Paroxysmal EEG Discharges Research Articles

Effects of Levetiracetam on EEG Activity and Regularity of the Menstrual Cycle in Women Suffering from Epilepsy

Epilepsy itself and its treatment with anticonvulsants noticeably affect the reproductive function in women suffering from this disease. Levetiracetam (LEV) was shown to be highly effective for the reduction of clinical seizures and EEG epileptic activity. At the same time, its impact on the reproductive/endocrine functions is still unclear. The aim of our study was to evaluate the influence of LEV on the frequency of seizures and epilepsy-related EEG discharges, and also on the regularity of menstrual cycles (MCs) among women with epilepsy (WE) in Georgia. Seizures entirely disappeared in all examined WE with focal and bilateral tonico-clonic seizures (BTCSs), as well as in all cases with juvenile myoclonic epilepsy (JME) (P = 0.008). Six months after starting LEV monotherapy, a reduction in single and burst EEG epileptic discharges was observed in all eight women with JME (P = 0.031); weakening of burst discharges was also revealed in all patients with focal epilepsy (P = 0.046). Among examined WE with regular MCs, oligomenorrhea was observed in two cases from eight patients with focal epilepsy and in one case from seven women with JME treated with LEV. In general, LEV effectively suppresses paroxysmal EEG discharges and also improves clinical seizure control. There was no significant influence of LEV on the MC disturbances, while oligomenorrhea was found in some cases; thus, the respective effects on the MC were at least relatively moderate. More data are needed to establish the level of association between LEV therapy and reproductive endocrine disorders in WE.

Long-term outcome in children with neonatal seizures: A tertiary center experience in cohort of 168 patients

PurposeThe purpose of this study was to evaluate long-term outcome and assess predictors of prognosis in children with neonatal seizures (NS). MethodThis retrospective study includes children with NS treated at our Institute from January the 1st 2005 until December the 31st 2015. The data were collected from medical charts and the electroencephalogram (EEG) database at the Institute. The predictive value was evaluated for following parameters: (1) characteristics of the patients, such as gender, gestational age, birth body weight, Apgar score, artificial ventilation; (2) etiology; (3) characteristics of seizures such as type, time of onset, resistance to treatment; and (4) EEG background activity and paroxysmal discharges. The outcome of NS was assessed at the end of the follow-up period and was categorized as one of the following: (1) lethal outcome, (2) neurological abnormalities, (3) intellectual disability, and (4) epilepsy. Univariate and multivariate logistic regression analyses were used to assess predictors of NS outcome. ResultsThe study included 168 children with NS (of which 109 are males, and 59 are females), mean aged 5.6 (SD 3.5) years at the end of the follow-up (with a range of 1 to 12 years). There was normal neurological development without epilepsy in 131 patients (78%), neurological abnormality in 31 (19.0%), intellectual disability in 28 (17.2%), epilepsy in 12 (7.4%), and lethal outcome in 7 patients (4.17%). ConclusionsLong-term outcome in children with NS could be favorable in most patients, and it appears to be related to specific early clinical and paraclinical variables. Newborns with an abnormal background EEG activity, with seizures resistant to antiepileptic drugs and/or low Apgar score are at a higher risk of a poor outcome. Females are at a much higher risk of lethal outcome than males.

Особенности изменений ЭЭГ у детей с фармакорезистентными формами эпилепсий

Выполнен корреляционный анализ ЭЭГ у 64 детей с фармакорезистентными эпилепсиями и 26 детей курабельными формами эпилепсий. Проведена программная и визуальная оценка ЭЭГ-паттернов, а также количественная оценка неспецифических изменений биоэлектрической активности мозга, среднего интервала между эпилептическими разрядами, количества эпилептических очагов в зависимости от наличия фармакорезистентности и диагностированной эпилептической энцефалопатии. Показано, что по данным только визуального анализа ЭЭГ невозможно различить пациентов с резистентными и курабельными формами эпилепсии. Исключение составляют только нозологические специфичные паттерны — вспышка-подавление, гипсаритмия, генерализованные комплексы острая-медленная волна, CSWS-синдром. Выявлена связь фармакорезистентности и развития эпилептической энцефалопатии с интенсивностью неспецифических изменений и количеством эпилептических очагов. Развитие эпилептической энцефалопатии коррелирует с высокой частотой пароксизмальных разрядов на ЭЭГ.

Focal EEG abnormalities might reflect neuropathological characteristics of pervasive developmental disorder and attention-deficit/hyperactivity disorder

Neurophysiological characteristics in electroencephalograms (EEG) were investigated for patients with pervasive developmental disorder (PDD) and for patients with attention-deficit/hyperactivity disorder (AD/HD). This study examined 64 PDD children and 22 AD/HD children with no history of epilepsy or progressive neurological or psychiatric disorder. We used multivariate analysis to compare EEG abnormalities, clinical symptoms, and intelligence levels between PDD and AD/AD patient groups. Paroxysmal discharges at the frontopolar–frontal (Fp–F) brain regions and background EEG abnormalities tended to be detected preferentially in the PDD group, although paroxysmal discharges at central–temporal (C–T) regions tended to be detected preferentially in the AD/HD group. The paroxysmal discharges observed in patients expressing persistence and impulsivity are apparently localized respectively in the Fp–F and C–T regions. A combination of EEG abnormalities, including background EEG abnormalities and paroxysmal discharges at Fp–F and C–T regions, might be useful diagnostic hallmarks to distinguish PDD with AD/HD from AD/HD alone using a logistic regression model. The dysfunction of specific brain areas associated with EEG abnormalities might explain characteristics of clinical symptoms observed in PDD and AD/HD patients.

A Case of Hemiconvulsion-hemiplegia Syndrome in a 2-year-old Girl with Exanthema Subitum Who Experienced Prolonged Seizures Followed by Right Hemiparesis Featuring Non-convulsive Status Epilepticus

A 2-year-old girl was admitted to our hospital because of prolonged seizures (right hemiconvulsions) and high-grade fever. A diazepam suppository was ineffective in treating the seizures, because an acetaminophen suppository had already been administered in an attempt to control the fever; thus, both suppositories were ineffective. An intravenous injection of flunitrazepam finally inhibited the hemiconvulsions, which had lasted 70 minutes. Thereafter, no jerking was observed, but the right hemiparesis and depressed consciousness persisted. The fever abated on the 5th day, and rashes developed over the entire body surface on the 6th day. Electroencephalograms (EEGs) recorded on the 5th day showed continuous irregular sharp waves in the left frontal area, suggesting non-convulsive status epilepticus. A further intravenous injection of flunitrazepam attenuated the paroxysmal EEG discharges and revived her consciousness, but the right hemiparesis remained. Human herpes virus 6 (HHV-6) DNA was detected in a blood sample, so exanthema subitum was diagnosed. Hemiconvulsion-hemiplegia syndrome was also diagnosed, because diffusion weighted magnetic resonance imaging on the 15th day showed high intensity areas in the cortices of the left-hemisphere and in the subcortical white matter of the left occipital lobe. Exanthema subitum is a common infectious disease in infants, and accompanying febrile seizures are not unusual in those affected. However, when febrile seizures are accompanied by such symptoms as prolonged seizures, hemiconvulsions followed by hemiparesis, and persistent depressed consciousness, early EEG recordings should be made.

非けいれん性てんかん重積状態をくりかえした成人発症ＩＩ型シトルリン血症の１例

Adult-onset type II citrullinemia (CTLN2) is a hereditary metabolic disorder characterized by highly elevated plasma citrulline and ammonia. Recent studies have identified the "citrin gene" (SLC25A13) as the causative gene for CTLN2. Various neurobehavioral symptoms seen in this disease, such as unconsciousness, disorientation, abnormal behavior, and epilepsy, are thought to be caused by encephalopathy mostly due to hyperammonemia. A 47-year-old woman presented with repeated unconsciousness and abnormal behavior. The high plasma anmonia level was not always associated with her neurobehavioral symptoms (unconsciousness, disorientation, abnormal behavior, and epilepsy), but paroxysmal EEG discharges were invariably associated with these symptoms. Her symptoms and abnormal EEG discharges were sometimes treated with diazepam simultaneously. Based on these findings, we considered that her symptoms were caused by nonconvulsive status epilepticus (NCSE). Until date, neurobehavioral symptoms of CTLN2 are considered to be caused by hyperammonemia or other metabolic factors. We suggest that encephalopathy of CTLN2 is caused not only by hyperammonemia but also by NCSE. Therefore, repeated EEG monitoring is recommended in the follow up of patients with CTLN2.

Double‐blind, Randomized Controlled Pilot Study of Bilateral Cerebellar Stimulation for Treatment of Intractable Motor Seizures

The efficacy and safety of cerebellar stimulation (CS) was reevaluated in a double-blind, randomized controlled pilot study on five patients with medically refractory motor seizures, and especially generalized tonic-clonic seizures. Bilateral modified four-contact plate electrodes were placed on the cerebellar superomedial surface through two suboccipital burr holes. The implanted programmable, battery-operated stimulator was adjusted to 2.0 microC/cm(2)/phase with the stimulator case as the anode; at this level, no patient experienced the stimulation. Patients served as their own controls, comparing their seizure frequency in preimplant basal phase (BL) of 3 months with the postimplant phases from 10 months to 4 years (average, eight epochs of 3 months each). During the month after implantation, the stimulators were not activated. The patient and the evaluator were blinded as to the next 3-month epoch, as to whether stimulation was used. The patients were randomized into two groups: three with the stimulator ON and two with the stimulator OFF. After a 4-month postimplantation period, all patients had their stimulator ON until the end of the study and beyond. Medication was maintained unchanged throughout the study. EEG paroxysmal discharges also were measured. Generalized tonic-clonic seizures: in the initial 3-month double-blind phase, two patients were monitored with the stimulation OFF; no change was found in the mean seizure rate (patient 1, 100%, and patient 5, 85%; mean, 93%), whereas the three patients with the stimulation initially ON had a reduction of seizures to 33% (patient 2, 21%; patient 3, 46%; patient 4, 32%) with a statistically significant difference between OFF and ON phase of p = 0.023. All five patients then were stimulated and monitored. At the end of the next 6 months of stimulation, the five patients had a mean seizure rate of 41% (14-75%) of the BL. The second patient developed an infection in the implanted system, which had to be removed after 11 months of stimulation; the seizures were being reduced with stimulation to a mean of one per month from a mean of 4.7 per month (BL level) before stimulation. At the end of 24 months, three patients were monitored with stimulation, resulting in a further reduction of seizures to 24% (11-38%). Tonic seizures: four patients had these seizures, which at 24 months were reduced to 43% (10-76%). Follow-up surgery was necessary in four patients because of infection in one patient and lead/electrode displacement needing repositioning in three patients. The statistical analysis showed a significant reduction in tonic-clonic seizures (p < 0.001) and tonic seizures (p < 0.05). The superomedial cerebellar cortex appears to be a significantly effective and safe target for electrical stimulation for decreasing motor seizures over the long term. The effect shows generalized tonic-clonic seizure reduction after 1-2 months and continues to decrease over the first 6 months and then maintains this effectiveness over the study period of 2 years and beyond.

Sleep disturbances in Ube3a maternal-deficient mice modeling Angelman syndrome

Angelman syndrome (AS) is a severe neurodevelopmental disorder with electroencephalographic (EEG) abnormalities and sleep disturbances. It results from lack of the functional maternal allele of UBE3A, which encodes a ubiquitin-protein ligase. Different mechanisms of UBE3A inactivation correlate with clinical phenotypes of varying severity; the majority of cases of AS are due to a de novo maternal deletion of the 15q11-q13 region. Ube3a maternal-deficient mice (Ube3a m-/p+) were generated in a C57Bl/6J background. This study compares cortical EEG and architecture of the sleep-waking cycle in adult Ube3a m-/p+ mice compared with those of age-matched WT (m+/p+) mice, under baseline conditions or after 4-h sleep deprivation (SD). Ube3a m-/p+ mice exhibited: reduced slow-wave sleep (SWS) amount with increase waking (W) at the dark/light transitions; increased SWS and W episode numbers; and deterioration of paradoxical sleep (PS) over 24 h [amount: -44%; episode duration: -46%; episode number: -40%; theta peak frequency (TPF) acceleration: 7.6 Hz vs. 7.0 Hz in WT mice]. Characteristic paroxysmal EEG discharges are observed during W and SWS associated with synchronous muscle bursting activity during hypoactive W. During the recovery period following SD, Ube3a m-/p+ mice exhibited no rebound either in slow-wave activity (+89% in WT) or in delta-power spectra but a slight rebound in PS amount (+20%). These data validate the mouse model produced by null mutation of the maternal Ube3a gene and provide useful results to investigate and better understand the molecular basis of sleep disturbances in AS patients.

Atypical Lennox–Gastaut syndrome successfully treated with removal of a parietal dysembryoplastic tumour

Focal brain lesions may be associated with the atypical form of Lennox–Gastaut syndrome (LGS). We describe a drug resistant LGS patient with daily seizures and a left parietal dysembryoplastic neuroepithelial tumour. Pre-surgical evaluation showed, in addition to diffuse paroxysmal EEG discharges associated with atonic and tonic axial seizures, lateralizing EEG and clinical signs pointing to left hemisphere origin of the seizures. The patient was treated with lesionectomy and after 12 months of follow-up is still seizure free. This case suggests that in patients with LGS and focal lesions the possibility of correct identification of the epileptogenic zone using anatomo-electro-clinical correlations may be the key element for ‘curative’ surgery.

Amygdala‐Kindling and Pentylenetetrazole‐Induced Seizures in Glutamate Transporter GLAST‐Deficient Mice

Purpose: A number of previous ncurophysiological studies have indicated that the glutamatergic system is important in the induction of epileptiform activity and the dcvelopment of epileptogenesis. Clutamate transport is the primary mechanism of inactivation of syiiaptically released glutamate. GLAST is classified BS an astrocytic transporter and occurs in high concentrations in the ccrebcllum. The pathophysiologic rolc of GLAST in epilepsy is not known in detail. To investigate the role of thc astroglial glutamatc transporter GLAST in epileptogenesis, we compared amygdalu‐kindling and pentylenctetrazolc (PTZ) induced seizures in GLAST‐deficient mice (GLAST(‐/‐)) wild‐type mice (GLAST(+/+)), and maternal C57Black6/J mice (C57). Methods: Kindling: All mice were between 10–1 I weeks of age. Under diethyl ether anesthesia, a chronic tripolar electrode w taxically implanted into the left amygdala (CS7: n = 6, GLAST(+/+): n = 3, CLAST(‐I‐): n = 5). All rats underwent kindling stimulation once daily that coiisistcd of 2 second duration of 100 Hz monophasic square pulses at the intensity of thc afterdischarge (AD) threshold. The seizure responses of thc kindled mice were classified as follows: stage 0, no response; stage 1, mouth and facial movement; stage 2, forclimb clonus; stage 3, bilateral forclimb clonus and tail up. The numbers of stimulations and AD durations required eliciting stage I or stage 2 werc compared, and the mean AD duration, latency and acizurc duration or five consecutive stagc 3 scizures (generalized scizures) were compared in each type of mouse. PTZ: PTZ was injected i.p. at a dose of SO mg/kg (GLAST(+/+): n = 13, GLAST(‐/‐): n = I3), and each mousc was observed for 30 min after the injection. Seizure rcsponses to PTZ werc rated as follows: stage 0, no response; stage I, isolated twitches; stagc 2, tonic‐chic convulsion; stage 3, tonic extension or death. Results: Kindling: No significant differcnces wcre scen in the first responses of amygdala‐kindled GLAST knockout mice. Nor were any significant differences seen in kindling seizure development. The mean AD duration, latency, and scizure duration of 5 consccutive stage 3 seizures in GLAST(‐/‐), GLAST(+/+), and C57 were compared. No significant differences were seen in AD duration and latency, but the generalized seizure duration (stage 3) of the AM‐kindled scizures in the GLAST(‐/‐) was significantly (approximately 35%) longer than in CS7. PTZ: GLAST(‐/‐) showed more severe scizurc stages of PTZ induced generalized seizures than GLAST(+/+) (p &lt; 0.02, MannWhitney rank sum test), and seizure latency was significantly shortcr in the mutant mice (p &lt; 0.005, unpaired t‐test). Conclusions: The results of present study clearly demonstrate that GLAST has different roles according to the type of epilepsy. In amygdala‐kindling, a limbic partial epilepsy model with secondary generalization, GLAST seems to have little role in seizure induction or the development of epileptogenesis in the limbic focus. Secondarily generalized seizures, on the other hand, may be modulated by GLAST, since the duration of bilateral forelimb clonus was found to be significantly longer in GLAST knockout mice. Several previous experiments have suggested significant increases in GLAST mRNA expression after amygdala‐kindled seizures or systemic administration of kainic acid. In contrast to kindled seizures, GLAST is closely related to the neuronal mcchanism underling seizure induction and severity in PTZ‐induced seizures, a primary generalized epilepsy model. GLAST may participate in the modulation of generalized tonicchic seizure activity in the cerebral cortex, because GLAST is widely localized i n the cerebral cortex, and the basic mechanism underling PTZ‐induced seizures is rclated to thalamocortical circuitry. Although no spontaneous seizures or EEG paroxysmal discharges were observed in GLAST knockout mice, it is concluded that GLAST is involved in the molecular mechanism of genetic idiopathic generalized epilepsy.

Childhood occipital epilepsy: seizure manifestations and electroencephalographic features

Childhood epilepsy with occipital paroxysms (CEOP) is an idiopathic localization-related epilepsy. A typical seizure in CEOP begins with visual symptoms, followed by hemiclonic seizures, complex partial seizures or generalized tonic-clonic seizures. Benign nocturnal childhood occipital epilepsy (BNCOE), characterized by nocturnal seizures with tonic deviation of the eyes followed by vomiting, has the same electroencephalographic features as CEOP. In this study, we report the seizure symptoms and electroencephalographic features of 21 cases with CEOP or BNCOE. Out of these patients, nine had BNCOE, six had CEOP, four had CEOP and BNCOE and the remaining two belonged to the incomplete syndrome because of no paroxysmal discharges in EEG. When the patients with BNCOE awoke from sleep, they had tonic deviation of the eyes and could describe visual symptoms. Patients with CEOP had seizures beginning with visual symptoms followed by loss of consciousness but no generalized convulsions. In three cases, in addition to the occipital spikes, independent centro-temporal spikes were recorded and in another three cases generalized spike-wave discharges were recorded. Such a combination suggests the idiopathic nature of these epilepsies. We concluded that in the diagnosis of CEOP and BNCOE, the seizure symptomatology is important even if the EEG can be considered normal.

Anterior corpus callosotomy: effects in a patient with congenital bilateral perisylvian syndrome and oromotor seizures

Anterior corpus callosotomy was performed in a patient with pseudobulbar palsy, mild mental retardation and intractable epilepsy related to congenital bilateral perisylvian cortical dysplasia. Before surgery, she had daily atonic drop attacks, rare and mainly sleep-related oromotor seizures, and multifocal and diffuse paroxysmal EEG discharges; after callosotomy, less abrupt atonic drop attacks recurred monthly and the EEG epileptiform abnormalities disappeared. Video-EEG sleep recordings revealed the clinically unsuspected serial recurrence of oromotor seizures, probably related to the clinically observed aggravation of dysarthria. New surgical techniques, in addition or alternative to callosotomy, should be developed in order to avoid or reduce the risk of aggravating some types of partial seizures in patients with bilateral cortical displastic lesions, intractable epilepsy and epileptic falls.

Reflex epilepsy in the Papio-papio baboon, particularly photosensitive epilepsy.

Papio-papio baboons may present two types of reflex paroxysmal manifestations: --Myoclonia and generalized seizures are induced by intermittent light stimulation in predisposed animals; this photosensitive epilepsy resembles that observed in some human patients; it involves mainly the cerebral cortex during myoclonia which are accompanied by EEG paroxysmal discharges, and the mesencephalic reticular formation during seizures; --Myoclonia of a different type, never accompanied by EEG paroxysmal discharged and never evolving into seizures, may occur during movement or agitation of predisposed animals; these myoclonia are considered "non-epileptic" since they do not involve the cerebral cortex but probably the lower brain stem; they resemble that observed in startle disease or in some human degenerative disorders. The paper demonstrates that these manifestations constitute two different entities with clinical and electrophysiological characteristics as well as pharmacological reactivities completely different one from the other. Their "epileptic" or "non-epileptic" nature is discussed.

DOES GLYCINE ANTAGONISM UNDERLIE THE EXCITATORY EFFECTS OF METHOHEXITONE AND PROPOFOL

We have investigated the pharmacological basis of CNS excitation that occurs in association with general anaesthesia in mice. Propofol produced sustained clonic movements during anaesthesia. Methohexitone produced intermittent non-rhythmic jerking during anaesthesia. Ethanol and pentobarbitone produced anaesthesia without associated clonic movements. Doses of all anaesthetic drugs were equipotent. Surface EEG recordings showed paroxysmal discharges consistent with interictal manifestations of cortical seizures with methohexitone or propofol, but not with ethanol or pentobarbitone. Strychnine, a glycine antagonist without effects on the cerebral cortex, and bicuculline, a GABAA antagonist with effects on the cerebral cortex, were used in doses that were equipotent-0.5 log units less than the ED10 for clonic convulsions. Strychnine potentiated both excitatory behaviour and EEG paroxysmal discharges when given with methohexitone or propofol, but not with ethanol or pentobarbitone. Bicuculline did not affect either behaviour or EEG with any of the anaesthetic drugs. Our data show that methohexitone and propofol produced CNS excitation, while pentobarbitone and ethanol did not. We propose that the pharmacological basis of this excitation may be glycine antagonism occurring in subcortical structures.

Pretransplant conditioning with busulfan and cyclophosphamide in acute leukemia patients: Neurological and electroencephalographic prospective study

A neurological and electroencephalographic (EEG) prospective study was performed in 34 leukemic patients receiving busulfan (BU) plus cyclophosphamide (CY) before bone marrow autologous transplant. During BU treatment and briefly thereafter, all patients were given anticonvulsant prophylaxis with phenobarbital. Neurological evaluations were performed daily and EEGs, recorded one week before and soon after the end of the BU regimen, were re-evaluated two months later. Basal EEGs were normal in 23 of the 34 patients, focal abnormalities were detected in 9 cases, and generalized epileptic discharges were present in one (one subject was not studied). EEGs performed at the end of BU administration showed generalized spike/polyspike-and-wave discharges in 21 of the 34 patients, with associated myoclonic epilepsy in 10 subjects appearing on the 3rd or 4th day of treatment. Focal abnormalities were present in 6 patients and constant EEG normality in 7. It is known that myoclonic epilepsy can be induced by drugs. Oral administration of high-dose BU is followed by a high-dose cerebrospinal fluid concentration of the drug. Therefore, myoclonic epilepsy and/or paroxysmal epileptiform EEG discharges may be observed in leukemic patients undergoing high-dose BU therapy.

Is Cerebral Arteritis the Cause of the Landau-Kleffner Syndrome? Four Cases in Childhood with Angiographic Study

Four children with Landau-Kleffner syndrome were studied over a six year period. They presented with acquired aphasia, epilepsy, and focal or generalized EEG discharges which were exacerbated during sleep. In addition, cerebral angiography demonstrated isolated arteritis of some branches of the carotid arteries in all cases. Computed tomographic and magnetic resonance images were normal. Nicardipine in a dose of 1 to 2 mg/kg/day, added to conventional anticonvulsant drugs provided effective supplementary control of seizures, of paroxysmal EEG discharges, and of language and behavioural disturbances, even several years after the onset of the disorder and in patients whose response to other medications, including steroids, had been poor. Interruption of nicardipine administration was followed by relapse of the language disorder. Repeat angiography was performed in all four patients and showed recanalization of obstructed vessels in two cases. Focal cerebral vasculitis may be the pathogenesis of the Landau-Kleffner syndrome and calcium channel blockers such as nicardipine may be effective and specific therapy.

Suppressive effects of l-5-hydroxytryptophan in a feline model of photosensitive epilepsy

We recently demonstrated that long-lasting photosensitivity is acquired as a result of kindling of the lateral geniculate nucleus (LGN), and that the LGN-kindled cat pretreated with d,l-allylglycine represents a useful model of epilepsy for drug studies. The present experiments studied anticonvulsant effects of a serotonin precursor, l-5-hydroxytryptophan (5-HTP), on photosensitivity in the LGN-kindled cat under d,l-allylglycine and on LGN-kindled seizures. 5-HTP suppressed both myoclonic responses and paroxysmal EEG discharges induced by photic stimulation in a dose-related manner. Photically-induced seizures were completely blocked 1.5–2 h after injection of 20 mg/kg 5-HTP. 5-HTP was also effective in reducing the afterdischarge duration and behavioral seizure stage in LGN-kindled seizures; following 40 mg/kg administration, no electroclinical seizures were elicited in the LGN-kindled cats. Serotonergic mechanisms may play an important role in epileptic photosensitivity; the 5-HTP suppressive effect on photosensitivity is at least partly due to reduced neuronal activity at the level of the LGN via serotonergic inhibition.

Adult Follow-Up of the Acquired Aphasia-Epilepsy Syndrome in Childhood. Report of 7 Cases*

The authors report at adult age 7 patients (6 men, one woman) with the syndrome of "acquired aphasia-epilepsy", 6 of which had been previously studied as children. The results of the language, neuropsychological and socio-educational evaluation detailed many years after the onset of the aphasia are the subject of this report. One man has recovered completely, one has a normal oral language but is severely dyslexic, one has recovered normal comprehension but has severe expressive language problems. Four have absent language comprehension and lack of expressive speech, and only one of them has learned and is using sign language with some efficiency. None has developed functional written language. Attempts to offer a substitutive language to children with prolonged inability to understand and use oral language appears important but is fraught with problems. Although there are no conclusive data about the role of the continuous paroxysmal EEG discharges and the effect of their suppression with drug treatment on the prognosis of the aphasia, the definite fluctuations of the aphasia in some cases, the isolated recent case reports of definitive improvement with drug treatment justify further trials in this potentially severe and chronic condition.

Alumina cream-induced focal motor seizures in cats: Bilateral lesions of the mesencephalic reticular formation

The effect of bilateral lesions of the mesencephalic reticular formation on the EEG-EMG patterns of types B and C alumina cream-induced focal motor seizures was studied in cats with chronically implanted electrode and cannula lesion systems. EEG patterns included number, amplitude, and contralateral propagation of type B spikes and occurrence and duration of type C tonic-clonic discharges. EMG patterns included changes in muscular multiple-unit activity time locked to the onset of type B spikes and to the onset and end of type C tonic-clonic EEG paroxysmal discharges. The lesions persistently blocked the orienting response to visual, auditory, and tactile stimuli to both sides in all cats and produced other neurologic symptoms partially or totally recovered in some cats. The lesions significantly increased the number, amplitude, and contralateral propagation of type B EEG spikes and the occurrence, but not the duration, of type C EEG tonic-clonic discharges. Ipsi- and contralateral adversion of the tonic phase were completely blocked and the muscular contractions of the clonic phase were reduced and delayed. These facts suggest that in intact epileptic cats, the mesencephalic reticular formation has an ascending suppressive influence on the mechanism related to EEG spike generation and precipitation of seizures but also a descending facilitatory control on the corticospinal epileptic impulses mediated through pyramidal and estrapyramidal pathways.

Alumina cream induced focal motor epilepsy in cats. VI. Excision of the perilesional cortex

The effect of surgical excision of dorsolateral ventromedial and combined (dorsolateral-ventromedial) perilesional cortices on EMG-EEG patterns of alumina cream induced focal motor seizures was studied in cats with chronically implanted electrodes. EMG patterns included clinical convulsions and related EMG-multiple unit activity. EEG patterns included number, amplitude, polarity and contralateral propagation of type B isolated spikes and type C tonic-clonic paroxysmal discharges. 1. (1) Dorsolateral decortications abolished isolated jerks and related EMG-multiple unit activity and blocked propagation with no effect on number, amplidude and polarity of EEG spikes of type B seizures (epilepsia partialis continua). Dorsolateral decortications reduced contraversion and repetitive jerks and related EMG-multiple unit activity with no changes in number, amplitude, polarity and propagation of EEG tonic-clonic paroxysmal discharges of type C seizures (adversive epilepsy). 2. (2) Ventromedial decortications decreased the number but neither changed jerks and related EMG-multiple unit activity nor amplitude, polarity, propagation of EEG spikes of type B seizures. Ventromedial decortications abolished contraversion and jerks and related EMG-multiple unit activity and reduced number, amplitude and duration with no changes in polarity and propagation of EEG paroxysmal discharges of type C seizures. 3. (3) Combined decortications abolished jerks, contraversion and related EMG-multiple unit activity with a variable effect of EEG patterns of type B and C seizures. In 4 cats, combined decortications abolished while in other 2 cats decreased the amplitude and reversed the polarity of type B spikes and reversed the polarity and blocked the propagation of type C paroxysmal discharges.