In order to determine the extent to which specific forms of glomerulonephritis (GN) contribute to the pool of crescentic GN, renal tissues from 17 crescentic GN patients were examined with special attention to glomerular and interstitial neutrophil infiltration. Renal tissues from five normal kidneys served as normal controls. Renal biopsy tissues from five patients with postinfectious GN in which crescent formation was not observed were also examined as disease controls. The patients were put into both three groups according to immunofluorescence findings and two groups according to the active or inactive phase of the crescents: group 1 with anti-glomerular basement membrane crescentic GN, one case; group 2 with immune complex crescentic GN, ten cases; and group 3 with pauci-immune crescentic GN, six cases. Four of the nine individuals tested were positive for anti-neutrophil cytoplasmic antibody (44.4%). Glomerular and interstitial neutrophil infiltrations were prominent in both the active and inactive phase groups, compared to normal controls (p<.05). Glomerular neutrophil infiltration was significantly prominent in the active phase group, compared to the inactive phase group (p<.001). In both the active and inactive phase groups, interstitial neutrophil infiltration was prominent, compared to disease control groups (p<.05). These results support the concept of the participation of periglomerular leukocytes in the renal tissue damage of crescentic GN, although the role of neutrophils was not examined.
Adult ; Aged ; Female ; Follow-Up Studies ; Glomerulonephritis/pathology* ; Glomerulonephritis/immunology ; Glomerulonephritis/classification ; Human ; Kidney Glomerulus/pathology* ; Kidney Glomerulus/immunology ; Male ; Middle Age ; Nephritis, Interstitial/pathology* ; Nephritis, Interstitial/immunology ; Neutrophils/physiology*

A 38-year-old woman, affected by chronic myeloid leukemia, received a BMT from his HLA identical brother. A mild acute graft-versus-host disease (GVHD) developed during the first month after the BMT. A typical clinical and electrophysiological feature of myasthenia gravis (MG) developed 3 months after the BMT requiring medication with pyridostigmine and steroids. Laboratory findings including acetylcholine receptor antibody and other autoantibodies were negative. MG is a well-characterized autoimmune disease which, on rare occasions, is also diagnosed as chronic GVHD after BMT. We report a first case of MG during an acute GVHD period. Since the patient had a myasthenic symptom during an acute GVHD period and no evidence of antibody mediated autoimmunity, this is likely to be an immune complication of acute GVHD. (J Korean Neurol Assoc 19(1):60~61, 2001
Acetylcholine ; Adult ; Autoantibodies ; Autoimmune Diseases ; Autoimmunity ; Bone Marrow Transplantation* ; Bone Marrow* ; Female ; Graft vs Host Disease ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Myasthenia Gravis* ; Pyridostigmine Bromide ; Siblings ; Steroids

BACKGROUNDS: Recently, the cases with transient neurologic deficit and brain MRI abnormalities similar to hypertensive encephalopathy or eclampsia were reported in the organ transplanted patients, during the administration of cyclosporine with the hypothesis as "capillary lack syndrome". But in addition to cyclosporine, other immunosuppressive agents as cytabine and ant-lymphocyte globulin(ALG) may induce similar transient neurologic manifestations such headache, seizure, altered mental state and change of signal intensities in brain MRI. METHODS AND CASES: 11 patients who had suffered form hematologic disorder were included in the study. The patients were presented with a reversible transient neurologic manifestations and brain MRI abnormalities during administration of various immunosuppressant,. We analysed neourologic symptoms and signs, anatomic localizations and laboratory findings. RESULTS: The underlying hematologic disorder were severe aplastic anemia acute lymphocyte leukemia, multiple myeloma, chronic myelocytic leukemia and acute myelocytic leukemia. The cyclosporine was prescribed in six. ALG in three, idarubicin in two and prednisolone in one patient. The accompanied neurologic symptoms and sign were seizure(11/11), visual disturbance or cortical blindness(5/11) and mental status change(3/11). All the symptoms were spontaneously improved by conservative management. The insidious increase on blood pressure, hepato-renal impairment, sepsis, and hepatopathy were noted in some cases just before and after the neurologic manifestation. The ESR was elevated in all examined cases and the cholesterol level was normal. Serum cyclosporine was elevated in 2/6 cases. They showed typical MRI findings which were high signal intensity an T2WI and iso- to low signal intensity on TIWI with blunding of cortical sulci and with no enhancement. The involved lesions were the parieto-occipital area, frontal lobe, temporal lobe, and basal ganglia in series. One patient showed a petechial hemorrhage in the occipital area on both CT and MRI. In six cases, follow-up MRI showed nearly complete resolution of the lesions correlated with the clinical symptoms. CONCLUSION: We can't explain the exact mechanisms of the neurologic complication of immunosuppressants, but the characterstics of transient neurologic deficits and the corresponding reversible brain image are similar to those of hypertensive encephalopathy or eclampsia. It is suggested that the mechanism of clinical syndrome maybe a capiliary leak due to the cytokine-induced vasculopathy but future studies are warranted.
Anemia, Aplastic ; Basal Ganglia ; Blood Pressure ; Brain ; Capillaries* ; Capillary Leak Syndrome* ; Cholesterol ; Cyclosporine ; Eclampsia ; Female ; Follow-Up Studies ; Frontal Lobe ; Headache ; Hemorrhage ; Humans ; Hypertensive Encephalopathy ; Idarubicin ; Immunosuppressive Agents* ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid, Acute ; Lymphocytes ; Magnetic Resonance Imaging ; Multiple Myeloma ; Neurologic Manifestations ; Prednisolone ; Pregnancy ; Seizures ; Sepsis ; Temporal Lobe

OBJECTIVES: Deep brain stimulation (DBS) of subthalamic nuclei (STN) is one of the current modalities of refractory epilepsy, but its exact mechanism and route of action have not been elucidated yet. We investigated the effect of STN stimulation on the development and propagation of seizures in the rats with lithium-pilocarpine induced status epilepticus in its functional anatomy. METHODS: Both pilocarpine injection and high frequency stimulation on STN (HFSSTN) were provided to rats (STN group, n=12), but pilocarpine injection with no stimulation was done on the sham group (n=8). The latency to first discrete ictal discharges and the latency to status epilepticus (SE) were analyzed and the electrical stimulation lasted for 30, 60, 90, 120 minutes after its first discrete spikes. After stimulation, the rats were immediately decapitated for immunohistochemistry and histologic examination. RESULTS: Both the latency to first discrete ictal discharges and the latency to the onset of SE were delayed in the STN group than in the sham group. The latency to the first SE was also more delayed in the STN group (42.7+/-7.9 min) than in the sham group (p<0.05). Remarkably, there was marked Fos immunoreactivity (FIR) on the reticular thalamic nuclei in the STN group, but not in the sham group. CONCLUSIONS: Increased FIR in the reticular thalamic nuclei during HFSSTN suggested that the facilitation of the inhibitory thalamic output prevented generalized motor seizure behavior. We assume that HFSSTN has a pivotal role in the suppression or progression to SE, but cannot prevent seizure onset.
Animals ; Deep Brain Stimulation ; Electric Stimulation* ; Epilepsy ; Immunohistochemistry ; Pilocarpine ; Rats* ; Seizures ; Status Epilepticus* ; Subthalamic Nucleus* ; Thalamic Nuclei

We experienced a rare clinical manifestation of a digoxin induced catatonic stupor without other features of digoxin toxicity. This case suggests that the neurological manifestation of digoxin toxicity can occur without the usual side effects. Also, a serum digoxin level should be checked in any elderly patient presenting with abnormal cerebral func-tions, irrespective of whether or not the dose of digoxin has been changed. (J Korean Neurol Assoc 19(4):438~439, 2001)
Aged ; Digoxin ; Humans ; Neurologic Manifestations ; Stupor*

Pericarotid syndrome is the combination of a postganglionic Horner's syndrome and ipsilateral head and facial pain, which is caused by diverse pathologic processes in and around the internal carotid artery. We report a case of peri-carotid syndrome which presented Horner's syndrome and ipsilateral periodic severe hemicrania associated with malig-nant lymphma lapping internal carotid artery. After surgical removal of the mass and chemotherapy, miosis, ptosis, and ipsilateral hemicrania improved.
Carotid Artery, Internal ; Drug Therapy ; Facial Pain ; Head ; Headache ; Horner Syndrome ; Lymphoma* ; Miosis ; Pathologic Processes

Anteromedial force to the knee in an extended position can cause an avulsion fracture of the proximal fibula with combined injuries to the posterolateral ligaments. Avulsion fractures of the proximal fibula are rare and current management of these fractures is based on few descriptions in literature. Various surgical methods of fixation for these fractures have been reported, but there is still no standard treatment modality. Anatomic reduction of these fractures is technically difficult, and failure of reduction may cause posterolateral instability, secondary arthritis and other complications. We present our experience with two such cases of comminuted avulsion fractures of the proximal fibular with posterolateral ligament ruptures surgically fixated with a locking compression hook plate and non absorbable sutures.
Arthritis ; Collateral Ligaments ; Fibula ; Knee ; Ligaments ; Rupture ; Sutures