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Scope and presumed mechanisms of hallucinations in partial epileptic seizures
F. Mauguière
perception of an actual stimulus, the presence of which can be confirmed by an observer, while the latter refer to abnormal perceptions, in the absence of any external stimuli. However, both are subjective experiences to which the observer has no access except through the patient’s report. The distinction between illusions and hallucinations resulting from a focal epileptic discharge is not so obvious on the basis of our present knowledge of the neurophysiological processes which subserve perception [1, 2]. Indeed, the sensory inputs are conveyed from the primary sensory areas through distributed networks of cortical areas, interconnected via feed forward and feedback projections, which process in parallel the physical attributes of the stimulus (for instance shape, colour, location and movement of a visual stimulus). Mental representations are thus supposed to result from time-locked coactivation of multiple subsets of cortical cells which can be distant in space. It can be assumed that during epileptic seizures, elementary sensations occur when the discharge affects the primary sensory areas, while illusions occur when the discharge disrupts the function of one, or several, of the areas involved in the processing of a specific attribute of a stimulus. Conversely hallucinations are produced when the discharge either releases an automatic activation of the whole network, as first proposed by Hughlings Jackson in 1879 [3] and later on supported by Ferguson et al. [4] and Halgren et al. [5], or reproduces, even with a degraded signal to noise ratio, the spatio-temporal pattern and sequencing of activation necessary for perception and complex mental functions [6]. In what follows, all of the above ictal phenomena will be considered as “hallucinations”, which can be classified as elementary, complex, formed or experiential, but which all reflect a focal discharge in part of the cortical network of perception.
Articles originaux
Epilepsy and paroxysmal movement disorders in families: evidence for shared mechanisms
R. Singh, R. Macdonell, I. Scheffer, K. Crossland, S. Berkovic
of certain familial epilepsies and paroxysmal movement disorders. We studied two families with the co-occurrence of epilepsy, movement disorders and migraine. Information was obtained on 147 individuals in the two families. In family WF, there was a co-occurrence of epilepsy (benign infantile convulsions, idiopathic generalized epilepsy), episodic ataxia (with cerebellar atrophy and without myokymia) and common migraine. In family CL, epilepsy (febrile seizures, febrile seizures plus), kinesigenic paroxysmal dyskinesia and migraine (including hemiplegic migraine) were observed in various combinations over 3 generations. The observations in these two families, together with review of the literature, suggest that the co-occurrence of epilepsy (particularly benign infantile convulsions), paroxysmal movement disorders and migraine is not due to chance. Thus, these distinct clinical phenomena could have a shared biological basis and ion channel defects are an attractive possibility.
Video-EEG telemetry: apparent manifestation of both epileptic and non-epileptic attacks causing potential diagnostic pitfalls
A. Raymond, W. Gilmore, C. Scott, D. Fish, S. Smith
important to identify such patients to avoid the hazards of inappropriate anticonvulsant withdrawal. To delineate the electroclinical characteristics and diagnostic problems in this group of patients, we studied the clinical, EEG and MRI features of 14 consecutive patients in whom separate attacks, considered to be both NES and ES were recorded using video-EEG telemetry. Only two patients were drug-reduced during the telemetry. Most patients had their first seizure (ES or NES) in childhood (median age 7 years; range: 6 months-24 years); 8/14 patients were female. Brain MRI was abnormal in 10/14 patients. Interictal EEG abnormalities were present in all patients; 13/14 had epileptiform and 1/14 only background abnormalities. Over 70 seizures were recorded in these 14 patients: in 12/14 patients, the first recorded seizure was a NES (p < 0.001), and 7 of these patients had at least one more NES before an ES was recorded. Only 3/14 patients had more than 5 NES before an ES was recorded. Recording a small number of apparently NES in an individual by no means precludes the possibility of additional epilepsy. Particular care should be taken, and multiple (> 5) seizure recording may be advisable, in patients with a young age of seizure onset, interictal EEG abnormalities, or a clear, potential aetiology for epilepsy.
Basal ganglia involvement in rotational seizures
L. Vercueil, P. Kahane, A. François-Joubert, E. Hirsch, D. Hoffmann, A. Depaulis, C. Marescaux
However, there are both experimental and clinical arguments which support the hypothesis of basal ganglia asymmetric activation during such complex motor behavior. We report a patient exhibiting rotational seizures which proved to arise from right anterior temporal lobe structures and the orbito-cingular cortex, as demonstrated during stereotactic EEG recordings. An ictal 99mTc-ECD-SPECT study was performed during an electrically induced seizure, similar to the seizures usually experienced by the patient but without a rotatory component, showing a marked increase of cerebral blood flow in the lenticular nucleus, ipsilaterally to the epileptogenic area. This finding suggests that lenticulate involvement might be necessary to produce an ictal circling behavior. As circling behavior can be observed during epileptic seizures originating from areas widely distributed in the cortex, one may postulate that the basal ganglia involvement is the “final common pathway” underlying the rotational part of the clinical symptomatology.
Tactile evoked spikes in children
P. de Marco, S. Calzolari
stimulation rate, the relation with middle-long latency somatosensory evoked potentials (MLSEP) and the relation between TES and spontaneous spikes in the same individual. New data were obtained by re-evaluating 566 children with TES, by assessing MLSEP from each finger, in 15 subjects with TES, and by studying MLSEP following posterior tibial nerve stimulation in 12 children with TES. TES appear to be enlarged components of MLSEP which are present in some children aged 4 to 14 years; they tend to increase during NREM sleep and to decrease during REM sleep; Their amplitude decreases at stimulation rates above 3 Hz. TES are associated with an increased risk of epileptic seizures, which usually have a benign prognosis. The possible neurophysiological mechanisms underlying this phenomenon are discussed.
Hemifacial spasm or subcortical epilepsy?
A. Arzimanoglou, F. Salefranque, F. Goutières, J. Aicardi
hemifacial spasm. Later in life he also developed independent, permanent abnormal eye and chin movements identical in rhythm to those seen in myorhythmias, suggesting involvement of the dentato-olivary pathway. MRI demonstrated a hamartomatous lesion at the level of the pontomedullary junction. We speculate that the nature of the lesion could be responsible for the partial seizures mimicking hemifacial spasm and that because of its location, this same lesion could also be implicated in the genesis of myorhythmias. The presence of a hamartomatous lesion in a region affected by the abnormal development of the first and second branchial arches is not fortuitous.
Seizure with prominent tonic initial signs followed by psychomotor features: a case report clinically manifesting an unusual ictal evolution
A. Ikeda, A. Sengoku, N. Aoyagi, Y. Kubota, R. Matsumoto, S. Ohara, T. Kunieda, K. Kimura, J. Takahashi, S. Miyamoto, H. Shibasaki
who had gliosis of the left temporal lobe and left hippocampal atrophy. Interictal epileptiform discharges were frequently seen in the left temporal area, and at the time of the tonic seizure phase, ictal spike discharges were continuously observed at the left posterior temporal area, which was recognized only by applying a high frequency filter (HFF) of 15 Hz to the digitally recorded EEG because EMG artifacts totally obscured the EEG with a HFF of 60 Hz. It is most likely that tonic seizure can occur in an adult patient with temporal lobe epilepsy, and it is speculated that an epileptogenic focus might activate a certain brain area which is regarded as a symptomatogenic zone for tonic seizures. If the tonic seizure phase is immediately followed by psychomotor features as seen in the present patient, the former could be due to focal epilepsy.
Focal seizures versus focal epilepsy in infancy: a challenging distinction
F. Gérard, A. Kaminska, P. Plouin, B. Echenne, O. Dulac
(EEG) recording before the end of the first year of life [3]. Focal epilepsy can be confirmed relatively easily when focal seizures of a single type are combined with neuroradiological evidence of a focal lesion affecting the same area.
Compte-rendu de cas
Benign epileptic seizures in infancy followed by paroxysmal choreo-athetosis during adolescence
C. Koch, N. Bednarek, J. Motte
paroxysmal choreo-athetosis. We were able to record one of these attacks by EEG video. This clinical association has been recently reported in four families [4].
