OBJECTIVETo observe the effects of moxibustion therapy on the improvements of clinical symptom scale score and neuropeptide substance in vascular dementia (VD) and investigate a part of mechanism of moxibustion on Vd.

METHODSEighty-seven cases of VD were divided randomly into a moxibustion group (43 cases) and a western medicine group (44 cases). In moxibustion group, the isolated moxibustion with Typhonium Rhizome was applied to Baihui (BL 20), and suspended moxibustion was used on Shenting (BL 24) and Dazhui (GV 14). In western medicine group, Piracetam tablet was taken orally. After 4-session treatment, the scores in Hasegawa's Dementia Scale (HDS), Mini Mental Status Examination (MMSE) and Activity of Daily Living Scale (ADL) as well as the content of active substances, somatostatin (SS) and arginine vasopressin (AVP) in cerebral spinal fluid relevant with learning and memory were compared with those before treatment.

RESULTSThe total effective rate was 81.4% (35/43) in moxibustion group, which was superior to 63.6% (28/44) in western medicine group (P < 0.01). The scores in HDS, MMSE and ADL after treatment were all improved as compared with those before treatment in two groups (P < 0.05, P < 0.01). The improvements of the scores in MMSE and ADL in moxibustion group were superior to those in western medicine group (both P < 0.05). After treatment, SS and AVP content in cerebral spinal fluid increased remarkably as compared with those before treatment in two groups (all P < 0.01), and SS and AVP levels after treatment in moxibustion group were improved significantly as compared with those in western medicine group (P < 0.05, P < 0.01).

CONCLUSIONMoxibustion therapy is superior to oral administration of western medicine no matter in the improvement of symptom scores or in the regulation of neuropeptide substances relevant with learning and memory, which deserves to be promoted in application.

Aged ; Dementia, Vascular ; cerebrospinal fluid ; therapy ; Female ; Humans ; Male ; Middle Aged ; Moxibustion ; Neuropeptides ; cerebrospinal fluid

Catecholamines ; blood ; cerebrospinal fluid ; metabolism ; Child ; Humans ; Neuropeptides ; blood ; cerebrospinal fluid ; metabolism ; Neurotransmitter Agents ; blood ; cerebrospinal fluid ; metabolism ; Syncope, Vasovagal ; blood ; cerebrospinal fluid ; metabolism ; physiopathology

Cataplexy is one of the most pathognomonic symptoms in narcolepsy. This study was designed to investigate the frequency of the HLA-DQB1 allele and cerebrospinal fluid (CSF) hypocretin levels in Korean narcoleptics with cataplexy as compared with those who do not have cataplexy. Seventy-two narcoleptics were selected based on polysomnography and multiple sleep latency test as well as their history and clinical symptoms at Sleep Disorders Clinic. The patients were divided into a narcolepsy with cataplexy group (n=56) and a narcolepsy without cataplexy group (n=16). All patients were subjected to HLA typing to determine the frequency of DQB1 allele and to spinal tapping to measure the level of CSF hypocretin. In cataplexy-positive patients, as compared with cataplexy-negative patients, the frequency of HLA-DQB1*0602 was found to be significantly high (89.3% vs. 50.0%) (p=0.003). On the other hand, the frequency of HLA-DQB1*0601 was found to be significantly low (0% vs. 43.8%) (p<0.001). In 48 of 56 cataplexy-positive patients (85.7 %), hypocretin levels were decreased (< or =110 pg/mL). However, only 6 of 16 cataplexy-negative patients (37.5%) exhibited a decreased hyopcretin level (p<0.001). The high frequency of HLA-DQB1*0602, low frequency of HLA-DQB1*0601 and low hypocretin levels in cataplexy-positive groups suggest that cataplexy-positive narcolepsy might be an etiologically different disease entity from the cataplexy-negative.
Sleep, REM ; Neuropeptides/*cerebrospinal fluid ; Narcolepsy/cerebrospinal fluid/*genetics ; Middle Aged ; Male ; Intracellular Signaling Peptides and Proteins/*cerebrospinal fluid ; Humans ; HLA-DQ Antigens/*genetics ; Female ; Child ; Cataplexy/cerebrospinal fluid/*genetics ; *Alleles ; Aged ; Adult ; Adolescent

BACKGROUND: Although leptin and its principal mediators, neuropeptide Y (NPY) and -melanocyte stimulating hormone (MSH) are postulated to play a pivotal role in the energy balance in experimental animals, the physiologic roles of leptin and its molecular targets are not fully identified in cases of human obesity. METHODS: The subjects consisted of 16 obese women (mean BMI 35.6 kg/m2) before and after weight loss that was induced by a 2 week-very low caloric diet (800 kcal/day) and 14 normal weight women (who had a mean BMI of 20.4 kg/m2). We evaluated the plasma and cerebrospinal fluid (CSF) leptin, NPY and alpha -MSH levels and their relationship in normal weight and obese women. Additionally, changes of these peptides during a negative energy balance (800 kcal/day) were assessed in causes of human obesity. RESULTS: Obese subjects exhibited a 6.3-fold higher plasma leptin level (21.9+/-1.2 vs 3.5+/-0.4 ng/mL, p<0.05) and a 2.8-fold higher CSF leptin level (0.29+/-0.02 vs 0.10+/-0.01 ng/mL, p<0.05) compared to control subjects. The CSF/plasma leptin ratio in normal weight subjects was 2.3-fold higher than that in obese subjects. After a weight loss in obese subjects, the plasma leptin level decreased by 40% and the CSF level decreased by 51%. The CSF/plasma leptin ratio was slightly lower than the baseline level. There was a positive linear correlation between CSF and plasma leptin level at the baseline in obese subjects (r= 0.74, p<0.05) and a positive logarithmic correlation in normal weight subjects and in obese subjects after a weight loss (r= 0.66, p<0.05). The BMI negatively correlated with the CSF/plasma leptin ratio (r=-0.86, p<0.05) in any subjects. Neither the baseline plasma levels nor the baseline CSF levels of NPY were different between the normal weight subjects and obese subjects. After a weight loss the CSF NPY level decreased significantly compared to the baseline values in obese subjects. The alpha -MSH levels in plasma and CSF did not differ significantly from controls in obese subjects at the baseline or after a weight loss. The baseline CSF leptin level neither correlated with the baseline CSF NPY level nor the baseline CSF alpha -MSH level. CONCLUSION: These results demonstrated that the efficiency of leptin delivery to the CNS is reduced in human obesity and that the CNS leptin uptake involves the combination of saturable and unsaturable mechanisms. A marked reduction in the CSF leptin levels compared to the plasma level after a weight loss in obese subjects can be a potent stimulus for the body to regain weight. In contrast to the results that were observed in experimental animals, the CSF NPY and alpha -MSH did not differ from the controls in human obesity and there was no significant correlation between the CSF leptin and CSF of these neuropeptides. This could have resulted from leptin resistance in cases of human obesity although the mechanisms for this resistance remain to be determined.
alpha-MSH ; Animals ; Cerebrospinal Fluid* ; Diet ; Female ; Humans ; Leptin* ; Neuropeptide Y ; Neuropeptides ; Obesity ; Peptides ; Plasma* ; Weight Loss*

To observe the expression of drebrin in the distal cerebrospinal fluid contacting neurons (dCSF-CNs) of rats with chronic constriction injury (CCI) of sciatic nerve by immunofluorescence technique, male Sprague-Dawley rats were randomly divided into three groups: control group, sham surgery group and CCI group. The behavior of rats was scored. After choleratoxin subunit B-conjugated horseradish peroxidase (CB-HRP, 3 muL) was injected into the lateral cerebroventricle to trace dCSF-CNs, the expression of drebrin was observed in the dCSF-CNs through immunofluorescence double staining and laser scanning confocal microscopy technique. The results showed that only the pain threshold of CCI group was decreased. The dCSF-CNs were clearly displayed in three groups. No drebrin expression was observed in the control and sham groups. In CCI group, drebrin was markedly expressed in intracytoplasm. It is suggested that the technique displaying dCSF-CNs with immunofluorescence is successful and the dCSF-CNs are possibly involved in the transmission of nociceptive information under the neuropathic pain state.
Animals ; Cerebrospinal Fluid ; Constriction, Pathologic ; Male ; Neuralgia ; metabolism ; Neurons ; metabolism ; Neuropeptides ; metabolism ; Pain Threshold ; Rats ; Rats, Sprague-Dawley ; Sciatic Nerve ; injuries

OBJECTIVETo analyze the clinical diagnosis and treatment process of narcolepsy and epilepsy co-existence, and thereby to improve awareness of such cases.

METHODThe clinical manifestations of 2 cases were observed, and video-electroencephalogram (VEEG), multiple sleep latency tests (MSLT) were performed. Hypocretin 1 level in cerebrospinal fluid was examined in one case.

RESULTThe onset of disease of case one was started with epilepsy with myoclonic seizure. After half a year, catalepsy induced by emotion especially laughing and excessive daytime sleepiness appeared. MSLT was positive and hypocretin 1 level decreased. Narcolepsy-cataplexy was definitely diagnosed in this case. Valproate was given and seizure was controlled completely, but the excessive daytime sleepiness was aggravated. Combination of valproate, methylphenidate and clomipramine treatment improved the symptoms of narcolepsy and the patient was still free of epileptic seizures. The onset symptoms of case 2 were catalepsy and excessive daytime sleepiness. MSLT was positive. The treatment was ineffective because of bad compliance. After 2 years, episodes of impairment of consciousness with automatism occurred. VEEG showed slow waves and spikes in right temporal area. Complex partial seizure was determined. Oxcarbazepine was used and then the patients became seizures free, but the symptoms of narcolepsy were still obvious.

CONCLUSIONComorbidity of narcolepsy and epilepsy is a rare phenomenon. Clinical symptoms, predisposing factor, VEEG and MSLT can help diagnosis and differential diagnosis. The antiepileptic drugs might aggravate drowsiness. Based on therapy of epilepsy by using antiepileptic drugs, low dosage of central nervous system stimulants might improve the drowsiness and catalepsy symptoms of narcolepsy.

Adolescent ; Anticonvulsants ; administration & dosage ; therapeutic use ; Brain Waves ; physiology ; Central Nervous System Stimulants ; administration & dosage ; therapeutic use ; Child ; Comorbidity ; Diagnosis, Differential ; Electroencephalography ; Epilepsies, Myoclonic ; diagnosis ; drug therapy ; physiopathology ; Epilepsy ; diagnosis ; drug therapy ; physiopathology ; Humans ; Intracellular Signaling Peptides and Proteins ; cerebrospinal fluid ; Male ; Narcolepsy ; diagnosis ; drug therapy ; physiopathology ; Neuropeptides ; cerebrospinal fluid ; Orexins ; Polysomnography ; Sleep Stages ; physiology ; Treatment Outcome