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In a series of 645 patients with epilepsy only 38 had attacks exclusively during sleep. A further 111 had attacks while waking and sleeping. The total number of patients whose epilepsy started with sleep attacks and who later developed attacks when waking increased with each successive year. The prognosis of sleep epilepsy is important in relation to the granting of driving licences.
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One hundred cases of methohexitone activation of the EEG are reported. The technique seems to be especially valuable in the investigation of petit mal and temporal lobe epilepsy and adds valuable negative evidence in cases of suspected behaviour disorders.
Amygdaloidotomy was performed bilaterally on 15 and unilaterally on three patients exhibiting severe aggressive or self-mutilating behaviour. Nine subjects (50%) were improved a year after operation; improvement was maintained in seven (39%) for periods ranging from 27 months to nearly six years. Four non-epileptic cases had convulsions during the period of review; one of them has a persistent mild hemiparesis dating from the postoperative period. There was a tendency for epileptics to respond better than non-epileptics and for mentally retarded patients to respond poorly, but none of the differences was statistically significant.
Clonazepam was added to the treatment of patients with poorly controlled epilepsy in a double-blind trial and an open trial. Considerable improvement occurred with patients with myoclonic jerks and tonic-clonic convulsions, and with photosensitive epilepsy. Patients with atypical petit mal and focal epilepsies also improved. Drowsiness was initially common but lasted only a short time. No evidence was found for an action of clonazepam on the metabolism of other drugs, but treatment with phenobarbitone lowered serum concentrations of clonazepam. We conclude that clonazepam is particularly valuable in epilepsy with associated myoclonsu and in photosensitive epilepsy.
A double-blind cross-over trial between pheneturide and phenytoin in ninety-four outpatients with epilepsy is described. There was no significant difference between the frequency of seizures in the two groups. The difficulties in comparing two anticonvulsants of similar efficacy are discussed particularly in relation to ethical problems, the selection of patients and trial design.
Cerebellar stimulating equipment was implanted in a 24-year-old male with severe epilepsy. He received continuous alternating stimulation for at least two months, intermittent bilateral stimulation on demand for at least two months and numerous short bursts of stimulation during preliminary testing and calibration of the apparatus. The patient died during a prolonged grand mal seizure 16 months after implantation and this paper reports the findings at necropsy. A special study was made of the degree of tissue damage in the cerebellar hemispheres resulting from implantation of the electrodes and subsequent cerebellar stimulation. There was deep grooving of the upper aspect of the cerebellum under the electrodes but only a minor degree of neuronal loss and gliosis was observed in the underlying cortex. Purkinje cell populations in the cerebellum at necropsy were similar to those in a biopsy specimen taken 16 months previously during implantation. The electrodes were covered with a thick layer of fibrous tissue but they were not adherent to the cerebellar surface. Thus, the main significant findings in the present case were the very slight structural damage to the cerebellum in contact with the electrodes and the intense fibrosis around the electrodes themselves. These features are discussed in relation to the efficacy of long-term cerebellar stimulation.
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BACKGROUND: Non-convulsive status epilepticus (NCSE) is status epilepticus without obvious tonic-clonic activity. Patients with NCSE have altered mental state. An EEG is needed to confirm the diagnosis, but obtaining an EEG on every patient with altered mental state is not practical. OBJECTIVE: To determine whether clinical features could be used to predict which patients were more likely to be in NCSE and thus in need of an urgent EEG. METHODS: Over a six month period, all patients for whom an urgent EEG was ordered to identify NCSE were enrolled. Neurology residents examined the patients and filled out a questionnaire without knowledge of the EEG results. The patients were divided into two groups, NCSE and non-NCSE, depending on the EEG result. The clinical features were compared between the two groups. The sensitivity and specificity of the features were calculated. RESULTS: 48 patients were enrolled, 12 in NCSE and 36 not in NCSE. Remote risk factors for seizures, severely impaired mental state, and ocular movement abnormalities were seen significantly more often in the NCSE group. The combined sensitivity of remote risk factors for seizures and ocular movement abnormalities was 100%. CONCLUSIONS: There are certain clinical features that are more likely to be present in patients in NCSE compared with other types of encephalopathy. Either remote risk factors for seizures or ocular movement abnormalities were seen in all patients in NCSE. These features may be used to select which patients should have an urgent EEG.
The reciprocal synaptic relationship between the relay thalamus and surrounding thalamic reticular nucleus can lead to the generation of various rhythmic activities that are associated with different levels of behavioral states as well as certain pathophysiological conditions. Intrathalamic rhythmic activities may be attenuated by numerous neuromodulators that arise from a variety of brain stem nuclei. This study focuses on the potential role of a particular neuropeptide, vasoactive intestinal peptide (VIP). VIP and its receptors are localized within the thalamic circuit and thus may serve as an endogenous modulator of the rhythmic activity. Using extracellular multiple-unit recording techniques, we found that VIP strongly attenuated the slow, 2- to 4-Hz intrathalamic rhythm. This rhythm is similar to that observed during slow wave sleep and certain pathophysiological conditions such as generalized absence epilepsy. Using intracellular recording techniques, we found that VIP selectively depolarized relay neurons in the ventrobasal nucleus but had negligible actions on neurons in thalamic reticular nucleus. The VIP-mediated depolarization is produced via an enhancement of the nonselective cation conductance, Ih. The antioscillatory actions of VIP likely occur by shifting the membrane potential to decrease the probability of burst discharge by relay neurons, a requirement to maintain the rhythmic activity. Not only does VIP alter the intrathalamic rhythmic activity, this peptide that is endogenous to the thalamic circuit may also play a significant role in the regulation of information transfer through the thalamocortical circuit.
Thalamic nuclei can generate intrathalamic rhythms similar to those observed at various arousal levels and pathophysiological conditions such as absence epilepsy. These rhythmic activities can be altered by a variety of neuromodulators that arise from brain stem regions as well as those that are intrinsic to the thalamic circuitry. Vasoactive intestinal peptide (VIP) is a neuropeptide localized within the thalamus and strongly attenuates intrathalamic rhythms via an unidentified receptor subtype. We have used transgenic mice lacking a specific VIP receptor, VPAC(2), to identify its role in VIP-mediated actions in the thalamus. VIP strongly attenuated both the slow, 2-4 Hz and spindle-like 5-8 Hz rhythmic activities in slices from wild-type mice (VPAC(2)(+/+)) but not in slices from VPAC(2) receptor knock-out mice (VPAC(2)(-/-)), which suggests a major role of VPAC(2) receptors in the antioscillatory actions of VIP. Intracellular recordings revealed that VIP depolarized all relay neurons tested from VPAC(2)(+/+) mice. In VPAC(2)(-/-) mice, however, VIP produced no membrane depolarization in 80% of neurons tested. In relay neurons from VPAC(2)+/+ mice, VIP enhanced the hyperpolarization-activated mixed cation current, I(h), via cyclic AMP activity, but VIP did not alter I(h) in VPAC(2)-/- mice. In VPAC(2)-/- mice, pituitary adenylate cyclase activating-polypeptide (PACAP) depolarized the majority of relay neurons via I(h) enhancement presumably via PAC(1) receptor activation. Our findings suggest that VIP-mediated actions are predominantly mediated by VPAC(2) receptors, but PAC(1) receptors may play a minor role. The excitatory actions of VIP and PACAP suggest these peptides may not only regulate intrathalamic rhythmic activities, but also may influence information transfer through thalamocortical circuits.
1. Nucleus reticularis thalami (NRT) is a nucleus composed entirely of GABAergic neurons, which functions as a pacemaker to synchronize thalamocortical oscillations. To study the functional properties of GABAergic inhibition mediated through activation of gamma-aminobuturic acid-A (GABAA) receptors in these cells, neurons were isolated acutely from NRT at various postnatal developmental stages and recorded from using whole cell patch-clamp techniques. 2. Application of GABA to NRT neurons elicited a large, bicuculline sensitive current with an average reversal potential of -60.6 +/- 1.9 mV (mean +/- SD) in postnatal day (p) 19-21 neurons and -51.2 +/- 3.1 mV in p7 neurons, presumably mediated through activation of a GABAA-mediated chloride conductance. The potency of GABA in activating GABAA receptors decreased significantly with postnatal development in NRT neurons and was best fitted with EC50s of 24.9, 33.9, and 67.2 microM, in neurons isolated from p5-9, p18-25, and p58-74 rats, respectively. The density of GABAA receptors in the membranes of NRT neurons increased significantly with postnatal development. In addition, the GABA current decay rate slowed significantly in neurons isolated from older animals relative to early postnatal rat pups. 3. Both the potency and efficacy of benzodiazepine augmentation of GABAA responses in NRT neurons increased significantly with development. The EC50 of clonazepam decreased from 26 to 6 nM in p5-9 and p58-74 NRT neurons, respectively, whereas the efficacy increased from 126 to 163% augmentation over the same developmental range. 4. The elevated efficacy of clonazepam (CNZ) in NRT neurons relative to thalamic and cortical neurons, particularly in neurons isolated from adult (> p58) rats, is consistent with the anticonvulsant profile of this drug in controlling Generalized Absence epilepsy. Augmenting inhibition within NRT would enhance NRT/ NRT inhibitory connections and thereby decrease the amplitude of NRT-mediated synchronizing inhibitory postsynaptic potentials onto thalamus (where CNZ has low efficacy), in turn making it more difficult to elicit burst firing in thalamus due to deinactivation and subsequent activation of the low-threshold Ca2+ current. 5. The present developmental profile of GABAA responses in GABAergic NRT neurons provides data important in understanding the role of GABAergic inhibition within NRT in the modulation of normal and pathological thalamocortical rhythms in the brain and is also relevant in understanding potential differences in GABAA receptor physiology and pharmacology in GABAergic interneurons relative to glutamatergic neurons.
T-type Ca2+ channels were originally called low-voltage-activated (LVA) channels because they can be activated by small depolarizations of the plasma membrane. In many neurons Ca2+ influx through LVA channels triggers low-threshold spikes, which in turn triggers a burst of action potentials mediated by Na+ channels. Burst firing is thought to play an important role in the synchronized activity of the thalamus observed in absence epilepsy, but may also underlie a wider range of thalamocortical dysrhythmias. In addition to a pacemaker role, Ca2+ entry via T-type channels can directly regulate intracellular Ca2+ concentrations, which is an important second messenger for a variety of cellular processes. Molecular cloning revealed the existence of three T-type channel genes. The deduced amino acid sequence shows a similar four-repeat structure to that found in high-voltage-activated (HVA) Ca2+ channels, and Na+ channels, indicating that they are evolutionarily related. Hence, the alpha1-subunits of T-type channels are now designated Cav3. Although mRNAs for all three Cav3 subtypes are expressed in brain, they vary in terms of their peripheral expression, with Cav3.2 showing the widest expression. The electrophysiological activities of recombinant Cav3 channels are very similar to native T-type currents and can be differentiated from HVA channels by their activation at lower voltages, faster inactivation, slower deactivation, and smaller conductance of Ba2+. The Cav3 subtypes can be differentiated by their kinetics and sensitivity to block by Ni2+. The goal of this review is to provide a comprehensive description of T-type currents, their distribution, regulation, pharmacology, and cloning.
Stereotactic Forel-H-Tomy has been performed in 20 cases of epilepsy refractory to medication of which 15 have been followed from 2 to 7 years. The outcome of operation in 7 cases is judged as 'markedly effective' or 'effective'. In 3 cases the operation was ineffective. Effectiveness was greater in bilateral operation. Improvement of EEG was indicated by disappearance or marked reduction of spikes (or sharp waves) or spike and wave complex. Grand mal seizures alone or cases of minor seizure alone have responded more favorably than other clinical types. Six cases demonstrated improvement of personality and emotions.
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