• Sleep Medicine and Psychophysiology
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• v.14 no.2
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• pp.92-98
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• 2007

Objectives: Obstructive sleep apnea syndrome (OSAS) is the most common form of sleep-disordered breathing and often presents with comorbid depressive symptoms. In this study, we evaluated the relationship between depressive symptoms and sleep parameters as measured by nocturnal polysomnography (NPSG) and simultaneous wrist actigraphy. Methods: Two hundred sixty-four subjects with clinically suspected cases of OSAS underwent one-night polysomnography, while simultaneously wearing a wrist actigraphy device. They also completed two questionnaires；the Epworth Sleepiness Scale-Korean version (ESS-K) and the Beck Depression Inventory (BDI). Of the cases studied, 105 subjects were proven by NSPG to have OSAS without other sleep disorders. NPSG and wrist actigraphy data from the subjects were analyzed. Pearson correlation and paired t-test were used in order to evaluate the relationship between depressive symptoms and sleep-parameters. Results: Mean age of the subjects was $46.1{\pm}13.1$ years. Means of the ESS-K score and BDI scores were $10.9{\pm}4.7$ and $12.8{\pm}8.1$, respectively. NPSG sleep parameters significantly differed from those of wrist actigraphy. There was no correlation found between subjects' respiratory disturbance index (RDI) and BDI scores. When directly comparing sleep parameters between subjects who were more depressed versus subjects who were less depressed, both total sleep time and sleep efficiency were decreased in the more depressed. A correlation between RDI and ESS-K scores was also found in the more depressed group. Conclusions: Although our findings suggest that there is no relationship between RDI and depressive symptoms, there are other significant differences in the sleep parameters between subjects who are more depressed versus those without depression. We recommend that patients with depression should also be evaluated for clinical symptoms of OSAS.

• Sleep Medicine and Psychophysiology
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• v.18 no.1
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• pp.40-44
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• 2011

Narcolepsy is a sleep disorder, which is characterized by excessive daytime sleepiness (EDS) that is typically associated with cataplexy, sleep fragmentation and other REM sleep-related phenomenon such as sleep paralysis and hypnagogic hallucination. Narcoleptic symptoms can be developed from various medical or neurological disorders. A 17-year-old male patient admitted for the evaluation of EDS which started three-month ago. He slept more than 18 hours a day with cataplexy and hypnagogic hallucination. He was obese with body mass index (BMI) of 30.4 kg/$m^2$. After admission he was newly diagnosed to the thyrotoxicosis. T3 391.2 ng/dL (60-181), free T4 4.38 ng/dL (0.89-1.76), TSH <0.01 ${\mu}IU$/mL (0.35-5.5) were measured. His pulse rate ranged 70-90 beats per minute and blood pressure ranged 150/100-120/70 mmHg. Polysomnography revealed many fragmentations in sleep with many positional changes (81 times/h). Sleep onset latency was 33.5 min, sleep efficiency was 47.9%, and REM latency from sleep onset was delayed to 153.6 min. REM sleep percent was increased to 27.1%. Periodic limb movement index was 13.4/h. In the multiple sleep latency test (MSLT), average sleep latency was 0.4 min and there were noted 3 SOREMPs (Sleep Onset REM sleep period) on 5 trials. We couldn't discriminate the obvious sleep-wake pattern in the actigraph and his HLA DQB1 $^*0602$ type was negative. His thyroid function improved following treatment with methimazole and propranolol. Vital sign maintained within normal range. Cataplexy was controlled with venlafaxine 75 mg. Subjective night sleep continuity and PLMS were improved with clonazepam 0.5 mg, but the EDS were partially improved with modafinil 200-400 mg. Thyrotoxicosis might give confounding role when we were evaluating the EDS, though sleep fragmentation was one of the major symptoms of narcolepsy, but enormous amount of it made us think of the influence of thyroid hormone. The loss of sleep-wake cycle, limited improvement of EDS to the stimulant treatmen, and the cataplexy not supported by HLA DQB1 $^*0602$ should be answered further. We still should rule out idiopathic hypersomnia and measuring CSF hypocretin level would be helpful.

• Nuclear Medicine and Molecular Imaging
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• v.41 no.1
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• pp.9-15
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• 2007

Purpose: Repetitive transcranial magnetic stimulation (rTMS) has recently been clinically applied in the treatment of drug resistant depressed patients. There are mixed findings about the efficacy of rTMS on depression. Furthermore, the influence of rTMS on the physiology of the brain is not clear. We prospectively evaluated changes of regional cerebral blood flow (rCBF) between pre- and post-rTMS treatment in patients with drug resistant depression. Materials and Methods: Twelve patients with drug-resistant depression (7 male, 5 female; age range: $19{\sim}52$ years; mean age: $29.3{\pm}9.3$ years) were given rTMS on right prefrontal lobe with low frequency (1 Hz) and on left prefrontal lobe with high frequency (20 Hz), with 20-minute-duration each day for 3 weeks. Tc-99m ECD brain perfusion SPECT was obtained before and after rTMS treatment. The changes of cerebral perfusion were analyzed using statistical parametric mapping (SPM; t=3.14, uncorrected p<0.01, voxel=100). Results: Following areas showed significant increase in rCBF after 3 weeks rTMS treatment: the cingulate gyrus, fusiform gyrus of right temporal lobe, precuneus, and left lateral globus pallidus. Significant decrement was noted in: the precental and middle frontal gyrus of right frontal lobe, and fusiform gyrus of left occipital lobe. Conclusion: Low-frequency rTMS on the right prefrontal cortex and high-frequency rTMS on the left prefrontal cortex for 3 weeks as an add-on regimen have increased and decreased rCBF in the specific brain regions in drug-resistant depressed patients. Further analyses correlating clinical characteristics and treatment paradigm with functional imaging data may be helpful in clarifying the pathophysiology of drug-resistant depressed patients.