[Advances in clinical epileptology].
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Biomedical subjects
Publications and source records attributed to K Karbowski.
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There are many different causes for an alternate outbreak of different seizure manifestations in the same patient. According to Herpin's 'law of identity', this is more a question of differing degrees of intensity of the same seizure type. Subsequently, minor or partial seizures are to be interpreted as rudimentary forms of 'major' seizures. This may be true for some, but not for all cases. It would be daring to maintain that a typical absence is a rudimentary form of a 'grand mal' seizure. Their mutual pathogenetic relations are unknown. A series of other cases would likewise go beyond the scope of Herpin's law. A patient can show, even during a cerebral condition of the same etiology, several different localized epileptogenic foci which 'flame up' alternately and initiate different types of seizures. Progressive cerebral illnesses can lead to a change in the original seizure symptoms and can also trigger off additional seizure forms. This can occasionally occur during medication. Finally, it is necessary to consider the possibility of an alternate outbreak of epileptic and nonepileptic seizures in the same patient.
We recorded an EEG within the first few days of coma in 100 patients without history of trauma or drug intoxication, in 50 after cardiac arrest, and in 50 in coma of other, chiefly metabolic etiologies. The EEG findings were classified in 5 categories (I-V) in terms of increasing severity. We were especially interested in the question whether the degree of early EEG disturbances allows prognostic conclusions regarding the clinical fate of patients one month after the beginning of coma. It was found that very severe EEG changes (Grad IV-V) indicate a poor prognosis (death, persistent vegetative state or profound neurological deficits) in over 90% of coma both after cardiac arrest and of other etiologies. An EEG without very severe changes (grade I-III) does not allow definite prognostic conclusions. Depending on the etiology, recovery occurs in 10-33% of cases. The prognostic significance of certain EEG parameters can be summarized as follows: areactivity to external stimuli and the presence of an "alpha-coma" pattern are usually (but not necessarily) associated with a poor outcome. The same applies to coma patients with epileptiform patterns in the EEG and/or suffering from epileptic or myoclonic seizures. One-fourth of patients with triphasic EEG complexes recover completely.
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Clinically it is often very difficult to distinguish rudimentary psychomotor seizures from absence seizures and sudden nonepileptic disturbances, especially from transitory cerebral ischaemia. In contrast to absence seizures during which bifrontally accentuated spike-wave activity is registered in the EEG, absence like psychomotor seizures usually present with unilateral temporal or frontotemporal EEG discharges. Syncopal and psychomotor attacks may overlap in the following context: falls resembling syncope during psychomotor seizures, the so-called "temporal fainting spells"; cardiac arrhythmias during psychomotor attacks; psychomotor symptoms such as automatisms and/or "dreamy states" that occur during syncopal attacks with transient dysfunction of the limbic system; alternating psychomotor and syncopal attacks in the same patient Symptoms of intermittent vertebrobasilar insufficiency: non-systematic vertigo, brief blurring of consciousness and blackouts may all be misinterpreted as rudimentary psychomotor seizures. The further differential diagnosis includes psychogenic attacks as well as states of confusion due to a variety of diseases in internal medicine.
As a result of painstaking studies carried out over a period of almost 30 years, the German neurologist and psychiatrist Hans Berger, of Jena, published the first paper on the human electroencephalogram (Uber das Elektrenkephalogramm des Menschen') in 1929. Clinical electroencephalography, which reached a zenith in the 1950s and 1960s, increased the range of diagnostic techniques available for a series of brain diseases and revolutionized the study of epilepsy. Today, conventional electroencephalography no longer yields startling scientific discoveries. Nor can it complete with computer tomography and magnetic resonance imaging, in the diagnosis of structural disorders of the brain. In spite of this, the scope of its uses continues to increase and it remains an indispensable instrument of neurophysiological diagnosis, especially in its capacity as a 'seismograph' of the brain. The trend that is apparent throughout the world to cut back clinical electroencephalographic units in favor of other neurophysiological investigative techniques is both unjustified and dangerous. If it continues, it will inevitably lead to a decline in epileptology, which is an essential part of the work of many different medical specialists both in practice and in hospitals.
Reviewing a longterm-EEG magnet-recording on the video system of the play-back unit "Mobile Oxford Medilog 9000" EEG patterns appeared, which imposed as epileptiform discharges. They seemed to correlate with the paroxysmal clinical disturbances the patient had experienced and noted in a diary, and could be printed out on a normal EEG-apparatus. Following investigations demonstrated the artificial origin of this EEG patterns: They appeared in fact only using the switches of the play-back unit for the fast back- and forward winding. The time-correlation between clinical and electroencephalographic episodes was simulated by the search of selected EEG-sequences based on the clinical episodes noted from the patient.
Alterations of consciousness with impaired perception and drive persisting over hours to days can be due to a nonconvulsive status epilepticus. This possibility has to be considered not only in patients with already known epilepsy, but also in those with a negative history for seizure disorders. The immediately recorded electroencephalogram (EEG) provides decisive clues. In the case of petit mal status most frequently appear tiredness, reduced vigilance and lack of drive. The EEG shows a generalized spike-wave activity. In status psychomotoricus, the clinical symptomatology varies from case to case. It can be characterized by anxiety, dreamy states or productive-psychotic states with agitation, automatisms and hallucinations. In the EEG a temporal or temporally-accentuated epileptic activity will be recorded. Transitional and mixed forms of petit mal status and status psychomotoricus can also be found. I.v. injections of benzodiazepines (clonazepam, diazepam) are an appropriate therapy for any type of nonconvulsive status epilepticus. Phenytoin is indicated in status psychomotoricus, but contra-indicated in the case of petit mal status.
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In view of the possible occurrence of epileptic manifestations and possible factors predisposing to them, the clinical course of 90 cerebral infarct patients was studied retrospectively and prospectively in a medical rehabilitation department for an average of 29 1/2 months. The following results were obtained: "prodromal" seizures (i.e. those preceding a cerebral insult) were not detectable in any of the study patients. 25 patients (27.7%) suffered epileptic seizures, 1 (1.1%) in the acute insult phase only, 2 (2.2%) in this as well as in the later phase, and 22 (24.4%) in the late phase only. All seizures in the acute insult phase were focal-motor or secondary generalized. Among all 24 patients (26.6%), the latency of late epileptic manifestations ranged from 2 1/2 months to 3 3/4 years and averaged about 12 months. Patients with cortical or cortical-subcortical brain lesions suffered epileptic seizures-as reported in the literature-significantly more frequently than those with exclusively subcortical insults. Based on the features of the focal (motor or psychomotor) seizures and/or interictal focal EEG spikes, there was clear evidence of a focus giving rise to epileptic discharges in the insulted hemisphere in 75% of the patients with late seizures. Under antiepileptic therapy (chiefly with phenytoin), the seizure frequency was slight (not exceeding 2 per year in 3/4 of the patients).
After a change in her antiepileptic medication, a 29 year old woman, who had petit mal absences since childhood, developed an intoxication by phenobarbital and a intermittent absence status. The intravenous administration of clonazepam paradoxically produced a transitory increase of the spike-wave-activity. Only 8 days later, when the serum level of phenobarbital had dropped and the concentration of valproic acid and ethosuximide were near the "therapeutic range", did the absences remit.
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Our analysis of the course of illness in 14 patients, whose common electroencephalographic characteristic was epileptogenic activity in the occipital area, showed very different clinical symptoms. The first group comprised patients who presented bilateral amaurosis. In four of these cases, the occipital hypersynchronous EEG activity was merely a secondary symptom of either ischaemic hypoxia or of a degenerative process in the occipital visual cortex and was not responsible for the genesis of the actual blindness. In two further cases of monosymptomatic temporary loss of vision, it was difficult to make a differential diagnosis between ictal blindness, respectively status epilepticus amauroticus occurring in a occipital lobe epilepsy and a migraine attack involving the basilar territory. The second group comprised five patients with paroxysmal visual hallucinations respectively illusions. Three of them suffered from hallucinations of the elementary type, respectively flickering fits in the hemianopic field, symptoms which are based on discharges in the visual cortex of the occipital lobe. In a case of one patient with complex visual hallucinations as well as in a further case with visual illusions, it was not possible to find out with certainty their place of origin. A study of these cases shows that the cortical or sub-cortical functional disturbance within the visual system causing the various optical deformations and visual hallucinations, form an inhomogeneous group with different etiology. In the only patient belonging to the third group, whose seizures were i.a. characterized through motor phenomena in the field of the ocular organs and the tonic lateral turning movement of the bulbi of the eyes and of the head, an occipital epileptic crisis with spread of discharges from the occipital pole to the frontomesial surface should be assumed. The occurrence of complex partial seizures, respectively generalized tonic-clonic attacks in two patients of the fourth group who have definite epileptogenic EEG-activity in the occipital area, can be explained by a propagation of paroxysmal activity to the temporal lobe or to the motor cortex. Because of the marked tendency to propagation of the hypersynchronous activity originating in the occipital lobe, many combinations of sensory and/or motor symptoms can occur within the frame-work of occipital epileptic seizures. On the basis of one scalp EEG finding, no final localizing conclusions may be drawn here.
off authors analyzed the ictal clinical symptoms (in 6 cases with videotape monitoring) of 12 infants and young children, who had focal epileptic discharges in the temporal regions (fig. 3, 4, 5). The average age was 1 9/12 years with a range of 3 months to 5 years. In 6 cases the seizures were typical "psychomotor" with oral automatisms, aimless movements of the upper extremities and/or tonic versive motor manifestations (fig. 2). In 5 cases the seizures consisted of staring and arrest of any movement. In another case, automatisms of the upper extremities were accompanied by a psychomotor arrest reaction. It is probable that in this age group seizures with sudden arrest of activity ("temporal pseudoabsences") are more frequently the main expression of partial complex seizures than in older children and in adults.
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