Changes of the Video Head Impulse Test Gains by the Directions of Head Rotation at Different Target Distances and Rotation Speeds / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: The conventional instrument for video head impulse test (vHIT) records the movement of the right eye only. The aim of this study was to evaluate the changes in the gain of vHIT results qdue to different directions of head rotation directons at different target distances and rotation speeds. SUBJECTS AND METHOD: Horizontal head impulse was recorded by vHIT in 20 normal subjects. vestibulo-ocular reflex (VOR) gains to the right and left directions were compared at different test conditions. Two different impulses with low (50-150 deg/sec) and high (200-300 deg/sec) peak-head-velocities were tested and the subjects were also instructed to fixate a laser dot on a screen at different distances of 60, 100, and 200 cm. Eye movements were recorded on the right eye. RESULTS: Regardless of the target distances and peak-head-velocities, the VOR gains to the rightward head rotation were significantly greater than those to the leftward head rotation. In more than 85% of normal subjects, vHIT gain to the rightward head rotation was greater than that to the leftward head rotation. Mean gain asymmetries were 2.16-3.33% and the mean interaural vHIT gain differences were 0.04-0.07. CONCLUSION: Regardless of the target distances and peak-head-velocities, the VOR gains to the rightward head rotation were significantly greater than those to the leftward head rotation. Directional asymmetry of VOR gain should be considered when interpreting vHIT results in patients with vestibular disorders.

Causes, Clinical Features and Functional Outcome of Pediatric Stroke

OBJECTIVE: To investigate the changes of causes, clinical features, and functional outcomes in childhood strokes. METHOD: This study included 152 patients, aged from 1 to 18 years, who were diagnosed with stroke and admitted to a tertiary hospital between January 2000 and April 2004. All medical records and neurologic images of the patients were reviewed. A parental questionnaire was used to investigate patients' functional outcomes. These results were compared with those of the previous study performed in the same hospital in 2001. RESULTS: The number of hemorrhagic stroke was 78 (51.3%) and that of ischemic stroke was 74 (48.7%). When compared to the previous study, the incidence of hemorrhagic stroke especially above the age of 10 years decreased and that of ischemic stroke below the age of 10 years increased. The causes of stroke were arteriovenous malformation (AVM, 42.8%), Moyamoya disease (37.5%), vasculitis (5.3%), cardiac disease (3.9%), hematologic disease (2.0%), and undetermined (8.5%). Common clinical features were headache (53.8%), vomiting (43.6%) and loss of consciousness (28.2%) in the hemorrhagic stroke, and hemiparesis (94.6%), headache (35.1%) and speech disorder (31.1%) in the ischemic stroke. 86.0% of the hemorrhagic and 64.8% of the ischemic stroke patients were categorized in the 'good' outcome group. CONCLUSION: The incidence of ischemic stroke increased to the similar level of hemorrhagic stroke. The most common causes were AVM in the hemorrhagic and Moyamoya disease in the ischemic stroke. Most of these patients showed good functional outcome, regardless of the causes of stroke.

Characteristics of Cognitive Dysfunction in Intracerebral Hemorrhagic Patients with Basal Ganglia and Thalamic Lesion

OBJECTIVE: To evaluate the characteristics of cognitive dysfunction in the stroke patients with basal ganglia and thalamic lesion. METHOD: We studied 24 stroke patients ( <3 months after onset) with thalamus or basal ganglia lesion, retrospectively. Patients were divided into 3 groups according to the brain lesion (group 1, basal ganglia; group 2, thalamus; group 3, both area). Results of cognitive function tests including Mini-Mental State Examination, Neurobehavioral Cognitive Status Examination and detailed test of attention, memory and executive function using Computerized Neuropsychological Test were compared between groups. RESULTS: Most of the patients showed abnormal performancein all domains of cognitive function regardless of location of the lesion. Impairment in stroop test and trail making test was prominent, suggesting executive dysfunction. Attention and verbal memory were impaired, too. Group 3 showed most severe cognitive dysfunction in all domains although statistically not significant. There were no significant differences between group 1 and group 2. CONCLUSION: All domains of cognitive function were impaired in basal ganglia or thalamic stroke, especially in executive function. There were no significant differences in cognitive dysfunction between basal ganglia and thalamic groups in this study.

A Case Report of X-linked Recessive Bulbospinal Muscular Atrophy (Kennedy`s Syndrome)

We had 58-year-old-man with chronic lower back pain, progressive whole extremities and facial muscle weakness, dysarthria and recurrent aspiration during swallowing, without any sensory disturbance. His two brothers had similar symptoms from their 6th decade. He had muscle atrophy on tongue, both hand lower leg muscles with some fasciculations. All tendon reflexes were absent without pathologic pyramidal reflex. Nerve conduction studies revealed low median, ulnar, and sural sensory nerve action potential amplitude. On EMG study, there were chronic denervation potentials on most of muscles of extremities. On DNA analysis, there were abnormal expansions of CAG repeats in the androgen receptor gene. We confirmed a X-linked recessive bulbospinal muscular atrophy (Kennedy's syndrome).

Delayed Postanoxic Encephalopathy : Two cases report

Delayed postanoxic encephalopathy causes relapse of cognitive impairment and movement deterioration in a few weeks after clinically complete recovery from initial anoxic or hypoxic insult. Delayed postanoxic encephalopathy is a rare condition, and its clinical symptoms are characterized by abulia, apathy, akinesia, confusion, agitation, parkinsonism, chorea, dystonia and/or progressive neurologic deficits. We reported two distinguished cases caused by carbon monoxide intoxication and mixed respiratory and metabolic lactic acidosis.