SummaryNarcolepsy type 1 is characterised by an increase in body weight after disease onset, frequently leading to obesity. It was suggested that this weight gain may be counteracted by treatment with sodium oxybate. We here provide longitudinal body mass index data of patients with narcolepsy type 1 after starting treatment with sodium oxybate, compared with patients in whom treatment with modafinil was initiated. Eighty-one individuals with narcolepsy type 1 fulfilled the entry criteria for this retrospective study: 59 had newly started treatment with sodium oxybate and 22 had newly started modafinil. Gender-specific differences between both treatment groups were compared using Student's t tests and mixed effect modeling.Patients using sodium oxybate lost weight, with a mean body mass index decrease were predictors for body mass index decrease. In conclusion, treatment with sodium oxybate is associated with a body mass index reduction in narcolepsy type 1, whereas modafinil treatment is not. This effect is most pronounced in those who already have a higher baseline body mass index. K E Y W O R D Sweight loss, central nervous system stimulants, hydroxybutyrates, hypersomnia, dyssomnias

Background. In this study, we have investigated whether intrathecal (i.t.) lidocaine administration is accompanied with changes of cerebrospinal fluid (CSF) prostaglandin E 2 (PGE 2) levels. Methods. Rats were anaesthetized for i.t. implantation of a triple-lumen spinal loop dialysis catheter. CSF changes in PGE 2 after i.t. injection of saline, 400, or 1000 mg of lidocaine were measured. The impact of i.t. pretreatment with 5 mg MK801 (N-methyl-D-aspartate glutamate antagonist) or 10 mg SC76309A (COX-2 inhibitor) was also investigated. CSF dialysates for measurement of PGE 2 were collected for 4 h. During the whole procedure, motor and sensory blocks were evaluated. A separate group receiving i.t. lidocaine 400 mg (without dialysate sampling) was assessed for mechanical (Von Frey) and radiant heat pain. Results. PGE 2 levels increased to 400% of baseline and remained elevated for 90-120 min after i.t. lidocaine at both doses. Pretreatment with SC76309A and MK801 attenuated this increase. A 40 min period of enhanced pain response was observed after Von Frey filament stimulation during and after sensory and motor block recovery. Conclusions. I.T. lidocaine (400 or 1000 mg) increases PGE 2 levels in the CSF for 90-120 min along with a transient period of mechanical hyperalgesia after sensory and motor block recovery.

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