[Generalized epilepsy with 1st onset in old age (apropos of a case)].
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Biomedical subjects
Publications and source records attributed to F Gemignani.
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In a group of 400 epileptic inpatients of the Neurological Clinic of Parma, 82 were over 60 years of age. Only 59 of them presented fits for the first time after the 60th year of age and in 78% of these, a definite anatomical damage could be demonstrated (neuroradiological investigations). One half of the epileptic syndromes with known etiology were thought to be related to cerebrovascular disease, but only few cases followed a stroke with persistent neurological symptoms. Intracranial space-occupying lesions were found to be the cause of epilepsy in 17% of cases. Partial epileptic seizures, secondarily generalized seizures, clinical signs of neurological damage, slow focal changes in the E.E.G. were the main features of this group of patients. In 22% of cases, miscellaneous causes were found: head injuries, exogenous intoxications due to accidental or iatrogenic ingestion, or alcoholic abuse. Relatively frequent were the seizures appearing in the course of degenerative or slow viruses induced encephalopathies. In 22% no demonstrable cause was found. Adequate follow-up may help us to discover etiological factors which at present are not obvious, but some form of idiopathic epilepsy with onset in this age range cannot be definitively ruled out. Only in 15% of cases interictal E.E.G. changes consisted in specific generalized or focal paroxysmal discharges (spikes, polyspikes, polyspike-and-wave). In about half of the cases the interictal E.E.G. failed to provide valuable informations, but an ictal E.E.G. could be obtained in 13 cases out of 59.
A histological, histochemical and ultrastructural study on muscle changes in chronic arterial insufficiency has been carried out in 40 patients. Muscle biopsy probes were taken in each patient either from the gastrocnemius or rectus femoris. In 7 patients submitted for amputation of a lower limb due to a more severe vascular disease, specimens were also obtained from both the sciatic and sural nerve for light and electron microscopic study. Our findings confirm the previous histological, histochemical and ultrastructural data on chronic ischemia of the skeletal muscle, suggesting that muscle damage is mainly based on a neurogenic noxa initiated by an ischemic peripheral neuropathy. In addition, many morphologic features also show the presence of a primary myopathic noxa, possibly depending on the direct damage of the mitochondrial respiratory chain by the deficit of the muscle blood supply.
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Some antiepileptic drugs, when administered at toxic plasma levels or more rarely at levels within the therapeutic range, induce asterixis. We report the case of a patient with painful syndrome of central origin being treated with carbamazepine, in which asterixis appeared with toxic serum levels. A pharmacologic interference was also observed between carbamazepine and beta-methyldigoxin, which in our patient was being used to treat disease. The blood digoxin levels were inversely proportional to those of carbamazepine. The therapeutic effectiveness of digoxin being sharply reduced when carbamazepine reached toxic levels.
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Churg-Strauss syndrome (CSS) is a disease characterised by hypereosinophilia and systemic vasculitis occurring in patients with asthma and allergic rhinitis. In the course of CSS three phases may be distinguished. The prodromal phase, which may persist for many years, consists of allergic disease. The second phase is characterised by peripheral blood eosinophilia and eosinophilic tissue infiltrates that produce a clinical picture diagnosed as Loeffler's syndrome, chronic eosinophilic pneumonia or eosinophilic gastroenteritis. The third phase is dominated by systemic vasculitis in which skin, cardiovascular system, gastrointestinal tract and peripheral nervous system are frequently involved. Renal disease in CSS is less common and generally less severe than that classical polyarteritis nodosa and Wegener's granulomatosis. Genitourinary tract may be involved, too. In the postvaculitic phase, allergic rhinitis and asthma usually persist and clinical picture is characterised by the consequences of the vasculitic illness, most commonly in form of neuropathy and hypertension. The pathogenesis of CSS is unknown but its association with asthma and allergic rhinitis may indicate an abnormal immune reactivity. The recently reported association with antineutrophil cytoplasmic antibodies with antimyeloperoxidase specificity may suggest a their role in the pathogenesis of the disease. An important role may be played by eosinophils, too. The main therapy is that with corticosteroids, possibly in association with immunosuppressive drugs.
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