No abstract available.
Cleft Lip* ; Congenital Abnormalities*

No abstract available.
Scalp* ; Skin* ; Transplants*

OBJECTIVES: We investigated impulsivity and sensation seeking of pathological gambling, comparing with alcoholism and normal group. METHODS: 36 pathological gamblers, who were diagnosed by DSM-IV criteria, were compared with 31 alcoholism group and 26 healthy normal group with Barratt impulsivity scale and Zuckerman sensation seeking scale. RESULTS: 1) Pathological gamblers appeared to have much more impulsivity than alcoholism group or normal group. In respect to sensation seeking, no significant differences were founded among three groups. 2) Pathological gamblers tend to have more non-planning impulsivity, cognitive impulsivity, and motor impulsivity than alcoholic group. Comparing with normal group, pathological gamblers tend to have more non-planning impulsivity and motor impulsivity, but not in cognitive impulsivity. 3) There were no differences in three sub-scales including of thrill seeking, experience seeking and disinhibition out of four sub-scales of sensation seeking scale, among three groups. However, Boredom susceptibility was higher in pathological gamblers than alcoholics and normal group. CONCLUSIONS: These results suggested that personality of pathological gambler is most impulsive and boredom susceptible, which indicates that pathological gamblers is more serious pathological clinical disorder than alcoholism.
Alcoholics ; Alcoholism* ; Boredom ; Diagnostic and Statistical Manual of Mental Disorders ; Gambling* ; Humans ; Impulsive Behavior* ; Sensation

Raeder's syndrome, or Raeder's paratrigeminal syndrome, is a painful Horner's syndrome characterized by unilateral head pain, oculosympathetic paralysis (miosis, ptosis) and anhydrosis over the forehead with otherwise normal facial sweating. We report two cases of Raeder's syndrome whose cause had not been found despite of intensive investigation and one case associated with nasopharyngeal tumor. The first case had a headache, miosis, ptosis but had not cranial nerve palsy. The second case had a unilateral facial headache, oculosympathetic paralysis, aoydrosis of forehead and sensory change in the ipsilateral ophthalmic division of the trigeminal nerve. The third case had a headache, miosis, ptosis, anhydrosis of forehead and sensory change in the whole territory of the trigeminal nerve.
Cranial Nerve Diseases ; Forehead ; Headache ; Horner Syndrome ; Miosis ; Paralysis ; Sweat ; Sweating ; Trigeminal Nerve

No abstract available.

OBJECTIVE : We investigated the relationship between the severity of the disease and the abnormality of some ocular movements in parkinson's disease. BACKGROUND: Disorders of eye movements have been described in diseases of the basal ganglia for over a century and ocular motor deficits of the saccadic and pursuit system have been reported in parkinsonian patients. METHOD : We studied the electro-oculography of the eye tracking and saccadic movement in 26 patients (11 males, 15 females) with Parkinson's disease. The severity of the disease was divided into two groups by Hoehn & Yahr(H-Y) staging, H-Y stage 1, 2(group A) and H-Y stage 3, 4 (Group B). Some patients antiparkinsonian drugs of L-dopa, dopamine agonist and anticholinergics. RESULT : The velocity of smooth pursuit and the velocity and latency of saccade were calculated and compared between two groups. Eye tracking test revealed decreased pursuit velocity leading to catch-up saccades, but normal phase relationship between eye and target movement, while saccadic eye movement had increased latency. These results showed more profound severity in more advanced stages of the disease. CONCLUSION : We suggest that ocular movement be often chosen as a simple but relevant example of general motor function, as well as criteria for staging of Parkinson's disease and basal ganglia play significant role in ocular movement.
Basal Ganglia ; Cholinergic Antagonists ; Dopamine Agonists ; Eye Movements ; Humans ; Levodopa ; Male ; Parkinson Disease* ; Pursuit, Smooth ; Saccades

We evaluated the effect of carbamazepine-controlled release (CR) on the cognitive function. By using monotherapy study, we investigated the effects of carbamazepine on cognitive function in 10 epileptic patients and 17 normal controls. The evaluations were conducted before and one and six months after therapy using neuropsychological batteries(BUSCHKE SELECTIVE REMINDING TEST BSRT, REY OSTERRIETH COMPLEX FIGURE TEST ROCFT, CONCENTRATION ENDURANCE TEST d2 test, REY VISUAL DESIGN LEARNING TEST RVDLT, FINGER TAPPING TEST). In the patients treated with carbamazepine-CR monotherapy, follow up studies were made in one and six months later, respectively. It was found that the cognitive function determined in the three tests(consistent long-term retrieval : one item of BSRT, d2 test, and ROCFT : P 0.05). The mean anticonvulsant blood levels on the day of cognitive function tests were 6.48mg/ml (SD=l. 87) and 6.53mg /ml (SD=l.97) in one and six months respectively. This study showed carbamazepine-CR monotherapy had an adverse effect on the cognitive function.
Carbamazepine ; Fingers ; Follow-Up Studies ; Humans ; Learning

Inositol 1,4,5-trisphosphate receptors (InsP3Rs) modulate Ca2+ release from intracellular Ca2+ store and are extensively expressed in the membrane of endoplasmic/sarcoplasmic reticulum and Golgi. Although caffeine and 2-aminoethoxydiphenyl borate (2-APB) have been widely used to block InsP3Rs, the use of these is limited due to their multiple actions. In the present study, we examined and compared the ability of caffeine and 2-APB as a blocker of Ca2+ release from intracellular Ca2+ stores and Ca2+ entry through store-operated Ca2+ (SOC) channel in the mouse pancreatic acinar cell. Caffeine did not block the Ca2+ entry, but significantly inhibited carbamylcholine (CCh)-induced Ca2+ release. In contrast, 2-APB did not block CCh-induced Ca2+ release, but remarkably blocked SOC-mediated Ca2+ entry at lower concentrations. In permeabilized acinar cell, caffeine had an inhibitory effect on InsP3-induced Ca2+ release, but 2-APB at lower concentration, which effectively blocked Ca2+ entry, had no inhibitory action. At higher concentrations, 2-APB has multiple paradoxical effects including inhibition of InsP3-induced Ca2+ release and direct stimulation of Ca2+ release. Based on the results, we concluded that caffeine is useful as an inhibitor of InsP3R, and 2-APB at lower concentration is considered a blocker of Ca2+ entry through SOC channels in the pancreatic acinar cell.
Acinar Cells ; Animals ; Boron Compounds ; Caffeine ; Calcium ; Carbachol ; Inositol 1,4,5-Trisphosphate Receptors ; Membranes ; Mice ; Reticulum

Lacune is small infarct located in the deeper part of the brain and developed by occlusion of small branch of the large cerebral arteries. It occupies 10-30% of infarction in western countries but 53.1% in our study. We investigated 181 cases of lacunar infarction confirmed by clinical features and neuroimaging study. We analyzed lacunar stroke into 13 groups of symdrome based on the clinical features. The frequent lacunar syndromes were pure motor stroke (35.4%), sensori-motor stroke (26.5%), ataxic hemiparesis (11.6%), and pure sensory stroke (6.1%). The frequent sites for lacune were pons (25.4%), corona radiata (24.9%), and thalamus (18.2%). The major contributing risk factors were hypertension (65.8%) and diabetes (19.3%). The incidence of multiple lacune was 67.4%. The determining factor for clinical presentation of lacune was not the size of lesion but the location of lesion.
Brain ; Cerebral Arteries ; Hypertension ; Incidence ; Infarction ; Neuroimaging ; Paresis ; Pons ; Risk Factors ; Stroke ; Stroke, Lacunar* ; Thalamus

Ataxic hemiparesis is a stroke syndrome in which the main features are unusual combination of weakness and cerebellar-like ataxia involving the limb on the same side. We describe an analysis of 17 patients with ataxic hemiparesis who underwent magnetic resonance imaging or computed tomography. Ten patients had lacunar infarction in the contralateral pons. In six, lesions were found in the contralateral thalamus and the posterior limb of internal capsule. In one patient, infarct was located in the contralateral midbrain, They showed different clinical manifestations depending on the sites of lesion. This study may suggest that variable sites of lesion can cause ataxic hemiparesis and different clinical manifestations.
Ataxia ; Extremities ; Humans ; Internal Capsule ; Magnetic Resonance Imaging ; Mesencephalon ; Paresis* ; Pons ; Stroke ; Stroke, Lacunar* ; Thalamus