Transcript Investigating Psychosis

Investigating Psychosis
R.J.Hackett
This presentation concerns:
1) investigation of acute psychoses that may arrive
acutely on an adult or adolescent psychiatry ward
or EIT and
2) investigation of chronic or recurring psychoses,
often with negative symptoms. These are patients
who one often takes over, but in whom you start to
question the cause.
I have not covered late-onset psychoses in patients
with Parkinson’s disease or degenerative disorders.
Traditional Psychiatric Approach
• Psychiatric diagnoses are syndromes –
symptoms that occur together.
• Underlying causes are not exhaustively
sought.
• Treatments are symptomatic.
• Psychological theories of cause are widely
held.
Neurological Approach
• Underlying medical causes of syndromes are
always investigated.
• Extensive search for pathological cause.
• Extensive use of medical tests.
• Where possible treatment directed at
underlying cause.
Schizophrenia
A syndrome of positive psychotic symptoms:
• Auditory hallucinations (often)
• Delusions
• Patient often lacks insight (this can change
with treatment).
• With or without negative symptoms (apathy,
blunt affect, poverty of thought).
Considerations in Investigations
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Cost of the test?
Yield?
Cost of failing to identify treatable cause?
How common are the treatable causes?
Current standard admission work up
for new psychosis
• Urine for drugs.
• FBC, biochemistry, LFT, Thyroid, bone profile.
• Vitamin B12, serum folate (a recognised cofactor in psychosis).
Infective causes
• HIV
• Neurosyphilis
Recognised causes of syndrome of
schizophrenia
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Toxic causes: recreational
Autoimmune brain disease (5-10%?).
Medication.
Metabolic disorders.
Infection.
NB. Structural brain lesions (tumour, trauma,
stroke, MS plaque) very rarely cause psychosis.
Examination
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Full neurological examination.
History must include medications.
Brief test of anterograde memory.
History of stable learning difficulty or of
cognitive decline.
• Mental state examine for catatonic features.
Toxic Causes
Recreational drugs: Urine drug screen.
• Cannabis
• Amphetamine
• Cocaine
• Psilocybin (august to 1st frost)
Autoimmune causes
Features to look out for:
• Impaired recall for onset/admission.
• Impaired anterograde memory.
• Facial dyskinesia.
• Catatonic symptoms.
• Personal/family history autoimmune disease.
Note autoimmune causes can (often) be present
without any of these features.
Autoimmune causes
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NMDA receptor antibodies.
Voltage gated potassium channel antibodies.
Anti GAD antibodies.
Hashimoto’s encephalopathy (anti-thyroid
peroxidase antibodies)
• SLE.
Further evidence for CNS inflammation in
psychosis can be obtained from:
• CSF – oligoclonal bands, lymphocytosis.
• MR brain – high signal on FLAIR sequences.
Infective causes
• HIV
• Neurosyphilis
Special situations
• Psychosis immediately after childbirth and
other physiological stresses.
• Often accompanied by confusion.
Consider urea cycle disorders (plasma
ammonia↑, urinary orotic acid, plasma urea↓)
Special situations
Psychosis accompanying epilepsy
• Post-ictal psychosis (history typical, no
available test
If ictal or interictal consider:
• Porphyria
(other metabolic causes usually associated with
learning difficulties)
Limbic encephalitis
• full syndrome acute psychosis + amnesia +
seizures.
• Usually middle age or older.
• Occult malignancy (most commonly lung)
• Other neurological deficits common (eg periferal
neuropathy)
• Paraneoplastic antibody screen, imaging screen
for malignancy.
Summary: investigations for acute
psychosis
• Routine Bloods inc. B12, folate.
• Urine drug screen
If negative
• Antibodies NMDA receptor/voltage gated K
channel, GAD.
• Thyroid peroxidase antibodies, ANA.
• MR with flair sequences
• Plasma ammonia
Summary: investigation of acute
psychosis
• HIV/syphilis serology – depends on risk
factors.
• Consider CSF for oligoclonal bands.
Chronic psychosis – identifiable causes
• Consider metabolic disorders.
• Adult onset inborn errors of metabolism
(IEM).
• Many of the lethal infantile IEMs can present
in attenuated forms from adolescence until
middle age.
• Psychosis (sometimes on its own) is common
presentation.
• Prevalence is unknown because they are
never looked for.
• Rarely diagnosed ≠ Rare. i.e.probably many
unidentified cases in psychiatric populations.
• Some are treatable.
Investigation of chronic psychosis
Consider metabolic disorder if:
• Evidence of progressive cognitive decline.
• Ataxia.
• Movement disorder esp. dystonia (i.e. don’t
just blame antipsychotics!).
• Spasticity.
Metabolic disorders to consider
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Nieman Pick disease type C
Juvenile metachromatic leukodystrophy
Adult-0nset Tay Sach disease.
Fabry disease
Alpha mannosidosis
Cerebrotenindous xanthomatosis
Adrenoleukodystrophy
• Homocystinuria
cystathionine beta synthase def.
methylene tetrahydrofolate reductase def.
• Wilson’s disease.
• Neiman Pick disease type C
cognitive impairment, vertical gaze palsy,
ataxia. Test: Oxysterols (blood)
Lysosomal storage disease
Test: white cell enzymes
• Juvenile metachromatic leukodystrophy
psychosis for years →spasticity , ataxia.
• Tay Sach’s disease.
Ataxia, spasticity, LMN signs, dystonia.
• Fabry disease.
painful neuropathy, young stroke.
• Alpha mannosidosis.
pre-existing LD, ataxia, spastic, dysmorphic.
Test: very long chain fatty acids (blood)
• Adrenoleukodystrophy.
spasticity, seizures
Test: plasma cholestanol
• Cerebrotendinous xanthomatosis
tendon xanthomas, cataract, spasticity, ataxia.
Test: plasma amino acids + urinary amino acids
(homocysteinuria) + urinary organic acids.
• Cystathionine β synthase def.
marfanoid, young stroke, ataxia.
• Methylenetetrahydrofolate reductase def.
spasticity, young stroke, perif. Neuropathy.
Test: Plasma copper + caeruloplasmin
• Wilson’s disease
Summary: tests for chronic psychosis
• MR brain (for space occupying lesion or
leukodystrophy)
• Oxysterols
• White cell enzymes
• Plasma amino acids
• Urinary amino acids
• Urinary organic acids
• Very long chain fatty acids
• Plasma cholastanol
• Serum copper + caeruloplasmin