No abstract available.
Sarcoma, Endometrial Stromal*

The time course of recovery in vestibular neuritis varies between individuals. The aim of this study was to identify the predictors for the early or late recovery of vestibular neuritis. The inclusion criteria were patients 1) who had an acute onset of vertigo lasting at least 24 hours, 2) with a horizontal-torsional unidirectional spontaneous nystagmus, and 3) with a canal paresis of 20% or more on the bithermal caloric tests. The primary endpoint for this study was an early or late recovery of vestibular neuritis as a dependent variable. A functional level scale was used to define the late recovery (5 or more points) at seven days after the symptom onset. The secondary endpoint was the duration of hospitalization. One hundred twenty eight patients met the inclusion criteria for this study, and among them, 71 patients had an early recovery. Multiple logistic regression analysis showed that diabetes mellitus was the only independent significant variable for the prediction of a late recovery of vestibular neuritis. In addition, the diabetes mellitus was a predicting variable for long duration of hospitalization. Diabetes mellitus was a predictor for a late recovery of vestibular neuritis.

BACKGROUND: Steroid-responsive encephalopathy associated with subacute thyroiditis has, to our knowledge, not been reported previously. CASE REPORT: A 49-year-old woman was found collapsed and brought to our institution with decreased mentality, dysarthria, and gait disturbance. Brain magnetic resonance imaging and angiography were normal but blood tests revealed thyroid-autoantibody-negative thyrotoxicosis. Results of a (99m)technetium-pertechnetate scan were compatible with the thyrotoxic phase of subacute thyroiditis. 14-3-3 proteins were detected in cerebrospinal fluid. Her mental status began to improve from the day following steroid administration. Recurrent encephalopathy was found 2 months after the initial admission, which was also effectively treated with steroid. CONCLUSIONS:We speculate that steroid-responsive recurrent encephalopathy associated with subacute thyroiditis is a subtype of Hashimoto's encephalopathy, and consider that steroid treatment should not be delayed in suspected patients.
14-3-3 Proteins ; Angiography ; Brain ; Brain Diseases ; Dysarthria ; Female ; Gait ; Hashimoto Disease ; Hematologic Tests ; Humans ; Magnetic Resonance Imaging ; Middle Aged ; Thyroiditis, Subacute ; Thyrotoxicosis

Papillary eccrine adenoma, first described by Rulon and Helwig in 1977, is a rare benign adnexal neoplastn. It is usually present as a solitary dermal nodule on the distal extremities. It has characteristic histopathological findings, consisting of dilated ducts that contain eosinophilic secretions and are associated with intralummal papillations. On the basis of histological and histochemical studies it is believed to be an adnexal neoplasm of possible eccrine differentiation. We report two recent cases of papillary eccrine adenomas occuring in two young male patients without subjective symptoms who had firm dermal nodules on the extremities.
Adenoma* ; Eosinophils ; Extremities ; Humans ; Male

A cerebral infarction involving the nodulus usually produce contralateral lateropulsion and ipsilateral spontaneous nystagmus to the lesion. Here, we report a case of atypical isolated nodular infarction showed ipsilateral lateropulsion and contralateral spontaneous nystagmus to the lesion with a normal head impulse test. A right-handed 70-year-old man developed sudden vertigo with an unsteady gait. Neurologic examination revealed spontaneous left-beating nystagmus with a torsional component. He also displayed imbalance of walking and axial lateropulsion to the right side. Head impulse test was normal. Magnetic resonance imaging indicated acute infarction in the right nodulus on diffusion-weighted images.
Cerebral Infarction ; Gait Disorders, Neurologic ; Head ; Infarction ; Magnetic Resonance Imaging ; Neurologic Examination ; Vertigo ; Vestibular Neuronitis ; Walking

BACKGROUND AND PURPOSE: Sudden cardiac death is one of the leading causes of death in patients with myotonic dystrophy type 1 (DM1). It has been proposed that a prolonged QT interval is associated with sudden cardiac death in several neurological diseases, including multiple system atrophy, idiopathic Parkinson's disease, and diabetic autonomic neuropathy. However, analyses of the corrected QT (QTc) interval in DM1 patients are rare in the literature. The purposes of this study were to determine the association between the QT interval and DM1, and the affecting factors. METHODS: Thirty-nine patients diagnosed with DM1 through genetic testing were enrolled. The QTc interval (calculated using Bazett's formula: QTc=QT/radicalRR) was compared between these patients and 39 normal healthy controls. The clinical and laboratory factors affecting QTc interval in the patient group were investigated. RESULTS: The QTc interval was significantly longer in the DM1 group (411.2+/-44.7 msec, mean+/-SD) than in the normal control group (355.6+/-20.6 msec). Intragroup analysis revealed that a prolonged QTc interval in DM1 patients was associated with being female and older, having a longer disease duration, and exhibiting abnormal electrocardiography findings. CONCLUSIONS: The higher incidence of sudden cardiac death in the DM1 population is associated with the observed prolonged QTc interval in those patients.
Cause of Death ; Death, Sudden, Cardiac ; Diabetic Neuropathies ; Electrocardiography ; Female ; Genetic Testing ; Humans ; Incidence ; Multiple System Atrophy ; Myotonic Dystrophy ; Parkinson Disease

The coronary vasospasm has usually been readily reversible by sublingual, intravenous or intracoronary nitroglycerin. Relief of spasm, either spontaneous or following nitrate therapy, results in reperfusion. Occurence of ventricular tachyarrhythmia during release of coronary spasm is attractive as a possible cause of sudden death because of significant proportion of sudden death victims do not have acute myocardial infarction. Recently, we experienced a 36 year old man who developed spontaneous coronary vasospasm, and the patients suffered from repetitive reperfusion ventricular tachyarrhythmia, and died suddenly in spite of administration of isosorbide dinitrate, lidocaine and several trials of cardioversion and cardiopulmonary resuscitation, and we report.
Adult ; Cardiopulmonary Resuscitation ; Coronary Vasospasm ; Death, Sudden* ; Electric Countershock ; Humans ; Isosorbide Dinitrate ; Lidocaine ; Myocardial Infarction ; Nitroglycerin ; Reperfusion* ; Spasm ; Tachycardia*

Skeletal muscles are known to have tolerance to ischemia, but a prolonged ischemia can cause damage to muscular tissues. The ischemia-reperfusion injury results from the oxygen free radicals released by leucocytes and formed by the reaction of hypoxanthine and xanthine oxidase. Superoxide dismutase (SOD), one of major antioxidant enzymes ocurring in the various tissues of the body metabolizes or scarvanges the oxygen free radicals. Although many studies reported difference in tolerance to ischemia and reperfusion between white and red muscles, some other investigators failed in finding such difference. The present study was performed to examine effects of graded periods of ischemia and reperfusion on the cellular ultrastructure and activity of SOD in white and red muscles. The Sprague-Dawley rats (200~250 g) were used as experimental animals. Under pentobarbital (50 mg/kg IP) anesthesia, incision was made on lower abdomen and left common iliac artery was occluded by means of a vascular clamp for 2, 4 and 6 hour (hrs). Thereafter, the superficial portion of mid-belly of anterior tibial muscle and soleus muscles were excised at 0, 24 and 72 hrs after onset of reperfusion. The specimens were sectioned into slices, 2 mm in length, 1 mm in width and thickness. Some specimens were prepared for electron microscopic observation and others for determination of SOD activity by using antihuman Cu, Zn- and Mn-SOD antibodies. The results obtained were as follows. 1. In anterior tibial muscle, areas with loose electron-density and dilated cristae were observed in the mitochondria immediately after 2 hrs of ischemia, while widened intermyofibrillar spaces and dilated cisternae of sarcoplasmic reticulum were seen after 2 hrs and 24 hrs reperfusion. When subjected to 2 hrs ischemia and 72 hrs reperfusion, no significant change was found in the cellular ultrastructure. 2. In soleus muscle, electron density was loose in the matrix of mitochondria immediately after 2 hrs of ischemia, while cisternae of sarcoplasmic reticulum were dilalated after 2 hrs of ischemia and 24 hrs reperfusion. Following 2 hrs of ischemia and 72 hrs reperfusion, the electron microscopic findings were similar to those of normal rats. 3. The changes in cellular ultrastructure were more prominent in both the 4 hrs and 6 hrs ischemia groups, in which degree of ultrastructural changes were proportional to duration of reperfusion. 4. In anterior tibial muscle, trace or weak immunoreactivities of Cu, Zn- and Mn-SOD were seen, whereas trace immunoreactivity of Cu, Zn-SOD and trace or weak immunoreactivity of Mn-SOD were observed in soleus muscle. 5. The immunoreactivities of Cu, Zn- and Mn-SOD were not altered in 2 hrs ischemic and 72 hrs reperfused group, while they were increased slightly in 2 hrs ischemic and 24 hrs reperfused group. 6. In both muscles, the activity of SOD increased following 4 hrs or 6 hrs ischemia and 24 hrs or 72 hrs reperfusion. The changes in immunoreactivity of Mn-SOD were not different between two muscles, whereas immunoreactivity of Cu, Zn-SOD were higher in anterior tibial muscle. Consequently, it is suggested that significant ischemia reperfusion injuries are produced after 4~6 hrs ishemia followed by 24 hrs or 72 hrs reperfusion, that anterior tibial muscle is more susceptible to ischemic reperfusion injury and that the ischemic-reperfusion injury is closely related with activity of SOD.
Abdomen ; Anesthesia ; Animals ; Antibodies ; Free Radicals ; Humans ; Hypoxanthine ; Iliac Artery ; Ischemia* ; Mitochondria ; Muscle, Skeletal ; Muscles* ; Oxygen ; Pentobarbital ; Rats* ; Rats, Sprague-Dawley ; Reperfusion Injury ; Reperfusion* ; Research Personnel ; Sarcoplasmic Reticulum ; Superoxide Dismutase ; Xanthine Oxidase

To present a case of cauda equina syndrome (CES) caused by chronic inflammatory demyelinating polyneuropathy (CIDP) which seemed clinically similar to Charcot-Marie-Tooth disease type1 (CMT1). CIDP is an immune-mediated polyneuropathy, either progressive or relapsing-remitting. It is a non-hereditary disorder characterized by symmetrical motor and sensory deficits. Rarely, spinal nerve roots can be involved, leading to CES by hypertrophic cauda equina. A 34-year-old man presented with low back pain, radicular pain, bilateral lower-extremity weakness, urinary incontinence, and constipation. He had had musculoskeletal deformities, such as hammertoes and pes cavus, since age 10. Lumbar spine magnetic resonance imaging showed diffuse thickening of the cauda equina. Electrophysiological testing showed increased distal latency, conduction blocks, temporal dispersion, and severe nerve conduction velocity slowing (3 m/s). We were not able to find genetic mutations at the PMP 22, MPZ, PRX, and EGR2 genes. The pathologic findings of the sural nerve biopsy revealed thinly myelinated nerve fibers with Schwann cells proliferation. We performed a decompressive laminectomy, intravenous IgG (IV-IgG) and oral steroid. At 1 week after surgery, most of his symptoms showed marked improvements except foot deformities. There was no relapse or aggravation of disease for 3 years. We diagnosed the case as an early-onset CIDP with cauda equine syndrome, whose initial clinical findings were similar to those of CMT1, and successfully managed with decompressive laminectomy, IV-IgG and oral steroid.
Adult ; Biopsy ; Cauda Equina ; Charcot-Marie-Tooth Disease* ; Congenital Abnormalities ; Constipation ; Foot Deformities ; Humans ; Immunoglobulin G ; Laminectomy ; Low Back Pain ; Magnetic Resonance Imaging ; Nerve Fibers, Myelinated ; Neural Conduction ; Polyneuropathies* ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ; Polyradiculopathy* ; Recurrence ; Schwann Cells ; Spinal Nerve Roots ; Spine ; Sural Nerve ; Urinary Incontinence

No abstract available.
Carcinoma, Transitional Cell* ; Female ; Ovary