They suggested that a lack of neuronal connections had contributed to the occurrence of symptomatic narcolepsy. 9 performed MRI tractography on a patient with symptomatic narcolepsy following surgery for craniopharyngioma. Although CSF hypocretin level was not measured in the present case, our patient was thought to have functional impairment of hypocretin projection rather than damaged hypocretin-containing neurons as a result of surgery, resulting in symptomatic narcolepsy. 8 The present case showed a vascular lesion in the left thalamus, but not in the hypothalamus, as a sequelae of surgery. 7 In contrast, a few symptomatic narcoleptic cases of paramedian thalamic infarctions have been reported with hypocretin levels within a normal range and impairment of hypocretin projection has been suggested to cause narcolepsy. Similar to idiopathic narcolepsy with cataplexy, reduced CSF hypocretin levels are often seen in symptomatic narcolepsy with various etiologies. Therefore, the patient was diagnosed with symptomatic narcolepsy. Narcoleptic symptoms in our patient appeared two years after surgical removal of Rathke’s cleft cyst. Nishino and Kanbayashi 3 suggested that narcolepsy onset should be within three years if the causative diseases are acute neurological conditions. 6 To be diagnosed as symptomatic narcolepsy, the signs and symptoms of narcolepsy should be temporally associated with the underlying neurological process. These findings are compatible with the current diagnostic criteria for narcolepsy without cataplexy based on the third edition of the International Classification of Sleep Medicine. The preceding nocturnal PSG showed no sleep problems associated with daytime sleepiness. On MSLT, mean sleep latency was 2.6 minutes and SOREMPs within 15 minutes of sleep onset were recorded in three out of five nap trials. In our patient, excessive daytime sleepiness and/or daytime lapses into sleep appeared within two years after surgical removal of Rathke’s cleft cyst. Modafinil was prescribed with a dose up to 400 mg/day, but was not effective in reducing excessive daytime sleepiness. Based on the findings of both overnight PSG and MSLT, she was diagnosed with narcolepsy. On MSLT, mean sleep latency was 2.6 minutes and sleep-onset REM periods less than 15 minutes after sleep onset were detected in 3 of 5 nap trials.
A total of 10 episodes of hypopnea were recorded (apnea hypopnea index = 1.2/hr) and the respiratory disturbance index was 3.3/h. The sleep onset REM period (SOREMP) was not observed.
Sleep architecture was normal and was composed of 6.1% of non-rapid eye movement (NREM) stage 1, 48.4% of NREM stage 2, 26.5% of NREM stage 3 and 18.4% of REM stage sleep. 4), sleep latency was 3.5 minutes and total sleep time was 521 minutes with a normal percentage (18.4%) of REM stage sleep. On the night of polysomnography (PSG) ( Fig. To eliminate the possibility of nonconvulsive seizures, video-EEG monitoring was performed, and did not show interictal or ictalepileptiform discharges. Follow up brain MRI showed the focal lesion in the anterior-superior-medial part of the left thalamus had decreased in the horizontal field but was slightly extended longitudinally. There were no focal signs on neurologic examination and laboratory findings were in the normal range. At the time, the antiepileptic drug regimen was not changed because the seizures were relatively well controlled. She denied having cataplexy, sleep paralysis or hypnagogic hallucinations. In November 2013, when she was 20 years old, she admitted having excessive daytime sleepiness for the past 3 years.