Comparison of Catecholamine Levels in Hemiplegic Patients with and without Reflex Sympathetic Dystrophy

OBJECTIVE: To determine whether the cause of sympathetic dysfunction is due to increased regional sympathetic outflow or receptor supersensitivity to circulating catecholamines in the pathogenesis of reflex sympathetic dystrophy in hemiplegia. METHOD: Ten hemiplegic patients with reflex sympathetic dystrophy were instructed to refrain from smoking or using caffeine and alcohol, and medications that influence catecholamine metabolism were witheld for 24 hours before blood sampling. Patients with cardiovascular disease, diabetes or abnormal liver and renal function tests were excluded from the study. Patients with a history of sympathectomy were also excluded. Ten hemiplegic patients without reflex sympathetic dystrophy served as the control group. Both groups of patients rested in supine position in a quiet room for 30 minutes. A needle with heparin cap was inserted into the dorsal venous arches of the affected hand and patients rested for another 20 minutes, after which blood was drawn through the heparin cap. The blood samples were assayed using high-performance liquid chromatography (HPLC) and norepinephrine and epinephrine were detected electrochemically. 24 hour urine was collected during rest and vanillylmandelic acid (VMA) and metanephrine were also detected using HPLC. RESULTS: The mean plasma norepinephrine levels were 1.05 0.24 ng/ml and 0.47 0.06 ng/ml in RSD affected and unaffected groups respectively, and the plasma norepinephrine level was significantly higher in the patient group with reflex sympathetic dystrophy (p<0.05). The plasma epinephrine and 24-hour urine VMA and metanephrine levels were not significantly different in two groups. CONCLUSION: These results may support a hypothesis of increased regional sympathetic outflow in the pathogenesis of reflex sympathetic dystrophy in hemiplegia.

Activated Protein C Resistance and Factor V Leiden Mutation in Patients with Arterial Ischemic Stroke

BACKGROUND: In the western hemisphere, resistance to activated protein C (APCR) is the most common risk factor for venous thromboembolic disease. A one-point mutation in the coagulation factor V that renders it APCR is found in more than 90% of patients with APC-resistant venous thrombosis. In Hispanic and Caucasian patients with arterial ischemic stroke, the prevalence of APC-R is approximately 10%. To determine the prevalence of APC resistance and its causative factor V mutation (Arg 506 Gln) in Koreans, we screened a group of Korean ischemic stroke patients. METHODS: We evaluated 60 Korean patients with arterial ischemic stroke diagnosed by either magnetic resonance neu-roimaging, conventional angiogram, or both, after 2 weeks of symptom onset. The mean age of the subjects was 59.2 years (13-82 years). APC resistance was expressed as a ratio of the activated partial thromboplastin time (aPTT) with and without adding APC to the subject's plasma. The presence of the factor V Leiden (Arg 506 Gln) mutation was determined by a direct polymerase chain reaction-based assay on peripheral blood leukocytes. RESULTS: Only one patient (n=1/60, 1.6%) had APC resistance and none were found to have the factor V Leiden (Arg 506 Gln) mutation. CONCLUSIONS: APCR and the factor V Leiden mutation do not seem to be a significant genetic risk factor for arterial ischemic stroke in Koreans.

Comparison of Perfusion- and Diffusion-weighted MRI in Acute Ischemic Stroke

BACKGROUND: Perfusion imaging (PI) of magnetic resonance imaging (MRI) uses the signal loss that occurs during dynamic tracking of the first pass of intravenous paramagnetic contrast agent. Then different hemodynamic measurements can be calculated and displayed as perfusion maps. Diffusion-weighted imaging (DWI) measures diffusional movement of water molecules within the brain and it can identify acute ischemic injury or cytotoxic edema. We evaluated clinical usefulness of PI and DWI in acute ischemic stroke. METHODS: Fifteen patients with clinical diagnosis of acute cerebral infarction were imaged with PI, DWI, and magnetic resonance angiogram (MRA) including FLAIR within 24 hours after onset. Comparisons were made between infarct volumes measured by DWI and PI using the parameters including relative mean transit time (rMTT) map, relative cerebral blood volume (rCBV) map, and relative cerebral blood flow (rCBF) map. RESULTS: Two patterns were found. rMTT map in PI lesion is larger than in the DWI lesion (n=7/15), and rMTT map in PI lesion is the same size or smaller than in DWI lesion (n=8/15). The former pattern was shown in cases with severe stenosis or occlusion of the major cerebral artery (MCA, PCA, or ICA) on MRA. The majority of latter pattern was lacunes (n=6/8). Also, we found presence of infarction cores surrounded by hypoperfused areas in rMTT map in acute largearterial territorial infarction. CONCLUSIONS: Perfusion- and Diffusion- weighted MRIs may be useful in differentiating large-arterial territorial infarction from lacunes.