Paraproteinemia potentially causes peripheral neuropathy via an unknown underlying pathogenetic mechanism. We report a case of pathologically proven amyloid neuropathy with AL amyloidosis with an IgA kappa light chain, which was initially diagnosed as neuropathy associated with monoclonal gammopathy of undetermined significance. This case indicates that in cases of neuropathy with paraproteinemia, the other potential causes should be excluded by appropriate means, especially pathological evaluations.
Amyloid Neuropathies ; Amyloidosis* ; Immunoglobulin A* ; Monoclonal Gammopathy of Undetermined Significance ; Paraproteinemias* ; Peripheral Nervous System Diseases ; Polyneuropathies*

Acute hemorrhagic leukoencephalopathy is a rare condition associated with the influenza virus, but the role of influenza in this condition has not been clarified. We experienced a patient with influenza A and B virus co-infection who initially presented mild gastrointestinal symptoms and rapidly progressed to coma. Magnetic resonance imaging showed severe brain edema and multiple intracranial hemorrhagic lesions. The patient was treated with oseltamivir and corticosteroid, and her clinical course improved without neurological sequelae.
Brain Edema ; Coinfection* ; Coma ; Herpesvirus 1, Cercopithecine ; Humans ; Influenza, Human* ; Leukoencephalopathies* ; Magnetic Resonance Imaging ; Orthomyxoviridae ; Oseltamivir

Acute hemorrhagic leukoencephalopathy is a rare condition associated with the influenza virus, but the role of influenza in this condition has not been clarified. We experienced a patient with influenza A and B virus co-infection who initially presented mild gastrointestinal symptoms and rapidly progressed to coma. Magnetic resonance imaging showed severe brain edema and multiple intracranial hemorrhagic lesions. The patient was treated with oseltamivir and corticosteroid, and her clinical course improved without neurological sequelae.
Brain Edema ; Coinfection* ; Coma ; Herpesvirus 1, Cercopithecine ; Humans ; Influenza, Human* ; Leukoencephalopathies* ; Magnetic Resonance Imaging ; Orthomyxoviridae ; Oseltamivir

BACKGROUND: Despite the lack of supporting evidence, intravenous heparin is still given frequently in the treatment of cerebral ischemia. However, there is only one study for the use of heparin nomogram in ischemic stroke or TIA. We evaluated the usefulness of a patient-specific, as well as weight-based, nomogram for the intravenous heparin in patients with ischemic stroke or TIA. METHODS: From Sep. 2004 to Sep. 2005, we recruited ischemic stroke patients treated according to the specifically designed heparin nomogram. The therapeutic range (TR) of activated partial thromboplastin time (aPTT) and dose adjustment were specified as a ratio of each patient's baseline aPTT. The first time to achieve TR (TR-time), to exceed therapeutic threshold (TE-time) and the fraction of time in TR (total time in TR/total time of heparin use, %) were analyzed. RESULTS: A total of 45 patients were included. The mean fraction of time in TR was 72.7+/-14.4%. Although TR-time and TE-time did not differ according to the use of bolus injection, the fraction of first aPTT at 6 hours after start of infusion in TR was higher with bolus than without bolus (84.8 vs. 58.3, p<0.05). CONCLUSIONS: Our nomogram could achieve and maintain therapeutic heparin anticoagulation effectively. Initial bolus injection may be better to achieve therapeutic anticoagulation more rapidly.
Brain Ischemia ; Heparin* ; Humans ; Nomograms* ; Partial Thromboplastin Time ; Stroke*

BACKGROUND AND PURPOSE: Hyperglycemia after acute ischemic stroke (AIS) is associated with poor outcomes. However, there is no consensus as to the optimal method for glycemic control. We designed an insulin infusion protocol for aggressive glucose control and investigated its efficacy and safety. METHODS: We applied our protocol to patients within 48 hours after AIS or transient ischemic attack (TIA) with an initial capillary glucose level of between 100 and 399 mg/dL (5.6-22.2 mmol/L). An insulin solution comprising 40 or 50 U of human regular insulin in 500 mL of 5% dextrose was administered for 24 hours. Capillary glucose was measured every 2 hours and the infusion rate was adjusted according to a nomogram with a target range of 80-129 mg/dL (4.4-7.2 mmol/L). Changes in glucose and overall glucose levels during insulin infusion were analyzed according to the presence of diabetes or admission hyperglycemia (admission glucose >139 mg/dL or 7.7 mmol/L) by the generalized estimating equation method. RESULTS: The study cohort comprised 115 consecutive patients. Glucose was significantly lowered from 160+/-57 mg/dL (8.9+/-3.2 mmol/L) at admission to 93+/-28 mg/dL (5.2+/-1.6 mmol/L) during insulin infusion (p<0.05). Laboratory hypoglycemia (capillary glucose <80 mg/dL or 4.4 mmol/L) occurred in 91 (71%) patients, 11 (10%) of whom had symptomatic hypoglycemia. Although glucose levels were significantly lowered and maintained within the target range in all patients, overall glucose levels were significantly higher in patients with diabetes or hyperglycemia (p<0.05). CONCLUSIONS: Our insulin-infusion protocol was effective in glycemic control for patients with AIS or TIA. Further modification is needed to improve the efficacy and safety of this procedure, and tailored intervention should be considered according to glycemic status.
Capillaries ; Cohort Studies ; Consensus ; Glucose ; Humans ; Hyperglycemia ; Hypoglycemia ; Insulin ; Ischemic Attack, Transient ; Nomograms ; Stroke