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Neuropsychiatric Disorders > Neuropsychiatry of Encephalitis > Flashcards

Neuropsychiatry of Encephalitis Flashcards

1
Q

What are the two types of immune-mediated encephalitis?

A

▪️ Post-infectious
▪️ Autoimmune

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2
Q

What is a paraneoplastic autoimmune encephalitis and how might it occur?

A

▪️ Associated with cancer
▪️ Immune response to cancer may initiate cross-reactivity with brain proteins

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3
Q

Why might prevalence of autoimmune encephalitis be increasing?

A

▪️ Better recognition
▪️ Environmental factors
▪️ Development of new cancer immunotherapies

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4
Q

How does HSV-1 encephalitis typically present?

A

▪️ 2-12 days latency
▪️ Predominantly in limbic lobes (limbic encephalitis)
▪️ Headache, fever, seizures, confusion
▪️ Essentially haemorrhagic

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5
Q

Who is most at risk to HSV encephalitis?

A

▪️ Diabetic
▪️ Presence of malignant tumour
▪️ Immunocompromised
▪️ Deficits in toll-like receptor

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6
Q

What psychiatric symptoms are commonly seen in the acute phase of HSV encephalitis?

A

▪️ Agitation
▪️ Confusion
▪️ Psychosis, especially hallucinations
▪️ Mania
▪️ Delirium
▪️ Confabulation
▪️ Catatonia

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7
Q

What psychiatric symptoms are commonly seen in chronic HSV encephalitis?

A

▪️ Cognitive impairment, especially anterograde amnesia with variable retrograde
▪️ Executive/frontal dysfunction
▪️ Disinhibition
▪️ Aggression
▪️ Kluver-Bucy syndrome (hyperorality and hypersexuality)

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8
Q

What is autoimmune antibody-associated encephalitis?

A

▪️ Autoantibodies target and bind to ion channels/receptors/associated proteins on neuronal cell surface
▪️ Typically downregulate function
▪️ Leading to often acute/subacute presentations such as cognitive impairment, seizures, or movement disorder

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9
Q

What is the characteristic progression of acute encephalopathy seen with anti-NMDAR encephalitis?

A
  1. Prodromal malaise/flu-like
  2. Psychiatric (incl. sleep disturbance)
  3. Movement disorder (incl. catatonia/dyskinesia)
  4. Seizures
  5. Autonomic dysfunction
  6. Coma
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10
Q

What is anti-NMDAR encephalitis commonly associated with?

A

Ovarian teratoma/malignancy

(Although decreasing now)

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11
Q

What psychiatric symptoms are commonly seen in anti-NMDAR encephalitis?

A

▪️ Anxiety
▪️ Agitation
▪️ Psychosis (delusions, paranoia, hallucinations)
▪️ Catatonia
▪️ Echolalia

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12
Q

What is the main investigation for identifying NMDAR encephalitis and what is usually found?

A

Lumbar puncture
▪️ 80% show abnormality
▪️ Typically increased white blood cells and oligoclonal bands (immunoglobulins)

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13
Q

What imaging can you used to identify NMDA encephalitis and what might you find?

A

▪️ MRI - 33% abnormal, usually non-specific
▪️ EEG - 80-90% abnormal, usually slowing (‘extreme delta brush’)

(BUT important to differentiate encephalopathic EEG slowing from effects of psychiatric medication)

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14
Q

What is the predominant feature or autoimmune (NMDAR) encephalitis?

A

Psychiatric/behavioural disturbance

(Is possible to get isolated presentation, particularly at relapse)

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15
Q

What psychiatric disorder is the psychiatric phenotype of NMDAR encephalitis most similar to?

A

Schizophrenia/First episode psychosis

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16
Q

What is the primary presenting symptom in most cases of NMDAR encephalitis in children?

A

Psychosis

(typically older children)

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17
Q

How do anti-NMDAR antibodies causes disease?

A

▪️ Targets NMDA receptor and internalises it
▪️ Leads to fewer receptors at synapse = hypofunction

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18
Q

Why do acute doses of ketamine produce symptoms similar to schizophrenia and NMDAR encephalitis?

A

It binds to NMDA receptors

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19
Q

What are the two possible target proteins associated with voltage-gated potassium channel encephalitis?

A

▪️ LGI1
▪️ CASPR2

(DO NOT REQUEST VGKC ANTIBODIES)

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20
Q

What is the main prodromal sign of LGI1 antibody disease?

A

Personality change

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21
Q

What intrinsic risk factors may increase the risk of developing LGI1 antibody disease later in life?

A

▪️ Male gender
▪️ HLA (human leukocyte antigen)

22
Q

Disease related to which antibody may present with sleep disorders such as REM and NREM parasomnia?

A

IgLON5

23
Q

What is the issue with only testing for antibodies in people who appear encephalopathic?

A

Many identified cases of ‘isolated psychiatric’ presentations would be missed

BUT we can test everyone with psychiatric presentation?

24
Q

How common is autoantibody-mediated psychosis?

A

NMDAR-Ab found in around 5% of FEP, indistinguishable from the others

25
Q

Can we make diagnoses based off blood tests?

A

No!

26
Q

What are the main onconeural antibodies associated with paraneoplastic immune-mediated encephalitis?

A

▪️ Anti-Yo
▪️ Anti-Hu
▪️ Anti-Ri
▪️ Anti-Ma
▪️ PCA-2

27
Q

Why is it important to detect cases of psychosis with anti-neuronal antibodies?

A

So that we can treat them appropriately with immunotherapy or tumour removal

28
Q

What is lymphocytic pleocytosis?

A

Abnormal increase in amount of lymphocytes in CSF (T and C WBCs)

29
Q

What is rituximab?

A

A monoclonal antibody that targets CD20 on B cells, stopping the production of antibodies

30
Q

What are the main problems with Graus criteria for autoimmune encephalitis?

A

▪️ Too focused on neurological signs and symptoms
▪️ ‘Possible’ criteria assumes EEG/MRI has been done - unclear which psychiatric patients to investigate
▪️ ‘Definite’ criteria is too liberal? - accept serum antibodies for diagnosis but they are common

31
Q

How does the new Pollak criteria for autoimmune encephalitis differ from the Graus criteria?

A

▪️ Reduced emphasis on serum test - not enough for diagnosis
▪️ Primary focus on CSF analysis
▪️ Need abrupt onset alongside just one of the possible signs to be sent for a lumbar puncture (e.g., movement disorder, adverse response to antipsychotics, decreased consciousness etc)

32
Q

What are the main symptoms of encephalitis lethargica?

A

▪️ Initial pharyngitis
▪️ Sleep disorder (hypersomnolence/sleep inversion/insomnia)
▪️ Basal ganglia signs (parkinsonism/dyskinesia/hyperkinetic)
▪️ Neuropsychiatric symptoms (e.g., psychosis)

33
Q

What are the main forms of encephalitis lethargica?

A

▪️ Somnolent-ophthalmoplegic
▪️ Hyperkinetic
▪️ Parkinsonian
▪️ Psychotic

34
Q

What are the most common chronic sequelae of encephalitis lethargica?

A

▪️ Parkinsonism
▪️ Compulsive behaviour
▪️ Psychosis
▪️ Catatonia

35
Q

What antibodies have been associated with modern cases of encephalitis lethargica?

A

▪️ Basal ganglia antibodies
▪️ NMDAR/D2R antibodies

36
Q

What is postviral autoimmune encephalitis?

A

Autoimmune encephalitis following initial viral encephalitis

Most commonly NMDAR antibodies following HSVE

37
Q

How does postviral autoimmune encephalitis typically present?

A

▪️ Choreoathetoid movement disorder in children
▪️ Cognitive dysfunction in adults
▪️ Seizures
▪️ Occasionally isolated psychiatric cases?

38
Q

How might postviral encephalitis lead to autoimmune encephalitis?

A

▪️ Damage to limbic system exposes NMDA receptor epitopes which trigger a second immune response?
▪️ Molecular mimicry?

39
Q

When is an onconeural antibody screen mandatory?

A

If a patient has a known cancer

40
Q

How does risk of encephalitis change postpartum?

A

It increases - can mimic postpartum psychosis

41
Q

What is Hashimoto’s encephalopathy?

A

▪️ Encephalopathy of presumed autoimmune origin
▪️ Characterised by massively increased levels of anti-TPO/TG antibodies, not necessarily with thyroid disease
▪️ Responds rapidly to steroids

42
Q

How do we treat psychiatric symptoms in encephalitis?

A

Focus on treating the causes (e.g., antivirals, antibiotics, immunotherapies)

43
Q

What contraindications must you consider when treating psychiatric symptoms in encephalitis?

A

▪️ High dose steroids can precipitate mania and/or psychosis
▪️ Methotrexate and cyclophosphamide can cause mood changes
▪️ Immunosuppression leaves individual vulnerable to opportunistic infection

44
Q

What treatments can you use for agitation and/or catatonia in encephalitis?

A

Benzodiazepines but may require very high dose

45
Q

What should you avoid when treating psychotic symptoms in encephalitis?

A

Typical neuroleptics/antipsychotics because:
▪️ Increased risk of neuroleptic malignant syndrome (especially in NMDAR encephalitis)
▪️ Can reduce seizure thershold

46
Q

What symptoms of autoimmune encephalitis are often the most persistent and why?

A

Psychiatric symptoms - symptom resolution often mimics symptom onset

47
Q

What residual cognitive impairment may be apparent following NMDAR encephalitis?

A

▪️ Episodic memory
▪️ Processing speed
▪️ Executive function

Often subtle!

48
Q

What is the prognosis of cognitive impairment following LGI1 encephalitis?

A

Majority do not return to baseline cognition, particularly with memory deficits due to MTL/hippocampal atrophy

49
Q

How likely is relapse following AE and how does it typically present?

A

Common!

Most likely isolated psychiatric or cognitive symptoms

50
Q

What autoantibodies are especially associated with persistent subacute encephalopathy?

A

LGI1 and CASPR2

(Low threshold for repeaT LP/MRI/EEG)

51
Q

What factors may contribute to the worse long-term psychiatric outcomes seen in individuals following encephalitis?

A

▪️ Premorbid factors
▪️ Encephalitis-associated neuronal damage
▪️ Psychological impact of illness experience (e.g., ICU)
▪️ Quality of psychosocial support - over 30% don’t return to work/school

INCREASED SUICIDALITY = IMPORTANCE OF COMMUNITY PSYCHIATRIC FOLLOW-UP

Neuropsychiatric Disorders (30 decks)

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