We report the clinical features in one patients with episodic positional vertigo and apogeotropic direction changing horizontal positional nystagmus that does not fatigue, beating to the right with the head turned to the left and beating to the left with the head turned to the right. This syndrome probably represents a horizontal semicircular canal variant of benign positional vertigo. Free-floating debris and Cupula attached debris in one horizontal semicircular canal may explain many of the clinical and oculographic findings.
Fatigue ; Head ; Humans ; Nystagmus, Physiologic ; Semicircular Canals ; Vertigo*

Myoclouns is a complicated and poorly-understood phenomenon caused by many pathological conditions. Myoclonus which is triggered by sensory stimuli has been termed reflx myoclonus and divided into cortical, reticular and spinal types depending on the generator sites. Segmental myoclonus of spinal origin consists of synchronous rhythmical jerks confined to a group of muscles supplied by either one segment or several contiguous segments of the spinal cords. We present two cases of spinal reflex myoclonus. One was 50 years old female who showed complex myoclonic jerks involving the abdominal wall and paraspinal muscibs resembling 'belly dance'. The other was 26 years old male who showed intermittent synchronous upper cervical axial muscle contractions. In both cases, jerks were increased with certain stimuli, but disappeared during sleep. They showed normal EEGs and absence of enhancement of SSEPS.
Abdominal Wall ; Adult ; Electroencephalography ; Female ; Humans ; Male ; Middle Aged ; Muscle Contraction ; Muscles ; Myoclonus* ; Reflex ; Spinal Cord

We report a 18 years old man of brainstem encephalitis with acute ataxia, areflexia and gaze evoked vertical and horizontal nystagmus which is mimicking Miller Fisher syndrome. He had evidences of both peripheral neuropathy in nerve conduction studies and a brainstem encephalitis in MR findings. The possible relationship of the Miller Fisher syndrome and brainstem encephalitis are discussed with brief review of literature.
Adolescent ; Ataxia ; Brain Stem* ; Encephalitis* ; Humans ; Miller Fisher Syndrome* ; Neural Conduction ; Nystagmus, Pathologic ; Peripheral Nervous System Diseases

High dose intravenous immunoglobulin (IVIg) therapy can improve the clinical course of several immune mediciated diseases. We evaluated clinical effects and side effects of IVIg in Guillain-Barre syndrome (GBS). 19 Patients with GBS were studied prospectively in a placebo-controlled trial. 11 Patients were received high dose IVIg (400mg/kg for 5 days) and controls received only conservative treatment. The disability scores using modified Rankin scores before and after treatment of each group were compared. Four weaks later, mean Rankin Score of IVIg group was 2.5 + 0.7 and control group was 3.3+ 0.5which showed significant difference(p<0.05). There were no serious advers effer of promote early improvement with safety in acute phase of Guillan-Barre syndrome.
Guillain-Barre Syndrome* ; Humans ; Immunization, Passive* ; Immunoglobulins* ; Immunoglobulins, Intravenous ; Prospective Studies

OBJECTIVES: To analyze the motor evoked potential (MEP) responses to a degree of voluntary contraction and stimulus intensity and to suggest the standardized optimal stimulation for MEP responses. METHODS: MEPs induced by a cortical stimulation were elicited at the thenar muscles in 15 normal subjects during the rest and gradual voluntary contraction, using the 10% of maximal voluntary contraction (MVC), 30%, 50%, and MVC. During rest and during each contraction, excitability threshold at rest (RET) and at contraction (CET) were determined. Consecutive stimuli were applied, according to the intensity of ratio increment (110% to 150% of excitation threshold). RESULTS: The RET showed a remarkable decrease (57.1+/-8.2% --> 47.4+/-8.7%) after the voluntary contraction (P<0.05). Shortening of latency reached the saturation level with 10% of MVC, irrespective of stimulus intensity. Amplitude reached a saturation level at 30% of MVC with 62.7% intensity of maximal output, which is equal to 140% intensity of its CET, and to 110% of RET. MEP amplitude at rest and at 10% of MVC were influenced by the excitation threshold (P<0.05), but those at above 30% of MVC were not related. CONCLUSION: The procedure for optimal facilitation for the MEPs is as follows; for minimal latency of MEPs, minimal contraction (10% of MVC) with RET intensity is enough. For maximal amplitude of MEPs, moderate contraction (30% MVC) with 110% intensity of RET is adequate.
Evoked Potentials, Motor ; Muscles ; Transcranial Magnetic Stimulation*

OBJECTIVES: This study was designed to measure sympathetic skin responses (SSRs) following magnetic stimulation of the cervicothoracic spine and to evaluate its clinical usefulness. METHODS: Fifteen healthy volunteers who had no dysautonomic symptoms or signs and a patient with C6 spinal cord transection participated in this study. To evoke SSR, we stimulated the C7 spinous process (SP) and T2 SP with 90 mm circular coil (Magstim 200). We recorded the sensory nerve action potential (SNAP) from the right middle finger to ascertain whether the C7 dorsal root was depolarized by the C7 SP stimulation. The same stimulation intensity by which SNAP had been obtained was used to evoke the SSR by the C7 and T2 SP stimulation. The recording of SSR was done in both palms. SNAP was recorded by the magnetic stimulation on the C7 SP in all subjects. RESULTS: By the C7 SP stimulation, the latency of SSR was 1.35 sec in the right palm, 1.33 sec in the left palm and by the T2 SP stimulation, the latency was 1.24 sec, 1.23 sec in order. The right-left difference was not found by each SP stimulation, but the latency of SSR by the T2 SP stimulation was faster than that by the C7 SP stimulation (p<0.01). The latency difference of C7 and T2 SP stimulation was 0.11 sec in the right palm, 0.10 sec in the left palm. In a case of C6 cord transection, SSR was evoked neither by the right median electric stimulation, nor by the C7 SP magnetic stimulation. However, SSR was successfully evoked by the T2 SP stimulation. CONCLUSION: We believe that the latency difference of C7 and T2 spinous process stimulation reflects the central conduction time of SSR.
Action Potentials ; Electric Stimulation ; Fingers ; Healthy Volunteers ; Humans ; Skin* ; Spinal Cord Injuries ; Spinal Nerve Roots ; Spine

OBJECTIVE: To evaluate the prevalence and prosthetic uses of lower extremity amputee in one Korean county. METHOD: We asked community health worker in Hwa Sung Goon to recruit lower extremity amputees. We contacted them by telephone and tried to know their prosthetic uses, adaptations and their behavior about prosthetic usage. Also, we recruited all lower extremity amputees in Hwa Sung Goon. RESULTS: In Hwa Sung Goon, the prevalence of lower extremity amputees was 35 persons per 100,000. 93.8% of them had prostheses, more than half of them were not satisfied with their prosthetic use. For last 10 years, they changed into new prosthesis per 2.3 years. CONCLUSION: In one Korean county, the prevalence of lower extremity amputees was 0.03%. Most of them used their prosthesis, and walked independently. Their compliances with rehabilitative intervention were very low.
Amputees* ; Community Health Workers ; Humans ; Lower Extremity* ; Prevalence ; Prostheses and Implants ; Telephone

Expression of protein kinase C-delta (PKC delta) is up-regulated by apoptosis-inducing stimuli. However, very little is known about the signaling pathways that control PKC delta gene transcription. In the present study, we demonstrate that JNK stimulates PKC delta gene expression via c-Jun and ATF2 in response to the anticancer agent doxorubicin (DXR) in mouse lymphocytic leukemia L1210 cells. Luciferase reporter assays showed that DXR-induced activation of the PKC delta promoter was enhanced by ectopic expression of JNK1, c-Jun, or ATF2, whereas it was strongly reduced by expression of dominant negative JNK1 or by treatment with the JNK inhibitor SP600125. Furthermore, point mutations in the core sequence of the c-Jun/ATF2 binding site suppressed DXR-induced activation of the PKC delta promoter. Our results suggest an additional role for a JNK signaling cascade in DXR-induced PKC delta gene expression.
Activating Transcription Factor 2/*physiology ; Animals ; Anthracenes/pharmacology ; Antibiotics, Antineoplastic/*pharmacology ; Apoptosis ; Cell Line, Tumor ; Doxorubicin/*pharmacology ; Mice ; Mitogen-Activated Protein Kinase 8/*physiology ; Mutation ; Promoter Regions, Genetic ; Protein Kinase C-delta/genetics/*metabolism ; Proto-Oncogene Proteins c-jun/antagonists & inhibitors/*physiology ; Signal Transduction/physiology ; Transcription, Genetic

Warfarin is widely used for the prevention of cerebral infarction, especially in patients with atrial fibrillation or artificial valve. Although hemorrhagic problems are well known, skin necrosis is a rare complication. Failures of early diagnosis or management may lead to serious results. We report a case of skin necrosis induced by warfarin therapy.
Anticoagulants ; Atrial Fibrillation ; Cerebral Infarction ; Early Diagnosis ; Humans ; Necrosis ; Skin ; Warfarin

BACKGROUND: Surgical hepatic inflow obstructions such as the Pringle Maneuver (PM) or hepatic vascular exclusion (HVE) can reduce bleeding during hepatic resection, but ischemia/reperfusion injury of the liver and systemic hemodynamic changes are also inevitable during and after PM or HVE. Nitric oxide plays a pivotal role in ischemia/reperfusion injury. We evaluated hemodynamic changes and changes of nitric oxide during liver ischemia/reperfusion injury excluding the effects of intestinal ischemia. METHODS: Liver ischemia was induced by clamping of the portal triad, infrahepatic and suprahepatic inferior vena cava for 90 minutes. To exclude the effects of intestinal ischemia during liver ischemia, portal and iliac venous blood was bypassed to the jugular vein using a pump. Hemodynamic parameters and nitric oxide were measured serially; before and during ischemia, and after reperfusion. RESULTS: Mean arterial blood pressure (MAP) was well-maintained during ischemia, but after reperfusion, MAP, cardiac output (CO) and stroke volume (SV) significantly decreased (35 - 40, 30 - 40 and 30%, respectively) postischemia. Compared to preischemia, systemic vascular resistance and heart rate did not change after reperfusion. Pulmonary vascular resistance and mean pulmonary arterial blood pressure significantly increased (220 - 250% and 60 - 70%) after reperfusion. Nitric oxide (NO) did not change until 20 minutes after reperfusion, but after 40 minutes reperfusion, NO significantly decreased (20%) compared to preischemia. CONCLUSIONS: After 90 minutes warm liver ischemia/reperfusion causes hypotension induced by decreased CO and SV. Increased PVR seems to be the cause of decreased CO and SV. NO-SVR interaction does not seem to be the cause of postreperfusion hypotension.
Arterial Pressure ; Cardiac Output ; Constriction ; Heart Rate ; Hemodynamics* ; Hemorrhage ; Hypotension ; Ischemia ; Jugular Veins ; Liver* ; Nitric Oxide* ; Reperfusion ; Stroke Volume ; Vascular Resistance ; Vena Cava, Inferior