No abstract available.
Hypophysectomy*

13 cases of atypical meningioma were analysed, which were proven surgically S.N.U.H. for 3 years since Marach,1979. CT findings of atypical meningioma were central low density in 8 cases, large cyst in 4 cases, calcifiedmass in 1 case and non-specific scalp mass in 1 case. All the CT findings of atypical meningioma werepathologically proven as follows. Central low density was tissue necrosis in 5 cases, multiple cyts in 2 cases andhemorrhage in a case. Large cyst was arachnoid cyst in all 4 cases. Calcified mass was massive calcium depositionon tumor. Non-specific scalp mass on temporal area was meningioma involving soft tissue, bone and dura.
Arachnoid ; Bone and Bones ; Calcium ; Meningioma ; Necrosis ; Scalp

The pathogenesis and mechanism of obstructive sleep apnea (OSA) has been under investigation for over 25 years, but its etiology and mechanism remains elusive. Skeletal (maxillary and/or mandibular hypoplasia or retrodisplacement, inferior displacement of hyoid) and soft tissue (increased volume of soft tissue, adenotonsillar hypertrophy, macroglossia, thickened lateral pharyngeal walls) factors, pharyngeal compliance (increased), pharyngeal muscle factors (impaired strength and endurance of pharyngeal dilators and fixators), sensory factors (impaired mechanoreceptor sensitivity, impaired pharyngeal dilator reflexes), respiratory control system factors (unstable respiratory control) and so on facilitate collapse upper airway. Therefore, OSA may be a heterogeneous disorder, rather than a single disease entity and various pathogenic factors contribute to the OSA varies person to person. As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep disordered breathing.
Compliance ; Humans ; Hypertrophy ; Macroglossia ; Mechanoreceptors ; Pharyngeal Muscles ; Sleep Apnea Syndromes ; Sleep Apnea, Obstructive*

Pulmonary Fibrosis*

We report a 37-year-old man with adrenomyeloneuropathy who presented as progressive gait disturbance. He had spastic paraparesis, hyperreflexia with Babinski's signs, a sensory level at T-4, and loss of the vibration sense in the legs. No adrenal insufficiency was noted. There were frontal white matter abnormalities but no cervical spinal lesions on MRI. A nerve conduction study showed distal axonal neuropathy predominantly in the lower extremities. The plas-ma level of the saturated very long chain fatty acids was elevated. (J Korean Neurol Assoc 19(4):431~434, 2001)
Adrenal Insufficiency ; Adrenoleukodystrophy* ; Adult ; Axons ; Fatty Acids ; Gait ; Humans ; Leg ; Lower Extremity ; Magnetic Resonance Imaging ; Neural Conduction ; Paraparesis, Spastic ; Reflex, Abnormal ; Reflex, Babinski ; Vibration

BACKGROUND: Cerebral white matter lesions(WMLs), such as leukoaraiosis, may be related to damage from cerebral ischemia and may also be associated with the degenerative process. The apolipoprotein E (APOE) 4 allele is a risk factor for degenerative diseases, such as Alzheimer`s disease, and ischemic brain damage through acceleration of atherosclerosis. No study has been performed regarding WMLs and APOE genotype in Korea. We investigated the association between WMLs and APOE among Koreans. METHODS: Brain MRI was performed in 225 subjects(ages 61 to 85 years) without neuropsychiatric disease randomly selected from the Ansan Health Cohort Study. WMLs observed on 225 MRI scans were rated in terms of severity by 2 raters. All study subjects underwent APOE genotyping. RESULTS: WMLs were observed in 109(48.4%) of subjects. In the subjects with WMLs, the distribution of APOE genotypes was 0.9% for epsilon 2/epsilon 2, 11.0% for epsilon2/epsilon3, 1.8% for epsilon2/epsilon4, 61.5% for epsilon3/epsilon3, 22.9% for epsilon3/epsilon4, and 1.8% for epsilon4/epsilon4, respectively. The distribution of APOE genotypes did not differ between subjects with and without WMLs. CONCLUSION: These data suggest that there is no association between WMLs and APOE genotypes in Koreans.
Acceleration ; Alleles ; Apolipoproteins E ; Apolipoproteins* ; Atherosclerosis ; Brain ; Brain Ischemia ; Cohort Studies ; Genotype ; Gyeonggi-do ; Korea ; Leukoaraiosis ; Magnetic Resonance Imaging ; Risk Factors

No abstract available.
Constriction, Pathologic* ; Stents*

BACKGROUND: The dominant innervation of airway smooth muscle is parasympathetic fibers which are carried in the vagus nerve. Activation of these cholinergic nerves releases acetylcholine which binds to M3 muscarinic receptors on the smooth muscle causing bronchocontraction. Acetylcholine also feeds back onto neuronal M2 muscarinic receptors located on the postganglionic cholinergic nerves. Stimulation of these receptors further inhibits acetylcholine release, so these M2 muscarinic receptors act as autoreceptors. Loss of function of these M2 receptors, as it occres in animal models of hyperresponsiveness, leads to an increase in vagally mediated hyperresponsiveness. However, there are limited data pertaining to whether there are dysfunctions of these receptors in patients with asthma. The aim of this study is to determine whether there are dysfunction of M2 muscarinic receptors in asthmatic patients and difference of function of these receptors according to severity of asthma. METHODS: We studied twenty-seven patients with asthma who were registered at Pulmonology Division of Korea University Hospital. They all met asthma criteria of ATS. Of these patients, eleven patients were categorized as having mild asthma, eight patients moderate asthma and eight patients severe asthma according to severity by NAEPP Expert Panel Report 2(1997). All subjects were free of recent upper respiratory tract infection within 2 weeks and showed positive methacholine challenge test(PC 20<16mg/ml). Methacholine provocation tests performed twice on separate days allowing for an interval of one week. In the second test, pre-treatment with the M2 muscarinic receptor agonist pilocarpine(180µg) through inhalation was performed before the routine procedures. RESULTS: Eleven subjects with mild asthma and eight aubjects with moderate asthma showed significant increase of PC20 from 5.30±5.23mg/ml(mean±SD) to 20.82±22.56mg/ml(p=0.004) and from 2.79±1.5mg/ml to 4.67±3.53mg/ml(p=0.012) after pilocarpine inhalation, respectively. However, in the eight subjects with severe asthma significant increase of PC20 from 1.76±1.50mg/ml to 3.18±4.03mg/ml(p=0.161) after pilocarpine inhalation was not found. CONCLUSION: In subjects with mild and moderate asthma, function of M2 muscarinic receptors was normal, but there was a dysfunction of these receptors in subjects with severe asthma. These results suggest that function of M2 muscarinic receptors is different according to severity of asthma.
Acetylcholine ; Asthma ; Autoreceptors ; Humans ; Inhalation ; Korea ; Methacholine Chloride ; Models, Animal ; Muscle, Smooth ; Neurons* ; Pilocarpine ; Pulmonary Medicine ; Receptors, Muscarinic* ; Respiratory Tract Infections ; Vagus Nerve

No abstract available.
Heart Ventricles* ; Hemodynamics*

BACKGROUND: The changes of cerebral hemodynamics during syncope have not been fully evaluated. We investigated the changes in the cerebral blood flow velocity during head-up tilt test (HUT) using transcranial Doppler ultrasonogra-phy (TCD) in patients with neurocardiogenic syncope or presyncope. METHODS: Thirty-three patients with a history of recurrent syncope or presyncope of unknown origin were evaluated using HUT for 30 minutes (baseline tilt test), fol-lowed by an infusion of intravenous isoproterenol if needed. Systolic (SV) and diastolic velocities (DV) of middle cere-bral artery were continuously monitored by TCD. Positive responses were defined as presyncope or syncope with hypotension, bradycardia, or both. RESULTS: Five patients had positive responses during baseline tilt and 14 patients dur-ing the isoproterenol infusion. During the baseline tilt test, there was a 86 +/- 23% drop in DV and a 41 +/- 34% drop in SV in patients with positive responses, and mean changes in those were less than 10% in patients with negative responses (p=.00, p=.00). During the HUT with an isoproterenol infusion, the TCD showed an 80 +/- 18% drop in diastolic velocity in patients with positive responses, and a 47 +/- 10% drop in patients with negative responses (p=.00), However, the change in systolic velocity did not differ. TCD showed three patterns during positive responses: loss of all flow, loss of end-diastolic flow, and a decrease in diastolic velocity. Loss of consciousness occurred in patients with loss of all flow or end-diastolic flow during positive responses. CONCLUSIONS: TCD shows different patterns of changes in cerebral hemody-namics during HUT. TCD can be used to investigate the pathophysiology of neurocardiogenic syncope.
Arteries ; Blood Flow Velocity ; Bradycardia ; Hemodynamics ; Humans ; Hypotension ; Isoproterenol ; Syncope* ; Syncope, Vasovagal ; Ultrasonography, Doppler, Transcranial ; Unconsciousness