ABSTRACT
An acute polyneuropathy with fever and blood eosinophilia (69%) developed in a 72-year-old woman with chronic bronchial asthma and weight loss for a few months. A muscle biopsy revealed necrotizing vasculitis with numerous eosinophilic granulocytes and neurogenic atrophy. The vasculitic changes were only minor in the sural nerve and limited to the epineurium. Signs of acute nerve-fibre disintegration were marked, while some fascicles were only affected in some sectors. The clinical and histological diagnosis suggested Churg-Strauss syndrome. The polyneuropathy, eosinophilia and abnormal erythrocyte sedimentation rate quickly disappeared on administration of initially 80 mg prednisolone and 100 mg azathioprine.
Subject(s)
Churg-Strauss Syndrome/complications , Polyneuropathies/etiology , Aged , Asthma/complications , Azathioprine/therapeutic use , Biopsy , Blood Sedimentation , Chronic Disease , Churg-Strauss Syndrome/diagnosis , Churg-Strauss Syndrome/drug therapy , Churg-Strauss Syndrome/pathology , Drug Therapy, Combination , Eosinophilia/diagnosis , Eosinophilia/drug therapy , Eosinophilia/etiology , Eosinophilia/pathology , Female , Humans , Muscles/pathology , Neurologic Examination , Polyneuropathies/diagnosis , Polyneuropathies/drug therapy , Polyneuropathies/pathology , Prednisolone/therapeutic use , Sural Nerve/pathologySubject(s)
Chickenpox/complications , Reye Syndrome/etiology , Valproic Acid/adverse effects , Adult , Aspirin/administration & dosage , Aspirin/adverse effects , Carbamazepine/administration & dosage , Drug Therapy, Combination , Epilepsy/drug therapy , Humans , Male , Reye Syndrome/chemically induced , Risk Factors , Valproic Acid/administration & dosageSubject(s)
Epilepsy/surgery , Electroencephalography , Epilepsies, Partial/surgery , Epilepsy/diagnosis , Evoked Potentials , Humans , PrognosisABSTRACT
In this article the efficacy of carbamazepine for seizure prophylaxis in severe head injuries is tested. In addition, conditions with high risk of seizures requiring prophylactic regimen, were defined. One hundred and thirty-nine patients above 15 years of age with severe head injuries were included in the study. They were randomly divided into two groups--carbamazepine versus placebo. Prophylaxis was started immediately after the accident and was continued for one and a half to two years. Carbamazepine dosage was adjusted individually to provide serum levels within therapeutic range. In case of a seizure all the necessary clinical management was initiated. Patients on carbamazepine showed a lower probability of post-traumatic seizures than those on placebo (p less than 0.05). This difference was statistically significant with regard to early seizures within the first week and with regard to the follow-up time in total, but not regarding late seizures per se. Brain lesions with a high risk of post-traumatic seizures were situated in the parietal and temporal areas and included acute subdural haematomas in all locations, temporal lobe contusions, parietal epidural haematomas accompanied by other lesions and the deep stages of coma. Brain stem contusions were accompanied by a rather low probability of seizures. The above mentioned types and locations of brain lesions with the exception of brain stem contusions justify antiepileptic prophylaxis. The regimen consists of oral carbamazepine 100 mg three times daily by gastric tube during the first two days increasing to about 200 mg three times daily on the third day corresponding to the serum level. If oral medication is not possible within the initial twelve hours, phenytoin in a dose of 750 mg Phenhydan-Infusion Konzentrate is given on the first day, followed by an intravenous dose of 250-500 mg on the second day or until oral carbamazepine administration is tolerated. Treatment should be continued for one year.
Subject(s)
Brain Injuries/complications , Carbamazepine/therapeutic use , Epilepsy, Post-Traumatic/prevention & control , Brain Concussion/complications , Carbamazepine/administration & dosage , Hematoma, Epidural, Cranial/complications , Hematoma, Subdural/complications , Humans , Parietal Lobe/injuries , Placebos , Temporal Lobe/injuries , Time FactorsABSTRACT
Paroxysmal symptoms of frequent recurrence and short duration occurring mostly unilaterally and without loss of consciousness have been described under a vast variety of headings. Brain stem origin of these symptoms was presumed. Electroencephalographic recordings usually did not show any paroxysmal discharges. 328 patients were found in the available literature including 9 patients of ours. The seizures were classified by their appearance. Tonic or dystonic, sensory, algetic, ataxic and akinetic-atonic fits were distinguished. The dystonic variety includes the "paroxysmal kinesiogenic choreoathetosis". The "paroxysmal dysarthria and ataxia" was subsumed under the ataxic type. By etiology, seizures were grouped into the cryptogenic and the symptomatic type. The symptomatic variety is frequently caused by multiple sclerosis, and rarely by tumours of the basal ganglia or by vascular disorders. Cranial computertomography showed subcortical lesions in three out of seven patients. In one case cerebral atrophy was found. All types of seizures respond very well to antiepileptic drugs. The prognosis is favourable with the cryptogenic type and unfavourable with the symptomatic variety depending on the underlying disease.
Subject(s)
Brain Stem , Seizures/diagnosis , Adult , Ataxia/diagnosis , Atrophy , Brain/pathology , Dysarthria/diagnosis , Electroencephalography , Female , Humans , Middle Aged , Prognosis , Seizures/diagnostic imaging , Tomography, X-Ray ComputedABSTRACT
Total creatine kinase (CK) activity in serum was increased post-ictally in 14 out of 17 patients (82%) admitted to the hospital after one or more generalized seizures. No correlation was found between increased CK levels and cerebral or extracerebral ictal injuries. A highly significant negative correlation exists between regular anti-epileptic treatment and elevated levels of the enzyme (p less than 0.01). The maximum value of CK activity was found on the 3rd or 4th post-ictal day in 10 out of 14 patients. Correspondingly, late CK-activity increases on the 2nd-4th post-ictal day were found in 6 out of 9 experiments with unrestrained cats. In cats immobilized by relaxant drugs, only an initial rise of the enzyme within 24 h after the electrographic seizures was observed. These findings suggest that sources other than the skeletal muscle alone contribute to the increased CK activity after grand mal seizures.
Subject(s)
Creatine Kinase/blood , Epilepsy, Tonic-Clonic/enzymology , Adult , Aged , Animals , Brain Injuries/enzymology , Cats , Epilepsy, Tonic-Clonic/drug therapy , Female , Humans , Male , Middle Aged , Muscle Relaxants, Central/therapeutic use , Muscles/enzymology , Time FactorsABSTRACT
In general, Adie's syndrome does not represent a serious diagnostic problem. In cases of cerebrospinal syphilis the Argyll-Robertson phenomenon or even absolute pupillary rigidity will be observed. Positive syphilis reactions will clarify these cases. The erroneous diagnosis of brain tumour may arise because of anisocoria. However, if pupillotonia can be ascertained by means of conjunctival instillation of drugs no further invasive diagnostics will be necessary. In some cases of Adie's syndrome concomitant emotional instability may be present. This dysautonomic reaction type of personality will hardly ever be confounded with the psychological disturbances encountered in brain tumours. Therapy is restricted to symptomatic measures. Pupillotonia can be influenced by strychnine and thymoxamine. Headache and facial neuralgia respond to the usual therapeutic schemes. Sweating disorder cannot be influenced. Neuropharmacological treatment may become necessary in periods of acute emotional disturbance.
Subject(s)
Adie Syndrome , Diagnosis, Differential , Fludrocortisone/therapeutic use , Humans , Neurosyphilis/diagnosis , Neurotic Disorders/diagnosis , Reflex, Pupillary , Strychnine/therapeutic use , Sympatholytics/therapeutic use , Tachycardia/drug therapySubject(s)
Adie Syndrome/diagnosis , Adult , Female , Headache/etiology , Humans , Hypertension/genetics , Male , Middle Aged , Neurologic Examination , Pupil , Sweat Gland Diseases/etiology , Syncope/etiologyABSTRACT
Eighty-five patients were admitted to the hospital under the preliminary diagnosis of epileptic seizures. None of them had more than five seizures before admission. Sixty-five of these 85 patients had a neurological and electroencephalographic follow-up examination 5 to 7 years later. Another 8 had been readmitted before. From these 8 the diagnosis of cerebral tumor was made in 3 patients. In almost half of the remaining 70 cases the etiology of seizures remained uncertain. The leading known etiologic factors were chronic alcoholism, head injury and perinatal brain damage. Before admission seizures recurred once or twice a year in most patients. After discharge from the hospital 25 patients were without further seizures, 15 of the seizure-free group never received anti-epileptic treatment. The remaining 10 were without medication for a period of time before the follow-up. All seizure-free patients were given the diagnosis of very rare grand mal seizures or seizures of uncertain origin. Only two of the untreated group (total of 17) had seizures after discharge. These findings show that recurrence of seizures was predictable, when patients were discharged. Predictors of recurrance were "treatment" or "no treatment" given initially. Antiepileptic medication should be given in cases of one seizure or more a year, when epileptic origin is certain. Very rare seizures and seizures of uncertain origin may stay without antiepileptic treatment. Sporadic seizures are benign in most cases - comparable to seizures of late onset. Both groups overlap.
Subject(s)
Seizures/diagnosis , Adolescent , Adult , Aged , Alcoholism/complications , Anticonvulsants/therapeutic use , Brain Damage, Chronic/complications , Brain Injuries/complications , Brain Neoplasms/complications , Child , Electroencephalography , Follow-Up Studies , Humans , Middle Aged , Prognosis , Seizures/drug therapy , Seizures/etiologySubject(s)
Brain Stem/physiopathology , Epilepsy/physiopathology , Adult , Amitriptyline/therapeutic use , Ataxia/drug therapy , Ataxia/etiology , Ataxia/physiopathology , Brain Neoplasms/complications , Carbamazepine/therapeutic use , Epilepsy/drug therapy , Female , Humans , Male , Middle Aged , Muscles/physiopathology , Phenytoin/therapeutic useABSTRACT
The review of the syndrome is centered on time course, prognosis and prophylaxis. Prophylactic anticonvulsive treatment depends on the prognosis. The latter is dependent on the risk to develop epilepsy after a certain type of head injury. Treatment should begin in the high risk group of patients before seizures become overt. In order to avoid preventive treatment in unselected posttraumatic cases, predicting the risk in each case is most important. Therefore the literature was reviewed selecting injuries and complications of high risk. Knowledge on pathophysiologic mechanisms in the epileptogenic focus to a large extent stems from animal experiments using a model of chronic recurrent seizures. Basic electrophysiologic mechanisms responsible for focal electroencephalographic changes were studied by recording from single cells. Profound abnormalities in patterns of neuronal discharge were found as well as morphological and functional changes of glia in the epileptogenic scar. It appears that glia is important in generating focal electroencephalographic spiking. By controlling intercellular potassium transport glia modulates neuronal activity.
Subject(s)
Epilepsy, Post-Traumatic , Animals , Astrocytes , Cats , Craniocerebral Trauma/complications , Electrophysiology , Haplorhini , Humans , Membrane Potentials , Neuroglia/pathology , Neuroglia/physiopathology , Neurons/physiopathology , Potassium/metabolismSubject(s)
Epilepsy/history , Adolescent , Adult , Anticonvulsants/therapeutic use , Child , Epilepsy/drug therapy , Epilepsy/surgery , Germany , Greece , History, 15th Century , History, 16th Century , History, 17th Century , History, 19th Century , History, 20th Century , History, Ancient , History, Medieval , Hospitals, Special/history , Humans , Lithium/therapeutic use , RomeABSTRACT
Methodological questions of clinical observation and classification of drug-induced extrapyramidal symptomatology are discussed. In our experimental approach we examined two groups of 20 acute schizophrenic patients each. The patients were treated for 4 weeks under double-blind conditions with the butyrophenone derivative Haloperidol and with the benzoxazepine derivative Loxapin respectively. The extrapyramidal disturbances appearing under these medications were studied. The patients were examined by means of the EPS-scale by Simpson and Angus weekly, before, during and after this treatment as well as under a subsequent therapy with a longacting neuroleptic. Extrapyramidal disturbances appearing between these fixed rating times were noted in a check list. According to a classification propased by Chien and Di-Mascio the symptomatology of extrapyramidal disturbances under neuroleptic therapy can be divided into "permanent neuroleptic manifestations" on the one hand and "paroxysmal neurodysleptic manifestations" on the other. While Haloperidol caused more distinct symptoms of permanent neuroleptic manifestations, acute neurodysleptic reactions appeared more frequently under Loxapin therapy.