[Neuromyelopathy caused by treatment with muzolimine].
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Biomedical subjects
Publications and source records attributed to P Berlit.
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Uric acid examination in 554 epileptic out-patients under long-term anticonvulsant medication revealed significantly lower serum concentrations compared to a group of normal controls. In patients taking enzyme-inducing drugs, uric acid levels were found to be lower than in those under valproate sodium. In addition, uric acid concentrations showed a negative correlation with duration of therapy in epileptic males. At this time, we can only speculate on the mechanism involved in the reduction of uric acid by enzyme-inducing anticonvulsants as well as on the possible implication of this finding in the treatment of hyperuricemia.
The case of a patient with a cauda syndrome without sensory deficits following radiation therapy to the lumbosacral cord is reported. This patient received a total dose of 38 Gy to the lumbar vertebrae because of bone metastases of a carcinoma of the breast. On autopsy, degeneration of cauda equina nerve roots with an irregular distribution was found. Anterior horn neurons showed central chromatolysis. No definite ischemic lesions were detectable. This is the first case report on neuropathological findings in lumbosacral radiation myelopathy.
The clinical characteristics of dysarthria in neurological disease are reviewed in relation to the site of the lesion, giving special attention to dysarthria as an early symptom and to paroxysmal dysarthria. Iatrogenic and toxic causes of speech disorder are enumerated and the principles of diagnosis and therapy summarized.
In 6 patients with repeating seizures early after stroke periodic lateralizing epileptiform discharges were detected in EEG. Computed tomography scans showed border-zone infarctions including the territories of the middle and the posterior cerebral artery in four patients; sonographic and angiographic findings were suspicious of embolic stroke in five cases. Seizures and EEG-discharges resolved during a short term treatment with anticonvulsants. In contrast to cerebral infarctions of other regions with comparable EEG-changes long term treatment was necessary in none of the patients.
A case of cervical radiation myelopathy following telecobalt-radiation therapy to the cervical lymph-nodes in Hodgkin's disease is described. After a latent period of 3 months neurological symptoms presented with a pure spastic paraparesis of the upper extremities. Diagnosis was confirmed neuropathologically. A review is given on clinical signs of cervical radiation myelopathy.
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The clinical and computed tomographic findings in 22 civilian cases of craniocerebral gunshot injury are reported. Fifteen out of the 19 male cases were suicidal attempts; the 3 women were shot by their husbands. In 2 cases the injuries resulted from use of a slaughterer's gun. The level of consciousness is a valuable predictor of outcome from the clinical point of view. CT findings such as bihemispheric injury and detection of intraventricular blood or air were associated with a poor outcome. Surgical intervention appears to be justified only in patients with extensive subdural or epidural hematoma. The mortality rate in this study was 45%.
Abuse of ergotamine-containing suppositories was followed by generalized vessel stenoses in a pregnant 29-year-old migraine patient and led to a space-occupying great brain infarction in the area supplied by the right internal carotid artery. Impressive improvement of clinical, computed tomography and ultrasound findings was observed during treatment with nimodipine. The literature about cerebral symptoms of ergotism is reviewed.
Three cases of allergic granulomatosis (Churg-Strauss syndrome) are reported. The patients all presented 2-10 years after the onset of pulmonary symptoms with a mononeuritis multiplex, accompanied by sharp pain in the extremities involved. In one patient, the neurological findings improved under treatment with corticoids and cyclophosphamide; the other two patients responded to treatment with thioguanine and cytarabine. In the first patient, the diagnosis was confirmed by a biopsy specimen of the sural nerve.
In a retrospective study the reports of 211 cases of cardiogenic cerebral embolism--diagnosed on the base of neurological and cardiological findings--were analyzed in view of signs and findings of prognostic value. There were 21 patients with TIA, 39 cases of RIND and 151 patients with cerebral infarction, 60 of which showed mild and 91 severe neurological symptoms. 38 patients died during the period of hospitalization. While sex of the patients as well as vascular risk factors (hypertension, diabetes mellitus, cigarette smoking) did not influence the clinical course of the disease, patients with TIA or RIND in general were younger (about 5 years) than those with severe stroke. Prognosis of cardiogenic cerebral embolism depended to a great degree on the underlying heart disease. Cerebral embolism after myocardial infarction showed a better remission of symptoms than embolism in atrial fibrillation. In the group of valvular diseases the course of embolic strokes in mitral lesions was worse than in aortal valve disease. Prognosis was worst in endocarditis, both in view of neurological deficit and of mortality. Mostly, the cardiogenic emboli lead to infarctions of the middle cerebral artery territory (78 per cent) with a predilection for the left hemisphere. In media-syndromes the clinical course was significantly worse in patients with additional homonymous visual defect compared to incomplete infarctions. Initial disturbance of conscience reduced prognosis quoad vitam et restitutionem significantly. Of the neuroradiological findings, the detection of arterial occlusion or circulatory disturbance in angiography as well as the finding of an ischemic lesion in computed axial tomography (CAT) was correlated with a severe course of the embolic stroke. While 7 patients with hemorrhagic infarction in CAT-Scan showed no differences in the clinical course, the 14 patients with pathological cerebral spinal fluid findings in embolism had an unfavourable prognosis. The development of epileptic seizures did not influence the further course of the infarction to a significant extent. Results are compared with the current world literature.
A review is given on symptoms, etiology, pathogenesis and prognosis of central pontine myelinolysis (CPM). Since 1959, 315 cases of CPM have been reported in world literature, 41 per cent of the patients described developed their neurological symptoms in the course of chronic alcoholism. In about 32 per cent CPM was connected with electrolyte disturbance, especially hypo- or hypernatremia. Beside the complications of alcoholism, accompanying diseases were malignancies (9%) infections of the lung (10%) and diseases of the central nervous system (7%). Current theories about etiology and pathogenesis of CPM are reviewed with special reference to the syndrome of inappropriate secretion of the antidiuretic hormone (IADH). Own experiences with clinical diagnosis of CPM are reported. Seven patients with neurological symptoms in hyponatremia have been seen prospectively during one year. In three cases clinically, in one patient neuropathologically the diagnosis of CPM was made.
Two cases of falx-meningiomas are reported. In both cases there was tumor infiltration of the skull base, orbital caves and paranasal sinus at the time of diagnosis. The histological diagnoses were hemangiopericytic meningioma and atypical meningotheliomatous meningioma. Prognosis and therapy are briefly discussed.
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Microbiologically determined plasma biotin levels in 404 epileptics under long-term treatment with anticonvulsants were markedly lower than in 112 controls (p less than 0.0005). Patients with partial epilepsy had lower biotin levels and higher average daily intake of AC than those with generalized epilepsy. Epileptics treated with valproate sodium in monotherapy showed considerably higher biotin levels than epileptics with monotherapy of primidone (PRM), carbamazepine (CBZ), phenytoin (PHT) or phenobarbital (PB). The group of epileptics with high average daily dose of anticonvulsants had lower biotin levels than the group with low dose. In three patients with newly recognized epilepsy biotin levels were normal before starting anticonvulsant medication, increased during the first week and fell under the starting level in the following weeks. Four epileptics treated with PHT, PB, PRM or CBZ had an increased urinary excretion of organic acids, as found in patients with a deficiency of biotin-dependent carboxylases. In 37 epileptics undergoing long-term treatment plasma lactate concentrations were determined; they had a higher mean concentration than that found in controls. Our results suggest, that the lowering of biotin in epileptics is caused by intake of anticonvulsants and has a biochemical effect in these patients. It is discussed, whether this could be a factor in the mode of action of anticonvulsants.