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Biomedical subjects

D R Fish

Publications and source records attributed to D R Fish.

At least 73 records · Page 4Linked to original sources
PubMed1996

Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy.

OBJECTIVE: To record non-invasively ictal cardiorespiratory variables. METHODS: Techniques employed in polysomnography were used in patients with epilepsy undergoing EEG-video recording at a telemetry unit. RESULTS: Apnoea (> 10, range > 10-63, mean 24 s) was seen in 20 of 47 clinical seizures (three secondary generalised, 16 complex partial, and one tonic) and 10 of 17 patients. Apnoea was central in 10 patients, but obstructive apnoea was also recorded in three of 10. Oxyhaemoglobin saturation (SpO2) dropped to less than 85% in 10 seizures (six patients). An increase in heart rate was common (91% of seizures). Bradycardia/sinus arrest was documented in four patients (mean maximum RR interval 5.36, range 2.8-8.6 s) but always in the context of a change in respiratory pattern. CONCLUSION: Ictal apnoea was often seen. The occurrence of bradycardia in association with apnoea suggests the involvement of cardiorespiratory reflexes. Similar mechanisms may operate in cases of sudden death in epilepsy.

Adolescent↗
PubMed1996

Startle provoked epileptic seizures:features in 19 patients.

OBJECTIVES: To define the clinical characteristics of a group of patients with startle provoked epileptic seizures (SPES). METHODS: Nineteen patients were identified during the course of a larger study of clinical seizure patterns. A witnessed seizure account was obtained in all patients; interictal EEG in 18, video-EEG-telemetry in eight, CT in 18, and high resolution MRI in eight. RESULTS: The onset of SPES was in childhood or adolescence in 14 of 19 patients. It was preceded by exclusively spontaneous seizures in nine patients and SPES had been replaced by exclusively spontaneous seizures in two patients. Sudden noise was the main triggering stimulus and somatosensory and visual stimuli were also effective in some patients. The clinical seizure pattern involved asymmetric tonic posturing in 16 of 19 patients. Focal neurological signs were present in nine patients, mental retardation in six, and 10 were clinically normal. Ictal scalp EEG showed a clear seizure discharge in only one patient with a tonic seizure pattern; over the lateral frontal electrodes contralateral to the posturing limbs. Brain CT showed a porencephalic cyst in three patients, focal frontal atrophy in one, and generalised atrophy in one. Brain MRI was undertaken in five normal subjects and three neurologically impaired patients, six with normal CT. It showed a porencephalic cyst in one patient. In six patients, there were dysplastic lesions. They affected the lateral premotor cortex in three patients and the perisylvian cortex in three patients, one with bilateral perisylvian abnormality. CONCLUSIONS: SPES are more frequent than is generally appreciated. They may be transient and occur relatively commonly without fixed deficit, by contrast with previous reports. The imaging abnormalities identified in those without diffuse cerebral damage suggest that SPES are often due to occult congenital lesions and that the lateral premotor and perisylvian cortices are important in this phenomenon.

Adolescent↗
PubMed1995

First seizures associated with playing electronic screen games: a community-based study in Great Britain.

Active surveillance by virtually all electroencephalographic departments throughout Great Britain identified 118 patients who had a first seizure while playing an electronic screen game during two 3-month periods. Patients were divided into Group A (46 patients)--those for whom there was thought to be a definite causal relationship (type 4 photoparoxysmal response); Group B (25 patients)--those for whom there was a probable causal relationship (types 1-3 photoparoxysmal response, clinical evidence of photosensitivity, subsequent recurrent seizures on repeat exposure to electronic screen games, and/or occipital spikes in the resting electroencephalogram); and Group C (47 patients)--those for whom there was no apparent causal relationship. The number of patients in Group C did not exceed that expected by the chance occurrence of two common events (playing electronic screen games and incidence of epilepsy). Most (103/118) of the patients were in the age range of 7 to 19 years. Within this age group the annual incidence of first seizures triggered by playing electronic screen games (Groups A and B combined) was estimated to be 1.5/100,000.

Adolescent↗
PubMed1995

Frameless stereotaxy and interactive neurosurgery with the ISG viewing wand.

Preliminary experience with the ISG wand for frameless stereotaxy is presented. The wand is a multijointed mechanical arm with a range of 25 inch radius sphere. The arm has a analog/digital hybrid transducers to locate the spatial position of the probe tip. The real time displays of triplanar 2D images with an optional 2D/3D image helps in surgical planning and interactive surgery. Seventeen patients underwent neurosurgical procedures with the help of wand. The wand was used to place minimal craniotomies, localise the brain-tumour interface and excise the lesions. The wand had an accuracy of 1.8 mm (SEM +/- 0.36 mm) in localising the lesions. Thus, the use of frameless stereotaxy has made easier and more precise surgical planning in several applications.

Adolescent↗
PubMed1995

Cortical dysgenesis: serial EEG findings in children and adults.

Cortical dysgenesis (CD) is becoming increasingly recognised as a cause of epilepsy in otherwise cryptogenic cases. We describe the serial EEG findings in 22 patients with focal/localised CD. The EEGs covered a minimum period of 5 years in each case (median = 13 years, range: 5-30 years), beginning in childhood. Median age at seizure onset was 3 years (range: 3 weeks-10 years, n = 21). The EEG was normal in the one patient, a 6 year old, who did not have epilepsy. Background rhythms appropriate for age were preserved in the majority of patients (18/22). Slow activity localised to the area of CD was seen in 11 patients; in 3 patients, this did not appear until the second decade of life. Epileptiform discharges were seen in at least one EEG in 20 patients: these were continuous or near-continuous (6 patients) or occurred recurrently in short runs (6 patients). In 6 patients, these discharges appeared only after the second decade of life and in 11 patients, they became more widespread over time. In the remaining patients, the EEG changes did not evolve. Sleep failed to produce new abnormalities (n = 15). None of the patients showed EEG features characteristic of lissencephaly or evolution to the Lennox-Gastaut syndrome. Even in this selected cohort of patients who had undergone serial clinical EEGs, the EEG abnormalities in focal/localised CD appeared relatively stable and showed only moderate changes over time. CD must be included in the differential diagnosis of any patient who presents with localised slow activity on EEG.

Adolescent↗
PubMed1995

Incidence of photosensitive epilepsy: a prospective national study.

We undertook a prospective nationwide study to determine the incidence of photosensitive epilepsy (PE). Virtually all EEG departments in Great Britain (providing approximately 90% coverage of all EEGs performed on people with newly diagnosed seizures) screened cases referred to them over a 3 month period and identified all new cases of epilepsy (defined as one or more recognised seizures) whose first EEG showed a photoparoxysmal response (PPR) on intermittent photic stimulation (IPS). 191 cases were identified, 143 of whom had type 4 PPRs (generalised spike and wave on IPS) on their first EEG. The annual incidence of cases of epilepsy with type 4 PPRs on their first EEG was conservatively estimated to be 1.1 per 100,000, representing approximately 2% of all new cases of epilepsy. When restricted to the age range 7-19 years, the annual incidence rose to 5.7 per 100,000-approximately 10% of all new cases of epilepsy presenting in this age range. To ascertain if there was a significant seasonal variation in PE, 5 EEG departments (which together contributed 15% of cases in the first study period) were visited during a second 3 month study period to identify all new cases of epilepsy with type 4 PPRs on their first EEG. No significant seasonal variation in incidence between summer and winter was found.

Adolescent↗
PubMed1995

Clinical correlations: MRI and EEG.

Main structural correlates of epileptogenesis include hippocampal sclerosis, cortical dysgenesis, foreign tissue lesions, gliosis, and dual pathology (a combination of any two). These structural abnormalities are now increasingly defined with MRI, enabling systematic EEG correlative analyses. Hippocampal atrophy (HA) and increased T2 signal in medial temporal structures predict the presence of mesial temporal sclerosis with a high degree of sensitivity and specificity. In 50 patients with clinical evidence of temporal lobe epilepsy and isolated HA, ictal scalp EEG was concordant to the atrophic temporal lobe in 33, nonlateralizing in 12, obscured in 3, and bilateral in 2, but it was discordant in none. Earlier reports of higher levels of discordance may be ascribed to the presence of dual pathology or to differing MRI and EEG criteria for localization. In a more inclusive group of 101 patients with unilateral HA, ictal scalp EEG was obtained in 99. It was unlocalized in 53, localized elsewhere in 9, and localized to the atrophic temporal lobe in 38. Of those, 51 patients had intracranial EEG: 12 were unlocalized, 29 were localized to the atrophic hippocampus, and 9 were localized elsewhere. There is thus a rare but definite subgroup of patients with unilateral HA who have EEG localization elsewhere than the atrophy. The successful cure of seizures in half these patients after removal of the EEG focus confirms the importance of this observation and emphasizes the search for more dual pathology that has remained undetected on MRI. About 10% of the patients with HA have significant atrophy bilaterally, and several series have confirmed that surgical success is predicted by removal of the EEG identified seizure onset area, not the more or less atrophic hippocampus. In patients with other kinds of dual pathology, including HA and foreign tissue lesions or cortical dysgenesis, EEG is also paramount in predicting the site of epileptogenesis for surgical intervention. EEG correlates of cortical dysgenesis are heterogeneous, but EEG has potential to provide accurate localization of the site of epileptogenesis in foreign tissue lesions also. In a study of 59 lesional patients, a small number of patients with low grade astrocytomas and oligodendrogliomas consistently localized by EEG to an area elsewhere than the lesion, and failed seizure control when the lesion was removed. Although MRI can demonstrate the structural correlate of the epilepsy in many situations, rare patients, particularly with certain tumors, cortical dysgenesis, and dual pathology, require EEG for accurate localization.

Atrophy↗
PubMed1995

Increasing the yield from volumetric MRI in patients with epilepsy.

Volumetric magnetic resonance imaging has become a routine investigation in the management of patients with chronic partial epilepsy. However, even with the use of reformatted images, an underlying cause for epilepsy cannot be found in many of these patients. We show that further processing of the data, including three-dimensional reconstruction and quantitative analysis of the volume and complexity of the images in three dimensions, reveals additional positive information in up to 75% of patients. This may be useful for surgical planning, prognostication, and understanding of the structure and development of the human brain.

Adult↗
PubMed1995

High-voltage pulsed current: its influence on diameters of histamine-dilated arterioles in hamster cheek pouches.

Results from five independent studies from our laboratory indicate that cathodal high-voltage pulsed current (HVPC) significantly curbs posttraumatic edema formation in several animal models. Conversely, anodal HVPC did not curb edema formation. The mechanism by which HVPC reduces edema formation is unknown. We hypothesize that HVPC causes a decrease in local blood flow by active vasoconstriction of arterioles. Because we had previously observed positive effects with cathodal HVPC but not anodal HVPC, we further hypothesized that cathodal but not anodal HVPC would reduce diameters of histamine-dilated arterioles. Changes in diameters of resistance arterioles (5 to 30 microns internal diameter) were measured directly in cheek pouches of anesthetized hamsters, using in vivo video microscopy. Three minutes after superfusion with the inflammatory mediator (histamine) was begun, sensory-level HVPC at 120pps was applied concurrently for 30 minutes. Five animals received cathodal HVPC and five received anodal HVPC. Four other animals received 30-minute treatments of both cathodal and anodal HVPC in random order. Three control animals received histamine without HVPC for 30 minutes. Diameter changes of one arteriole from each cheek pouch was measured every 20 seconds throughout the treatment period. One-way analysis of variance (ANOVA) with repeated measures showed that diameters of histamine-dilated controls varied little over 30 minutes, and that adding cathodal HVPC did not significantly alter diameters of arterioles superfused with histamine. However, applying anodal HVPC to histamine-dilated arterioles significantly reduced arteriolar diameters. These results do not support the hypothesis that cathodal HVPC curbs edema formation by increasing arteriolar tone in the injured area.

Animals↗
PubMed1995

Autosomal dominant nocturnal frontal lobe epilepsy. A distinctive clinical disorder.

The disorder of autosomal dominant nocturnal frontal lobe epilepsy has recently been identified, and is now delineated in detail. A phenotypically homogeneous group of five families from Australia, Britain and Canada, containing 47 affected individuals, was studied. The largest family contained 25 affected individuals spanning six generations. This disorder is characterized by clusters of brief nocturnal motor seizures, with hyperkinetic or tonic manifestations. Subjects often experienced an aura, and remained aware throughout the attacks. Seizures occurred in clusters (mean eight attacks/night) typically as the individual dozed, or shortly before awakening. The epilepsy usually began in childhood, and persisted through adult life, with considerable intra-family variation in severity. Seizures were often misdiagnosed as benign nocturnal parasomnias, psychiatric and medical disorders. Interictal EEG studies were unhelpful. Ictal video-EEG studies showed that the attacks were partial seizures with frontal lobe seizure semiology. Neuro-imaging was normal. Carbamazepine monotherapy was frequently effective. This disorder showed autosomal dominant inheritance. Recognition of this entity is clinically important for diagnosis, appropriate therapy and genetic counselling. Moreover, this disorder now offers an opportunity to identify a gene for partial epilepsy.

Adolescent↗
PubMed1995

Abnormalities of gyration, heterotopias, tuberous sclerosis, focal cortical dysplasia, microdysgenesis, dysembryoplastic neuroepithelial tumour and dysgenesis of the archicortex in epilepsy. Clinical, EEG and neuroimaging features in 100 adult patients.

Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes. We reviewed the clinical, EEG and neuroimaging features in 100 adult patients with CD. There were 39 men and 61 women with a median age of 27 years (range 15-63 years). All patients were referred because of medically refractory epilepsy. Median age at seizure onset was 10 years (range 3 weeks to 39 years); in 30 patients, onset was in adulthood. The epilepsy was classified as generalized in 16 patients and localization-related in 84. Of the latter, the epileptic syndromes in decreasing frequency were frontal (32%), temporal (31%), parietal (14%) and occipital (7%). Only 15% of patients had a history of status epilepticus. Prenatal/perinatal problems were reported in 32 patients but these were severe in only four: exposure to drugs (three) and infection (one) during the first trimester. Delayed developmental milestones were seen in 10%, mental retardation in 9%, additional congenital abnormalities in 4% and neurological deficits in 14% of patients. Diagnosis of CD was based on neuroimaging in 70, pathology in four and both methods in the remaining 26. The following subcategories were identified: agyria/diffuse macrogyria (four patients), focal macrogyria (16), focal polymicrogyria (one), focal macrogyria/polymicrogyria associated with a cleft (11), minor gyral abnormalities (seven), subependymal grey matter heterotopia (20), bilateral subcortical laminar grey matter heterotopia (eight), tuberous sclerosis (five), focal cortical dysplasia/microdysgenesis (seven) and dysembryoplastic neuroepithelial tumours (DNT) (21). Sixty-eight percent of patients had normal CT and 19 out of 36 patients had normal previous conventional MRI. MRI-based hippocampal volume measurements in 47 patients revealed ratios (smaller: larger hippocampus) of < 0.90 in 16, 0.90-0.94 in 14 and > or = 0.95 in 17 patients. EEGs were normal in only five patients. Alpha rhythm was preserved in 78 patients, including one patient with bilateral posterior macrogyria. Localized polymorphic slow activity was present in 43 patients. Five of 68 patients with focal/unilateral CD had only bilateral independent/synchronous spiking and 14 out of 32 with diffuse/bilateral CD only focal/unilateral spiking. In 60 patients with nondiffuse CD or with abnormal gyration or DNT, the epileptiform abnormalities were less extensive than coextensive with the lesion in 28, more extensive than and overlapped the lesion in 18 and remote from the lesion in five; nine patients did not have epileptiform abnormalities. There was poor correlation between the epileptic syndromes and EEG abnormalities and the location/extent of CD as defined by MRI and pathology.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1995

Widespread cerebral structural changes in patients with cortical dysgenesis and epilepsy.

Cerebral cortical dysgenesis (CD), as revealed by MRI is the second commonest cause of medically refractory chronic partial epilepsy. Surgical treatment is often disappointing in these cases. This has been attributed to the probable diffuse nature of the condition but proof of this in the human brain is lacking. We have quantitatively analysed MRI scans of 30 neurologically normal control subjects and 18 patients with CD, examining the regional distribution of grey and subcortical matter volumes. In 15 out of the 18 patients, we have demonstrated abnormalities of this distribution beyond the margins of the visualized lesion. Nine out of 10 patients with dysgenetic lesions visualized only in one hemisphere had volumetric abnormality in the apparently normal contralateral hemisphere. These abnormalities were not visible on reinspection of the MRI scans. Such abnormalities were not found in 10 patients with isolated hippocampal sclerosis (HS) although the history of generalized seizure activity and duration of epilepsy did not differ between the two groups of patients. Thus there is evidence for the existence of extensive structural disorganization outside visually identified focal lesions in the brains of patients with CD and chronic partial epilepsy. This disruption is not due to the effects of the epilepsy and must instead be associated with its cause. Possible mechanisms producing the abnormalities are discussed. The methodology described may be applied to other cortical diseases.

Adult↗
PubMed1995

Benzodiazepine-GABAA receptors in idiopathic generalized epilepsy measured with [11C]flumazenil and positron emission tomography.

The neurochemical basis of absence seizures and the mechanism of their suppression by valproate (VPA) are uncertain. We used positron emission tomography (PET) to determine whether an abnormality of [11C]flumazenil binding to benzodiazepine (BZD)-GABAA receptors exists in patients with childhood and juvenile absence epilepsy and to examine the effects of VPA on [11C]flumazenil binding. The regional cerebral volume of distribution (Vd) of [11C]flumazenil in patients not treated with VPA was not different from that in normal controls; Vd was lower in patients treated with VPA, and the number of receptors available for binding was significantly reduced in such patients as compared with normal controls. There was no evidence of a primary abnormality of the BZD-GABAA receptor in childhood and juvenile absence epilepsy (CAE/JAE), but the data suggest that treatment with VPA is associated with a reduction in [11C]flumazenil binding that may be relevant to its mode of action in CAE/JAE.

Adolescent↗
PubMed1995

Sudden death in epilepsy: a study of incidence in a young cohort with epilepsy and learning difficulty.

Sudden death, often seizure related, may occur in patients with epilepsy. Population-based incidence is probably on the order of 1:1,000/year. The incidence is much higher in selected groups, however. We wished to establish the incidence of sudden unexpected death (SUD) in a young cohort with severe epilepsy and learning difficulties. The study cohort included 310 pupils with epilepsy enrolled at a special residential school between April 1970 and April 1993. The follow-up period totaling 4,135 person-years included a period of residence at the school as well as time after leaving. Age and sex standardized overall mortality ratio was 15.9 [95% confidence interval (CI) 10.6-23.0], with 20 of 28 deaths considered epilepsy related. An incidence of sudden death cases of 1:295/year was noted. All 14 sudden deaths occurred when the pupils were not under the close supervision of the school and most were unwitnessed, which has implications for prevention.

Adolescent↗
PubMed1995

Benzodiazepine-GABAA receptor binding during absence seizures.

The role of benzodiazepine (BZD)-gamma-aminobutyric acidA (GABAA) receptors in the pathogenesis of absence seizures is uncertain. In this study, we examined the effect of absence seizures on the binding of flumazenil to the BZD binding site of the GABAA receptor. Five patients with idiopathic generalized epilepsy (IGE) were studied at rest and during absence seizures with [11C]flumazenil and positron emission tomography (PET). Normalized regional cerebral time-activity curves from the resting and ictal scans were compared with each other and with computed simulations showing the effects of changes in cerebral blood flow (CBF) and [11C]flumazenil binding. No evidence was found for a change in [11C]flumazenil binding with absence seizures. This result, together with those of a recent study showing no abnormality of [11C]flumazenil binding interictally in patients with childhood and juvenile absence epilepsy (JAE) does not support a primary role for the BZD binding site of the GABAA receptor in the pathogenesis of absence seizures.

Adolescent↗
PubMed1995

Magnetic resonance imaging in partial epilepsy: additional abnormalities shown with the fluid attenuated inversion recovery (FLAIR) pulse sequence.

Thirty six patients with a history of partial epilepsy had MRI of the brain performed with conventional T1 and T2 weighted pulse sequences as well as the fluid attenuated inversion recovery (FLAIR) sequence. Abnormalities were found in 20 cases (56%), in whom there were 25 lesions or groups of lesions. Twenty four of these lesions were more conspicuous with the FLAIR sequence than with any of the conventional sequences. In 11 of these 20 cases, lesions thought to be of aetiological importance were only seen with the FLAIR sequence. In eight this was a solitary lesion. In the other three, an additional and apparently significant lesion (or lesions) was only seen with the FLAIR sequence when another lesion had been identified with both conventional and FLAIR sequences. The 11 additional lesions or groups of lesions were seen in the hippocampus, amygdala, cortex, or subcortical and periventricular regions. No lesion was found with any pulse sequence in 16 (44%) of the original group of 36 patients. In the eight cases where a lesion was seen only with the FLAIR sequence, localisation was concordant with the electroclinical features. Two of the eight patients with solitary lesions seen only on the FLAIR sequence underwent surgery, after which there was pathological confirmation of the abnormality identified with imaging. In one patient with a congenital cavernoma, the primary lesion was best seen with a contrast enhanced T1 weighted spin echo sequence. In this selected series, the FLAIR sequence increased the yield of MRI examinations of the brain by 30%.

Adolescent↗
PubMed1995

Incidence of sudden unexpected death in an adult outpatient cohort with epilepsy at a tertiary referral centre.

Overall mortality, incidence of sudden unexpected death, and cause of death were determined in 601 adult outpatients with epilepsy at a tertiary referral centre. The patients were followed up from 1990 to 30 June 1993. There were 24 deaths among the 601 patients (1849 patient years) with a standardised mortality ratio of 5.1 (95% confidence interval 3.3-7.6) of which 14 were related to epilepsy. Underlying disease of which epilepsy was a symptom accounted for four deaths only. An incidence of sudden deaths (including seizure related) was of the order of 1:200/year. In conclusion, excess mortality in chronic epilepsy is more likely to be related to the epilepsy itself than to underlying pathology. The relatively high incidence of sudden deaths found in this hospital based cohort has important implications for patient management.

Adolescent↗