Narcolepsy and hypersomnolence — structured clinical viva

This is narcolepsy type 1 until proven otherwise: EDS plus classic cataplexy, hypnagogic hallucinations with insight, and occupational risk. “Conversion” and “psychosis” are mislabels until the sleep diagnosis is confirmed. Immediate priorities: driving safety, sleep-medicine work-up, and targeted wake/cataplexy therapy — not depot antipsychotics for sleep-bound phenomena.[1][2]

1. Hierarchy. Probable NT1; residual MDD; occupational/driving risk. Exclude insufficient sleep, OSA, sedating drugs, seizures/syncope, secondary hypothalamic disease if indicated.[1][2]

2. Discriminators. Cataplexy = atonia + preserved consciousness + emotional trigger. Hypnagogic hallucinations = sleep-edge, often with insight — not first-rank schizophrenia by default.[2][1]

3. Mechanism. Selective orexin/hypocretin neuron loss; low CSF hypocretin-1 supports NT1; REM atonia pathways intrude into wake as cataplexy.[6][1]

4. Investigations. Adequate sleep first; PSG then MSLT (classic: mean latency ≤8 min with ≥2 SOREMPs); CSF hypocretin when available/needed; HLA supportive only.[3][1]

5. Treatment. Behavioural naps and schedule. EDS: modafinil often 100–200 mg oral morning, titrate toward 200–400 mg/day with BP/psychiatric monitoring (product info). Cataplexy: sodium oxybate controlled protocol (no alcohol/sedatives) and/or antidepressant anticataplectics. European/AASM frameworks guide agent choice.[4][5][7][8]

6. Safety and psychiatry. Temporary driving stop per rules; document; treat mood without assuming SSRI fixes sleep attacks; avoid unnecessary antipsychotics for hypnagogic phenomena.[5][1]