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A syncope is defined as a sudden, temporary loss of consciousness, associated with loss of postural tone with spontaneous recovery. The incidence is high and the differential diagnosis broad; therefore, the first observations are essential for the management of the patient. In this review diseases will be described which manifest themselves with syncopes that fall under the auspices of either internal medicine or neurology. First, the etiologies of syncopes are discussed in the strict sense of the word, i.e. due to a global cerebral ischemia such as in orthostatic hypotension and vasopressor syncopes. Thereafter, a discussion concerning the differential diagnosis of syncopes will be introduced, including mainly psychogenic and epileptic seizures as well as vertebrobasilar hypoperfusion. Depending on the reason of the loss of consciousness, it can be a common benign disorder or a severe life-threatening disease. The personal history or witness account of the incidence provides the most useful information concerning diagnosis. The cardiological diagnostic procedures are discussed elsewhere. In some instances an EEG can further help with the diagnosis. In many cases an etiology can't be found, even if extensive investigations have been performed.

New antiepileptic drugs such as vigabatrin, lamotrigine, gabapentin, oxcarbazepine and felbamate have been lately marketed. This article provides an overview, showing known modes of action, pharmacokinetics, efficacy, tolerability, interactions and indications. A table showing selected data of antiepileptic drugs is included.

In epileptic seizures, the sensitivity of CT and MRI depends on different underlying pathologies and varies according to the age of the patient and the type of seizure. The different modalities are discussed in detail.

Single fits and epileptic illness are more frequent in advanced age; their occurrence reaches the same frequency as in the neonatal period. Their origin and the possibilities of treatment are tightly connected to the process of ageing, a fact that requires special consideration. The main reasons for new epileptic attacks in the group of age 65 or more are structural changes, i.e. ischemic infarctions, tumors and atrophic involution. For certain patients, the use of antiepileptic drugs may be limited by unavoidable side effects. Complete cure of the attacks in advanced age is rare, but with a well selected treatment sufficient control is often possible.

We present the concept of an 'epileptic syndrome' which is important for prognostic statements and the application of appropriate therapeutic measures. We then discuss the epileptic seizure and the assessment of suspected seizure, indications for admission to a hospital, diagnostic measures (EEG, CT scan, laboratory tests, lumbal puncture, MRI scan, PET scan, angiography), therapy and procedures for imminent status epilepticus. Finally, we try to answer the question whether anticonvulsant medication should be instituted after a first epileptic seizure.

In order to investigate whether sleep deprivation activates the photoconvulsive response 35 patients were investigated electroencephalographically after 24–36 h of waking. In 34 cases with sleep depri

Sodium valproate enteric-coated tablets were administered as monotherapy to 118 patients (median age, 19 years) with primary generalized epilepsies. More than half (56%) of these patients were transferred from prior drug therapy, most of them because of inadequate seizure control, and some because of adverse effects. Seventy-one percent of the patients experienced tonic-clonic seizures, either alone or in combination with other types of seizures, principally absences. Mean duration of follow-up was 18 months (median, 17 months; range, 1-68 months). At a mean daily dosage of less than 20 mg/kg, 83% of the patients became seizure-free. Therapy was equally effective against tonic-clonic seizures, absences, and myoclonic seizures. Tonic-clonic seizures were suppressed in 85% of cases (89% when patient had only one seizure type), absences in 82% (95% when patient had only one seizure type), and myoclonic seizures in 82%. Paroxysmal activity was present in 88% of the electroencephalogram (EEG) records before valproate monotherapy, and in 32.4% at the study's end. These results were achieved with generally mild and mostly transient side effects; side effects were reported by 16% of patients during the first month, and 2% at the last follow-up. No hematologic or hepatic toxicity was observed. The lag time between attaining steady-state serum concentrations and achieving maximal clinical improvement suggests that sodium valproate monotherapy should be given an adequate trial to ensure that patients derive the greatest possible benefit before adding or switching to another drug.

An EEG study was carried out in 4 epileptic patients. In each case, Ro 15-1788 caused the disappearance or marked reduction of the epileptic potentials. In 1 case the patient had been pretreated with diazepam; in the other cases there had been no prior benzodiazepine treatment. In the first case, it is possible that Ro 15-1788 acted by abolishing a paradoxical effect of diazepam; in the other cases, we postulate an intrinsic anticonvulsant effect of Ro 15-1788. This investigation would suggest further study of Ro 15-1788 in epileptic patients for clarification of its anticonvulsant properties. In addition, evaluation of its action on the sedation caused by benzodiazepine antiepileptic medication is suggested.

Computerized transaxial tomography was carried out on 112 patients with partial seizures with complex symptomatology. Structural abnormalities were defined in 33% of their studies: tumors in 8 patients, diffuse cerebral atrophy in 2, focal cortical atrophy in 27 and vascular abnormality in 1 case.

SUMMARY Two unusual cases of sensory precipitation of epileptic attacks are presented and briefly discussed. One patient had suffered from tonic and clonic seizures in her right arm for 11 years. The seizures were induced by touching this arm or even by carrying a heavy object. She never had a generalized seizure. The other patient had petit mal-like attacks when taking food, sometimes provoked by the mere sight of it. In both cases the epileptic nature was confirmed by the EEG and by successful anticonvulsant treatment. RESUME Deux cas inhabituels de declanchement sensoriel d'attaques epileptiques sont presentes et brievement discutes. L'un concerne une patiente souffrant de crises tonico-cloniques de son bras droit, depuis 11 ans, a l'exclusion de toute generalisation. Les crises etaient induites par le simple contact decebras, ou lorsqu'elle soulevait un objet lourd. L'autre patient avait des crises de type petit mal lorsqu'il absorbait de la nourriture ou meme parfois a la simple vue de celle-ci. Dans les deux cas, la nature epileptique a ete confirmee par l'E.E.G. et par les bons resultats d'une therapeutique anticonvulsivante.

In addition to the benzodiazepine antagonism we report, as a first observation, the effect of flumazenil on carbamazepine intoxication, where a mechanism other than benzodiazepine receptor antagonism must be supposed.

The authors report on the use of clonazepam in 63 adult epileptics over a period of 3 years. Clonazepam had a particularly good effect on focal epilepsies both when administered alone and when combine

In this overview the current state of knowledge concerning epilepsy is presented: diagnosis, classification, etiology, pathogenesis and therapy. The change in these aspects during the past epochs of medical history is described. Suggestions as to future prospects are discussed.

The clinical anti-convulsant effect of flumazenil in epilepsy has been demonstrated: (i) by acute i.v. administration under EEG control in an epileptic patient who had been previously heavily sedated with diazepam; (ii) in patients undergoing pharmaco-EEG studies whereby spike and wave counts were diminished following oral administration of 10 mg of flumazenil; and (iii) in a series of 27 epileptic patients treated chronically for periods of up to 42 months with flumazenil as monotherapy or as addition to basic therapy. The daily dose ranged from 10-90 mg. Before treatment all patients presented with frequent seizures and had an abnormal EEG. In these patients the anti-convulsant effect was good or very good in 70% of the previously untreated (naive) patients and in about half of the patients who had epilepsy of long duration and had been treated already with standard anti-convulsants. Side-effects with flumazenil were generally mild in nature and rarely led to discontinuation. About one-third of the patients expressed a feeling of well-being while under therapy with flumazenil. A possible mechanism of action is discussed.

After mentioning the therapeutic effect of anti-convulsant medication on the pathophysiology of epileptic seizures the principal anticonvulsive drugs are characterized in a table. Furthermore their interactions with non-anticonvulsive drugs are pointed out, as well as side-effects. Some statements are made concerning genetic and psychosocial considerations.

This paper reports on 294 patients with presumptive symptoms of epilepsy but no noteworthy, or only suspicious, EEG findings. With recording during sleep after 24-27 h of sleep deprivation, 138 persons showed definite epilepsy potentials. The remainder of the group showed no noteworthy findings. Nevertheless, on the basis of clinical observations and the course of the patient's illness, epilepsy was diagnosed in 27 patients of this second group. Neurophysiological aspects of the electroencephalographic provocation method are discussed.

193 patients with epilepsy were investigated by EEG and by computerized tomography (C.T.). 55.5% of the pathological C.T. scans were found in partial seizures with elementary symptomatology. In patients with generalized seizures the diagnosis of symptomatic epilepsy could be made in 40 cases (35.7%) with the help of computerized tomography. In 38 EEG there was a continual delta-wave focus, 18 of these with epileptogenic activity. Of these 38 patients, 34 showed a pathological result in computerized tomography. 19 tumors or metastases, 11 cases of atrophy (10 local and one diffuse) as well as one case of encephalitis could be diagnosed. The remaining 3 patients showed indefinate findings with C.T. 19 EEG showed intermittent theta-wave foci. Computerized tomography gave 5 pathological scans in these patients. If one compares the results of computerized tomography and EEG in cases of tumor, the agreement between positive tomography and the pathological EEG is very high (95%): 64 positive C.T. compared with 61 positive EEG. Our investigations with computerized tomography show organic findings in 67 of 193 epilepsies, that is about 35%.

Depakine® sodium di-n-propylacetate is a new anti-epileptic drug. Its action may be related to inhibition of GABA-transaminase. We report our results with Depakine treatment in 33 patients with Petit