Brainstem Encephalitis

A

subacute–> LESS THAN 4 WEEKS

30
Q

what is the symptom pattern seen in Bickerstaff’s Brainstem Encephalitis

A

progressive impairment of CONSCIOUSNESS
+
ATAXIA
+
bilateral, mostly symmetrical OPHTHALMOPARESIS

frequently develop pupillary abnormalities, bilateral facial palsy, babinskis sign and bulbar palsy
–> generalized limb weakness can occur and overlap with features of GBS

31
Q

when can a diagnosis of definitely Bickerstaff’s Brainstem Encephalitis be made

A

in presence of + IgG anti-GQ1b antibodies
–> even if bilateral ophthalmoplegia is not complete or ataxia cannot be assessed or if recovery occured within 12 weeks after onset

32
Q

what two criteria must be met to diagnose probable Bickerstaff’s Brainstem Encephalitis

A
  1. subacute onset (rapid progression of less than 4 weeks) of ALL of the following:
    decreased LOC
    +
    bilateral external ophthalmoplegia
    +
    ataxia
  2. reasonable exclusion of alternative dx
33
Q

what factors can be elevated in those with hashimotos encephalitis/encephalopathy

A

anti-TPO antibodies
anti-thyroglobulin antibodies
anti-dsDNA antibodies

34
Q

what 6 criteria must be met for diagnosis of hashimotos encephalitis/encephalopathy

A
  1. encephalopathy with seizures, myoclonus, hallucinations or stroke-like episodes
  2. subclinical or overt THYROID DISEASE
  3. brain MRI NORMAL or with nonspecific abnormalities
  4. presence of SERUM THYROID ANTIBODIES (thyroid peroxidase, thyroglobulin)
  5. absence of well characterized neuronal antibodies in serum or CSF
  6. reasonable exclusion of alternative causes
35
Q

is hashimotos encephalitis/encephalopathy usually associated with hyper or hypothyroidism

A

usually hypothyroidism

36
Q

what is normally seen on MRI in hashimotos encephalitis/encephalopathy

A

usually normal or with nonspecific abnormalities

37
Q

list RED FLAGS for suspicion of autoimmune encephalitis in patients with PSYCHOSIS

A
  1. infectious prodrome
  2. new onset severe headache or clinically significant change in headache pattern
  3. rapid progression
  4. adverse response to antipsychotics or presence of NMS
  5. insufficient response to antipsychotics
  6. movement disorder i.e catatonia or dyskinesia
  7. focal neuro disease
  8. decreased LOC
  9. autonomic disturbance
  10. aphasia, mutism or dysarthria
  11. seizures
  12. presence of a tumor or hx of recent rumor
  13. hyponatremia (not explained by side effects of medication)
  14. other autoimmune disorders
  15. parethesia
38
Q

what is required for a diagnosis of DEFINITE autoimmune psychosis

A

meet criteria for probable autoimmune psychosis + presence of IgG class anti-neuronal antibodies in CSF

(criteria for probable autoimmune psychosis include rapid progression of sx + symptom clusters + CSf WBC/MRI abn/EEG changes/CSF oligoclonal bands/serum anti-neuronal antibodies)

39
Q

list the NO paraneoplastic encephalopathies

A

hashimotos encephalopathy

sarcoidosis

lupus

sjogrens

celiac

Bechet’s

anti-VGKC encephalitis

40
Q

what is paraneoplastic limbic encephalitis

A

rare neuro syndrome assoc with cancer

selectively affects limbic system structures–hippocampus, hypothalamus, amygdala

caused by altered immune response to a malignancy that has antigens that resemble limbic antigens

41
Q

paraneoplastic limbic encephalitis is usually associated with what type of cancer

A

small cell lung cancer

42
Q

ddx for autoimmune encephalitis

A

HSV encephalitis

HHV-6 encephalitis

glioma

status epilepticus

neurosyphillis

whipples

HIV

CNS infections

septic encephalopathy

metabolic encephalopathy

drug toxicity

epileptic disorders

prion diseases

CVD

mitochondrial disorders

inborn errors of metabolism

kleine-levin

43
Q

what signs would indicate HSV encephalitis

A

fever + MRI hemorrphagic lesions

usually unilateral MRI changes

44
Q

what is a sign/symptom that is considered pathognomonic for autoimmune limbic encephalitis

A

faciobracial dystonic seizures

–> involuntary movements–> brief contractions affetcing ipsilateral face, arm or leg–> can last several seconds, and can occur hundreds of times a day

–> often refractory to treatment with anti seizure meds

45
Q

is there usually unilateral or bilateral involvement shown on MRI in the limbic encephalitises

A

usually bilateral (though can be unilateral or MRI can be normal)

46
Q

what EEG change is most specific for anti-NMDA receptor encephalitis

A

extreme delta brush

47
Q

what type of antibodies are associated with autoimmune encephalitises

A

all are IgG

48
Q

anti-NMDA receptor encephalitis predominantely affects what population

A

under age 45

more females

49
Q

what is the main tumor association with anti-NMDA receptor encephalitis

A

ovarian teratoma

50
Q

what receptor is associated with limbic encephalitis

A

AMPA receptor

51
Q

what tumors are more associated with limbic encephalitis

A

thymoma

small cell lung cancer

52
Q

what is first line therapy for autoimmune encephalitis

A

(if theres a tumor, treat the tumor first–this will be most important tx)
otherwise…

IV steroids (methylprednisone)
IVIG
Plasma exchange/PLEX
or both IVIG + PLEX

(second line = rituximab and cyclophosphamide)

53
Q

how do symptoms generally progress in anti-NMDA receptor encephalitis

A

initially prominent PSYCHIATRIC symptoms

then progresses to seizures, movement disorders, autonomic dysfunction, hypoventilation

*older adults may present with cognitive decline and catatonic feaures

54
Q

you have a young person admitted with psychosis, and they display antipsychotic intolerance–what should you consider

A

anti-NMDA receptor encephalitis

those with anti-NMDA receptor encephalitis often have antipsychotic intolerance i.e fever, unusual EPS rigidity, decreased alertness

55
Q

what other encephalitis can precede anti-NMDA receptor encephalitis

A

HSV encephalitis–> seroconversion rate of up to 30%

56
Q

what should you do if you have a patient who presents with a relapse of symptoms after recovering from HSV encephalitis

A

CSG analysis for anti-NMDA receptor encephalitis–> MANDATORY in these cases due to high seroconversion rate

**ask about hx of HSV encephalitis in patient presenting with new psychosis

relapsing HSV encephalitis affects 20% of patients

57
Q

in which populations should you suspect cryptococcal meningitis

A

those with HIV

can also affect other people who are immunosuppressed

58
Q

what psychiatric disorder can be misdiagnosed in those who actually have cryptococcal meningitis

A

dementia

59
Q

what are the most common clinical symptoms of cryptococcal meningitis

A

subacute headache and confusion

(less than 20% have the neck stiffness that we assoc. with meningitis)

60
Q

do people with cryptococcal meningitis usually present acutely

A

no–> subacute meningitis is the most common presentation–> can be steadily progressive up to years

61
Q

what are the symptoms of hepatic encephalopathy

A

cognitive impairment

ataxia

altered LOC

62
Q

what investigations should be done if you suspect hepatic encephalopathy

A

ammonia levels

abdominal U/S

EEGs (look for encephalopathy)

63
Q

in a patient on VPA, what should you consider if they present with decreasing LOC, focal neuro deficits, cognitive slowing, vomiting, drowsiness, lethargy

A

consider hyperammonemic encephalopathy–> check ammonia levels

can occure even when VPA levels are normal and LFTs are normal

14. Consult Liaison Psychiatry (7 decks)

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