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Biomedical subjects

C P Panayiotopoulos

Publications and source records attributed to C P Panayiotopoulos.

At least 19 recordsLinked to original sources
PubMed2001

Tooth brushing-induced seizures: a case report.

We report a 28-year-old woman of normal intellect, who had three late-onset seizures with unusual ictal features and secondary generalization during prolonged and vigorous tooth brushing. Neurologic examination and brain magnetic resonance imaging (MRI) were normal, but interictal EEG showed left frontal epileptiform activity. Reasonable precautions (regular but briefer and less vigorous brushing of her teeth) combined with a moderate dose of carbamazepine effectively prevented seizure recurrence. This case may be an example of cryptogenic form of reflex epilepsy with seizures induced exclusively by tooth brushing.

Adult↗
PubMed2001

Primary diffuse leptomeningeal gliomatosis simulating tuberculous meningitis.

Three patients are reported on who presented with communicating hydrocephalus due to presumed tuberculous meningitis. Subsequent clinical deterioration despite antituberculous chemotherapy prompted reassessment with FDG-PET scanning and meningeal biopsy in one case and repeat CSF cytology with special staining in the second. The third patient died and postmortem confirmed a diagnosis of primary diffuse leptomeningeal gliomatosis. In the first two patients, MRI of the entire neuraxis showed no evidence of a primary intraparenchymal tumour. These cases emphasise the need for repeated reassessment in patients with culture negative lymphocytic meningitis. In addition, this is the first report of FDG-PET scanning in leptomeningeal gliomatosis.

Adult↗
PubMed2001

Treatment of typical absence seizures and related epileptic syndromes.

Typical absences are brief (seconds) generalised seizures of sudden onset and termination. They have 2 essential components: clinically, the impairment of consciousness (absence) and, generalised 3 to 4Hz spike/polyspike and slow wave discharges on electroencephalogram (EEG). They differ fundamentally from other seizures and are pharmacologically unique. Their clinical and EEG manifestations are syndrome-related. Impairment of consciousness may be severe, moderate, mild or inconspicuous. This is often associated with motor manifestations, automatisms and autonomic disturbances. Clonic, tonic and atonic components alone or in combination are motor symptoms; myoclonia, mainly of facial muscles, is the most common. The ictal EEG discharge may be consistently brief (2 to 5 seconds) or long (15 to 30 seconds), continuous or fragmented, with single or multiple spikes associated with the slow wave. The intradischarge frequency may be constant or may vary (2.5 to 5Hz). Typical absences are easily precipitated by hyperventilation in about 90% of untreated patients. They are usually spontaneous, but can be triggered by photic, pattern, video games stimuli, and mental or emotional factors. Typical absences usually start in childhood or adolescence. They occur in around 10 to 15% of adults with epilepsies, often combined with other generalised seizures. They may remit with age or be lifelong. Syndromic diagnosis is important for treatment strategies and prognosis. Absences may be severe and the only seizure type, as in childhood absence epilepsy. They may predominate in other syndromes or be mild and nonpredominant in syndromes such as juvenile myoclonic epilepsy where myoclonic jerks and generalised tonic clonic seizures are the main concern. Typical absence status epilepticus occurs in about 30% of patients and is more common in certain syndromes, e.g. idiopathic generalised epilepsy with perioral myoclonia or phantom absences. Typical absence seizures are often easy to diagnose and treat. Valproic acid, ethosuximide and lamotrigine, alone or in combination, are first-line therapy. Valproic acid controls absences in 75% of patients and also GTCS (70%) and myoclonic jerks (75%); however, it may be undesirable for some women. Similarly, lamotrigine may control absences and GTCS in possibly 50 to 60% of patients, but may worsen myoclonic jerks; skin rashes are common. Ethosuximide controls 70% of absences, but it is unsuitable as monotherapy if other generalised seizures coexist. A combination of any of these 3 drugs may be needed for resistant cases. Low dosages of lamotrigine added to valproic acid may have a dramatic beneficial effect. Clonazepam, particularly in absences with myoclonic components, and acetazolamide may be useful adjunctive drugs.

Anticonvulsants↗
PubMed2000

Benign childhood epileptic syndromes with occipital spikes: new classification proposed by the International League Against Epilepsy.

In a recent proposal, the Commission on Classification and Terminology of the International League Against Epilepsy recognized early-onset childhood epilepsy with occipital spikes (Panayiotopoulos type), differentiating it from the only other type of childhood epilepsy with occipital spikes previously accepted: late-onset childhood epilepsy with occipital spikes (Gastaut type). The importance of this newly recognized syndrome of benign childhood partial seizures is that it is very common-only 2.4 times less frequent than benign rolandic epilepsy, and of equally excellent prognosis. It is characterized by a unique seizure type comprising a combination of autonomic and behavioral disturbances, vomiting, deviation of the eyes, and often with impairment of consciousness that can progress to convulsions. These commonly last for more than 3 minutes and in one quarter of cases for hours. One or more of these symptoms can predominate or be absent. Eyes can remain open without deviation, ictal vomiting might not occur, and autonomic and behavioral disturbances can predominate, particularly in the early stages of the ictus, and be missed in nocturnal seizures. Age at onset is 5 years, with a singular or a median of three seizures, which are predominantly nocturnal. Interictal electroencephalography (EEG) frequently shows occipital paroxysms or occipital spikes but one-fifth of the cases have only extraoccipital spikes on normal EEG. Treatment might not be needed. Panayiotopoulos syndrome, like rolandic epilepsy, needs recognition by the general pediatrician because of the invariably excellent prognosis and also because it can be misdiagnosed as an acute cerebral insult.

Age of Onset↗
PubMed2000

Clinical, genetic, and expression studies of mutations in the potassium channel gene KCNA1 reveal new phenotypic variability.

Episodic ataxia type 1 (EA1) is an autosomal dominant central nervous system potassium channelopathy characterized by brief attacks of cerebellar ataxia and continuous interictal myokymia. Point mutations in the voltage-gated potassium channel gene KCNA1 on chromosome 12p associate with EA1. We have studied 4 families and identified three new and one previously reported heterozygous point mutations in this gene. Affected members in Family A (KCNA1 G724C) exhibit partial epilepsy and myokymia but no ataxic episodes, supporting the suggestion that there is an association between mutations of KCNA1 and epilepsy. Affected members in Family B (KCNA1 C731A) exhibit myokymia alone, suggesting a new phenotype of isolated myokymia. Family C harbors the first truncation to be reported in KCNA1 (C1249T) and exhibits remarkably drug-resistant EA1. Affected members in Family D (KCNA1 G1210A) exhibit attacks typical of EA1. This mutation has recently been reported in an apparently unrelated family, although no functional studies were attempted. Heterologous expression of the proteins encoded by the mutant KCNA1 genes suggest that the four point mutations impair delayed-rectifier type potassium currents by different mechanisms. Increased neuronal excitability is likely to be the common pathophysiological basis for the disease in these families. The degree and nature of the potassium channel dysfunction may be relevant to the new phenotypic observations reported in this study.

Action Potentials↗
PubMed1999

F-chronodispersion in patients on thalidomide.

OBJECTIVES: To describe abnormalities of F-chronodispersion in patients treated with thalidomide. METHODS: We retrospectively studies F-wave latency, persistence and F-chronodispersion in 12 patients on thalidomide treatment and compared them with a control group of another 12 patients with similar dermatological conditions who did not receive thalidomide. Furthermore, we prospectively performed longitudinal neurophysiological studies in 4 patients before and during thalidomide treatment. RESULTS: Seven of 12 patients in the retrospective study had abnormal F-chronodispersion while this was normal in all patients of the control group (P = 0.014). All other neurophysiological parameters were similar in the two groups. Two of the thalidomide patients with abnormal F-chronodispersion later developed sensory neuropathy. In all 4 patients in the prospective study though F-chronodispersion was normal before thalidomide it became markedly abnormal after exposure to this drug. CONCLUSIONS: Thalidomide may affect smaller diameter motor nerve fibres even before changes in sural sensory nerve action potentials. F-waves and F-chronodispersion should be routinely monitored in patients on thalidomide treatment.

Adolescent↗
PubMed1999

Early-onset benign childhood occipital seizure susceptibility syndrome: a syndrome to recognize.

Early-onset benign childhood occipital seizures (EBOS) described by Panayiotopoulos constitute the commoner after the rolandic phenotype of a childhood seizure susceptibility syndrome. EBOS are the clinical representative of occipital spikes. Their cardinal features are infrequent (often single) partial seizures manifested with deviation of the eyes and vomiting, frequently evolving to hemi- or generalized convulsions. Ictal behavioral changes, irritability, pallor, and rarely cyanosis, and eyes wide open are frequent. Retching, coughing, aphemia, oropharyngolaryngeal movements, and incontinence may occur. Consciousness is usually impaired or lost, either from the onset or the course of the fits, but in a few children, it may be preserved. Duration varies from a few minutes to hours (partial status epilepticus). Seizures are usually nocturnal, but semiology is similar in nocturnal or diurnal fits. Onset is between 1 and 12 years with a peak at 5 years. One third of children have a single seizure, the median total number of fits is two to three, and the prognosis is invariably excellent, with remission usually occurring within 1 year from onset. A few children may later develop rolandic or other benign partial seizures. The likelihood to have seizures after age 12 years is exceptional and rarer than that of febrile convulsions. EEG shows occipital paroxysms demonstrating fixation-off sensitivity, but random occipital spikes, occipital spikes in sleep EEG alone, or normal EEG may occur. Centrotemporal and other spike foci may appear in the same or more frequently in subsequent EEGs. The EEG does not reflect clinical course and severity.

Age Factors↗
PubMed1999

Extraoccipital benign childhood partial seizures with ictal vomiting and excellent prognosis.

In a previous report of 900 patients with epileptic seizures, 24 children had ictal vomiting. Twelve had a previously unrecognised syndrome of early onset benign childhood occipital seizures (EBOS) and three had symptomatic epilepsy. The other nine children with extraoccipital EEG foci or normal EEG are described in this paper based on a prospective follow up for a median of 9 years after their first seizure. All had normal neurology, mental state, and development. All seizures of all but one patient occurred in sleep. Seizures manifested with ictal vomiting (nine), deviation of the eyes (four), speech arrest (three), hemiconvulsions (five), oropharyngolaryngeal symptoms, and hypersalivation (one) with or without impairment of consciousness. Median age at onset was 5 years, seizures were infrequent and remitted at a median age of 6. Four children had a single fit, four had two to three, and only one child had many seizures before the initiation of treatment. This study certifies that idiopathic childhood partial seizures with ictal vomiting may occur with EEG spike foci in other than the occipital regions or EEG may be normal. Despite some clinico-EEG differences from the EBOS, childhood seizures with ictal vomiting, and extraoccipital EEG foci are of equally excellent prognosis. Their existence on the border between rolandic and occipital seizures is consistent with a unified concept of a benign childhood partial seizure susceptibility syndrome.

Anticonvulsants↗
PubMed1999

Elementary visual hallucinations, blindness, and headache in idiopathic occipital epilepsy: differentiation from migraine.

This is a qualitative and chronological analysis of ictal and postictal symptoms, frequency of seizures, family history, response to treatment, and prognosis in nine patients with idiopathic occipital epilepsy and visual seizures. Ictal elementary visual hallucinations are stereotyped for each patient, usually lasting for seconds. They consist of mainly multiple, bright coloured, small circular spots, circles, or balls. Mostly, they appear in a temporal hemifield often moving contralaterally or in the centre where they may be flashing. They may multiply and increase in size in the course of the seizure and may progress to other non-visual occipital seizure symptoms and more rarely to extra-occipital manifestations and convulsions. Blindness occurs usually from the beginning and postictal headache, often indistinguishable from migraine, is common. It is concluded that elementary visual hallucinations in occipital seizures are entirely different from visual aura of migraine when individual elements of colour, shape, size, location, movement, speed of development, duration, and progress are synthesised together. Postictal headache does not show preference for those with a family history of migraine. Most of the patients are misdiagnosed as having migraine with aura, basilar migraine, acephalgic migraine, or migralepsy simply because physicians are not properly informed of differential diagnostic criteria. As a result, treatment may be delayed for years. Response to carbamazepine is excellent and seizures may remit.

Adolescent↗
PubMed1999

Interictal 18FDG PET findings in temporal lobe epilepsy with déjà vu.

The authors studied the functional anatomy of the déjà vu (DV) experience in nonlesional temporal lobe epilepsy (TLE), using interictal fluorine-18 fluorodeoxyglucose PET in 14 patients with and 17 patients without DV. Several clinical conditions, such as age at PET study, side of ictal onset zone, and dominance for language, were no different between the two groups. The patients with DV showed significant relative reductions in glucose metabolism in the mesial temporal structures and the parietal cortex. The findings demonstrate that ictal DV is of no lateralizing value. They further suggest that temporal lobe dysfunction is necessary but not sufficient for the generation of DV. Extensive association cortical areas may be involved as part of the network that integrates this distinct experience.

Adult↗
PubMed1999

Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine.

This is a systematic-prospective study of occipital seizures with elementary visual hallucinations in 18 patients with symptomatic occipital epilepsy. Qualitative and chronological analysis showed that visual seizures usually lasted for seconds to 1-3 minutes. Three patients also had longer visual seizures of 20-150 minutes. Elementary visual hallucinations mainly consisted of coloured and small circular patterns flashing or multiplying in a temporal hemifield. Flashing lights or non-circular patterns were rare. Three patients experienced achromatic flickering lights. None of the patients had the over 4 minute, linear, zigzag, and achromatic or black and white patterns characteristic of migraine visual aura. Blurring of vision could precede visual hallucinations. Visual seizures were usually frequent, often occurring in multiple clusters daily or weekly. They usually occurred alone but they often advanced to other occipital and extra-occipital ictal symptoms. In 7 patients they progressed to temporal lobe seizure manifestations, and in 6 to motor partial seizures or ipsilateral hemiconvulsions. All but 2 had secondary generalised tonic clonic convulsions. Ictal blindness ab initio occurred in 2 and ictal, mainly orbital headache in another 2 patients. One patient had ictal vomiting as an occasional symptom. Postictal headache, often severe and indistinguishable from migraine, occurred in two thirds of the patients, even after brief visual seizures without convulsions. Despite relevant structural lesions in brain imaging, 10 patients had a normal mental and neurological state. In 8 patients, EEG was also normal or nonspecific. Misdiagnosis of visual seizures as visual aura of migraine was common and 3 patients were misdiagnosed as suffering from migraine. The differential diagnosis between migraine and the occipital epilepsies is reviewed. It is concluded that elementary visual hallucinations, blindness or both, alone or followed by headache and vomiting of symptomatic occipital epilepsy are identical to those of idiopathic occipital epilepsy. Progress to temporal lobe structures is different and consistent with symptomatic occipital lobe epilepsy. The clinical diagnosis of visual seizures is easy if individual elements of duration, colour, shape, size, location, movement, speed of development and progress are identified. They are markedly different from visual aura of migraine, although they often trigger migrainous headache, probably by activating trigeminovascular or brain stem mechanisms.

Adolescent↗