Further investigation

Is there anything else you would especially like to know about this patient?

Some of the patient’s negative symptoms seem atypical

• – He tends to talk loudly

• – He speaks in close proximity to people

• – He often has an odd affect and odd prosody of speech

• – In discussions with his family at the initial visit, “he has always been that way”

  • He has had few friends, but has been content

  • He has not exhibited anxiety about missing a clear, distinct peer group

  • After his positive symptoms developed, these premorbid social interaction deficits have remained the same but have been labeled as “negative symptoms” instead of his premorbid personality style

Were these negative symptoms really present since childhood?

• – It is unlikely that these negative schizophrenia symptoms were a 20-year prodrome

• – The patient may have a developmental disorder such as an ASD which predates his first psychotic break

• – He does not meet ASD criteria formally

• – His IQ is likely low-average, e.g., 85–100, but has never been formally tested

• – There are no clear chromosomal abnormality stigmata nor maternal infectious exposure stigmata

• – He is a likeable, straightforward, socially awkward, talkative man

Case outcome: first interim follow-up visits through six months

Clinically continues without change

Risperidone (Risperdal) is lowered to 3 mg/d to avoid long-term movement disorder and metabolic risk, and due to the fact that he has been largely asymptomatic

Later reports an increase in anxiety over interpersonal interactions and states he now has insomnia

There are no re-emergent positive psychotic symptoms

Clonazepam (Klonopin) is increased to 2 mg/d taken at night to cover these anxiety and insomnia symptoms, with good effect

Later, risperidone (Risperdal) is lowered to 2 mg/d without incident

Question

Can traditional BZ sedative–anxiolytics be used as sedative–hypnotics too?

No, these are separate approvals and only sedative–hypnotics should be used to treat insomnia

No, sedative–anxiolytics are less sedating and tend not to promote sleep

Yes, both classes are BZs, which are PAMs at the GABA-A receptor and may promote fatigue, somnolence, and induce sleep

Yes, although off-label, the sedative–anxiolytics are less sedating than the sedative–hypnotics, but increasing the dose of the anxiolytic is often accompanied by increasing sedation and ultimately hypnosis

Case outcome: second interim follow-up visits through 12 months

There is no psychosis but an increase in insomnia is reported again

• – This stresses the patient as he is worrying about his lack of sleep and has the clinical feel of classic, primary insomnia

• – He is more irritable

• – He dislikes doing his usual activities as he is tired and not his usual self

• – He enjoys things less as such

• – He has no other worries outside his pending insomnia every night

Denies depression feelings and reports there are no acute stressful events at home or work

• – There is a possibility that the insomnia is the sentinel symptom of a depressive episode or a third psychotic episode