Epileptic Activity In Patients Research Articles

Symptoms related to the menopause and sex steroid treatments.

In the menopause transition, ovarian steroid production is gradually inhibited and around 35% of women will seek medical help for postmenopausal symptoms. The hot flush is a characteristic manifestation occurring in about 70% of women; it is associated with oestrogen withdrawal and disappears with oestrogen-based hormone replacement therapy. The exact mechanism behind it is still unclear but is probably related to heat loss mechanisms. The flush often occurs in parallel to changes in skin temperature, blood flow, pulse rate and pulses of luteinizing hormone (LH). These are probably secondary to a disturbance in the thermoregulatory centre of the CNS, which is anatomically close to neurons containing gonadotropin-releasing hormone. Depression is no more frequent in the menopausal transition than at other times in life. After surgical menopause, however, oestrogen improves low mood over placebo. In women with premenstrual syndrome, an increased feeling of well-being is associated with the pre-ovulatory oestrogen peak. Progestogens are associated with negative mood changes during the menstrual cycle, oral contraception and postmenopausal replacement therapy. Certain progesterone metabolites are anaesthetic and have anti-epileptic and anxiolytic properties, effects which are mediated via the type A gamma-aminobutyric acid (GABAA) receptor. Oestrogen is associated with increased sensory perception, locomotory activity, limb coordination and balance: this may help explain the increased frequency of bone fractures in the early postmenopausal period. Oestrogen improves memory and performance in patients with mild Alzheimer's dementia and increases epileptic activity in patients with partial epilepsy. These effects can be related to amplifying effects of oestrogen on excitatory amino acids in the CNS.

Independent component analysis of interictal fMRI in focal epilepsy: Comparison with general linear model-based EEG-correlated fMRI

The general linear model (GLM) has been used to analyze simultaneous EEG–fMRI to reveal BOLD changes linked to interictal epileptic discharges (IED) identified on scalp EEG. This approach is ineffective when IED are not evident in the EEG. Data-driven fMRI analysis techniques that do not require an EEG derived model may offer a solution in these circumstances. We compared the findings of independent components analysis (ICA) and EEG-based GLM analyses of fMRI data from eight patients with focal epilepsy. Spatial ICA was used to extract independent components (IC) which were automatically classified as either BOLD-related, motion artefacts, EPI-susceptibility artefacts, large blood vessels, noise at high spatial or temporal frequency. The classifier reduced the number of candidate IC by 78%, with an average of 16 BOLD-related IC. Concordance between the ICA and GLM-derived results was assessed based on spatio-temporal criteria. In each patient, one of the IC satisfied the criteria to correspond to IED-based GLM result. The remaining IC were consistent with BOLD patterns of spontaneous brain activity and may include epileptic activity that was not evident on the scalp EEG. In conclusion, ICA of fMRI is capable of revealing areas of epileptic activity in patients with focal epilepsy and may be useful for the analysis of EEG–fMRI data in which abnormalities are not apparent on scalp EEG.

A Probable Causative Factor for an Old Problem: Selenium and Glutathione Peroxidase Appear to Play Important Roles in Epilepsy Pathogenesis

Only recently has it become known that oxidative stress and generation of reactive oxygen species are the cause and the consequence of epileptic seizures. Due to the protective role of selenium (Se) and selenoproteins against oxidative damage and the ability to promote neuronal cell survival, we compared serum selenium level and red blood cell Glutathione peroxidase activity (RBC GPx) between epileptic and healthy children. In a case control study, 53 epileptic children were compared with 57 healthy children in the same age and community of residence. Serum Se and RBC GPx activity were measured with an atomic absorption spectrophotometry and Cayman standard glutathione assay kit, respectively. The mean (+/-standard deviation) of serum Se was 72.90 microg/L (+/-22.20) and 86.00 microg/L (+/-15.00) in patient and control groups, respectively. For RBC GPx activity the mean (+/-standard deviation) was 440.57 nmol/min/ml (+/-264.00) and 801.00 nmol/min/ml (+/-267.00) in patient and control groups, respectively. Statistical analysis showed a significant lower means of serum Se and RBC GPx activity in patient group compared to that of healthy control group (p < 0.001). Lower serum Se and RBC GPx activity in epileptic patients compared to healthy children may support the proposed crucial role of Se and GPx activity in the pathogenesis of epilepsy. However, RBC GPx activity in the case of selenium deficiency could not be a sensitive and specific indicator of Se status in serum that led us to supplant Se measurement with RBC GPx activity.

FMRI correlates of interictal epileptic activity in patients with idiopathic benign focal epilepsy of childhood: A simultaneous EEG–functional MRI study

EEG-correlated fMRI (EEG/fMRI) can identify alterations of brain function associated with interictal epileptiform discharges (IED). fMRI activation can localize the irritative zone and indicate functional disturbance distant from the spike focus. This might be of particular interest in paediatric epilepsy syndromes with frequent IED. Using simultaneous EEG/fMRI in a 3T MR scanner we studied blood oxygen level-dependent (BOLD) signal changes related to spontaneous IED in 10 children with typical and atypical benign focal epilepsy of childhood (BFE) or benign epileptic activity of childhood (BEAC). EEG artefacts were subtracted offline and IED were used as regressors for event-related fMRI analysis in SPM2. In four of the seven children with IED during EEG/fMRI we found IED related positive and negative signal changes (p<0.001, uncorrected). In three children we found only significant negative signal changes. At a more liberal threshold (p<0.05, uncorrected) these three children had positive signal changes congruent with the four children with significant positive signal changes. In summary, we found positive or negative signal changes in perisylvian, central, premotor and prefrontal regions. One child showed additional bilateral occipital fMRI activation. In addition to former reports our results indicated that frontal brain areas are functionally disturbed during IED corresponding to general neuropsychological findings in BFE and BEAC. We conclude that using EEG/fMRI it might be possible to localize generators of IED and functionally disturbed brain regions in children with BFE. Further studies are required to differentiate between BFE subtypes and to identify fMRI signatures of specific syndromes or corresponding neuropsychological deficits.

FMRI correlates of interictal epileptic activity in patients with idiopathic benign focal epilepsy of childhood: A simultaneous EEG-functional MRI study

EEG-correlated fMRI (EEG/fMRI) can identify alterations of brain function associated with interictal epileptiform discharges (IED). fMRI activation can localize the irritative zone and indicate functional disturbance distant from the spike focus. This might be of particular interest in paediatric epilepsy syndromes with frequent IED. Using simultaneous EEG/fMRI in a 3T MR scanner we studied blood oxygen level-dependent (BOLD) signal changes related to spontaneous IED in 10 children with typical and atypical benign focal epilepsy of childhood (BFE) or benign epileptic activity of childhood (BEAC). EEG artefacts were subtracted offline and IED were used as regressors for event-related fMRI analysis in SPM2. In four of the seven children with IED during EEG/fMRI we found IED related positive and negative signal changes (p<0.001, uncorrected). In three children we found only significant negative signal changes. At a more liberal threshold (p<0.05, uncorrected) these three children had positive signal changes congruent with the four children with significant positive signal changes. In summary, we found positive or negative signal changes in perisylvian, central, premotor and prefrontal regions. One child showed additional bilateral occipital fMRI activation. In addition to former reports our results indicated that frontal brain areas are functionally disturbed during IED corresponding to general neuropsychological findings in BFE and BEAC. We conclude that using EEG/fMRI it might be possible to localize generators of IED and functionally disturbed brain regions in children with BFE. Further studies are required to differentiate between BFE subtypes and to identify fMRI signatures of specific syndromes or corresponding neuropsychological deficits.

Correlation between metabolic alterations in 1H-MR spectroscopy and epileptic activity in patients with temporal lobe epilepsy

Correlation between metabolic alterations in 1H-MR spectroscopy and epileptic activity in patients with temporal lobe epilepsy

Mechanisms regulating GABAergic inhibitory transmission in the basolateral amygdala: implications for epilepsy and anxiety disorders

The amygdala, a temporal lobe structure that is part of the limbic system, has long been recognized for its central role in emotions and emotional behavior. Pathophysiological alterations in neuronal excitability in the amygdala are characteristic features of certain psychiatric illnesses, such as anxiety disorders and depressive disorders. Furthermore, neuronal excitability in the amygdala, and, in particular, excitability of the basolateral nucleus of the amygdala (BLA) plays a pivotal role in the pathogenesis and symptomatology of temporal lobe epilepsy. Here, we describe two recently discovered mechanisms regulating neuronal excitability in the BLA, by modulating GABAergic inhibitory transmission. One of these mechanisms involves the regulation of GABA release via kainate receptors containing the GluR5 subunit (GluR5KRs). In the rat BLA, GluR5KRs are present on both somatodendritic regions and presynaptic terminals of GABAergic interneurons, and regulate GABA release in an agonist concentration-dependent, bidirectional manner. The relevance of the GluR5KR function to epilepsy is suggested by the findings that GluR5KR agonists can induce epileptic activity, whereas GluR5KR antagonists can prevent it. Further support for an important role of GluR5KRs in epilepsy comes from the findings that antagonism of GluR5KRs is a primary mechanism underlying the antiepileptic properties of the anticonvulsant topiramate. Another mechanism regulating neuronal excitability in the BLA by modulating GABAergic synaptic transmission is the facilitation of GABA release via presynaptic alpha1A adrenergic receptors. This mechanism may significantly underlie the antiepileptic properties of norepinephrine. Notably, the alpha1A adrenoceptor-mediated facilitation of GABA release is severely impaired by stress. This stress-induced impairment in the noradrenergic facilitation of GABA release in the BLA may underlie the hyperexcitability of the amygdala in certain stress-related affective disorders, and may explain the stress-induced exacerbation of seizure activity in epileptic patients.

Levetiracetam reduces frequency and duration of epileptic activity in patients with refractory primary generalized epilepsy

Levetiracetam (LEV) is a new antiepileptic drug highly effective as add-on treatment in refractory partial epilepsies. In animal models, LEV is effective against absence seizures. A limited number of case reports and series indicate that LEV reduces seizure frequency in patients with generalized epilepsies. We evaluated with continuous EEG eight adult patients with idiopathic generalized epilepsy (IGE). All patients were refractory to the conventional therapy for IGE. Four patients received LEV as add-on therapy, and in four, a conversion to LEV monotherapy was undergone. Epileptic activity was analyzed in order to determine spike-wave density as well as median and maximal duration of spike-wave discharges. Each patient underwent a 24h EEG baseline monitoring before starting LEV therapy. A second 24h EEG examination was performed after a mean follow-up period of 136 days. Spike-wave density (spikes/h) was reduced by 78% after LEV administration. Median spike-wave duration decreased by 72% (p < 0.05). Maximal spike-wave duration was 6s before, and 1.5s after LEV with a percentage change of 81% (p < 0.05). The four patients on LEV monotherapy evidenced also a considerably improvement after conversion. This study showed that LEV produces a consistent long-term reduction of interictal epileptic activity in patients with refractory IGE. The reduction in the spike-wave activity additionally correlated with a clinically relevant antiepileptic effect. Our results support the concept that LEV could be an alternative therapy in primary generalized epilepsies.

FMRI Correlates of Interictal Epileptic Activity in Patients with Idiopathic Benign Focal Epilepsy of Childhood. A Simultanous EEG- Functional MRI Study

The localization of the epileptic zone or related brain regions plays an important role in patients with focal epilepsy. So far there are no established non-invasive methods that allow such diagnostic procedure, especially in children with idiopathic focal epilepsy. Our aim was to demonstrate EEG-correlated functional MRI (EEG-fMRI) as a feasible method in children and to correlate our data with clinical and EEG findings. Using simultaneous EEG-fMRI in a 3 Tesla MR scanner (Siemens Trio, Erlangen) we detected blood oxygen level-dependent (BOLD) signal changes related to spontaneous interictal epileptic activity. We studied 10 children with typical or atypical benign focal epilepsy of childhood (BFE) or benign epileptic activity of childhood. This is the largest published patient number examined by these methods so far. EEG artefacts were subtracted offline and epileptic activity discharges were marked after visual inspection using the analyzer software (Brain Products, Munich). These discharges were used as regressors for event-related fMRI analysis in SPM2. In the seven children with interictal epileptic activity (IED) during EEG-fMRI we found IED related activation or deactivation in the perisylvian, central and frontal regions in seven children. One child showed additional bilateral occipital fMRI activation. FMRI activation represented the affected brain areas in accordance to EEG localization. Additionally to former reports our results indicated that frontal brain areas are functionally disturbed during IED corresponding to clinical neuropsychological findings in BFE. We conclude that EEG-fMRI is a useful diagnostic tool to localize epileptic activity and functionally disturbed brain regions in children. Further studies are required to differentiate between BFE subtypes and to identify fMRI signatures of specific syndromes.

Correlation between metabolic alterations in 1H-MR Spectroscopy and epileptic activity in patients with temporal lobe epilepsy

Correlation between metabolic alterations in 1H-MR Spectroscopy and epileptic activity in patients with temporal lobe epilepsy

The Effects of Sevoflurane and Hyperventilation on Electrocorticogram Spike Activity in Patients with Refractory Epilepsy

We investigated the effects of sevoflurane and hyperventilation on intraoperative electrocorticogram (ECoG) spike activity in 13 patients with intractable epilepsy. Grid electrodes were placed on the brain surface and ECoG was recorded under the following conditions: 1) 0.5 minimal alveolar anesthetic concentration (MAC) sevoflurane, 2) 1.5 MAC sevoflurane, and 3) 1.5 MAC sevoflurane with hyperventilation. The number of spikes per 5 min and the percentage of leads with spikes were assessed in each condition. In 4 patients with chronically implanted-subdural electrodes, the leads with seizure onset and with spikes during the interictal periods in the awake state were compared with those during sevoflurane anesthesia at 0.5 MAC and 1.5 MAC. The number of spikes and the percentage of leads with spikes were significantly more under 1.5 MAC sevoflurane anesthesia compared with those under 0.5 MAC sevoflurane (P < 0.05). The induction of hyperventilation significantly increased the number of spikes and percentage of leads with spikes (P < 0.05). With 0.5 MAC sevoflurane, the leads with spikes were similar to those at seizure onset in the awake state, whereas with 1.5 MAC sevoflurane, spikes were similar to those occurring during interictal periods in the awake state. These results indicate that sevoflurane and hyperventilation can affect the frequency and extent of ECoG spike activity in patients with intractable epilepsy. Careful attention should be paid to the concentration of sevoflurane used and ventilatory status when intraoperative EcoG is used to localize epileptic lesions. Electrocorticogram can be used to define the location and extent of epileptic foci during epilepsy surgery. However, electrocorticogram can be affected by anesthetic technique. The present study found that sevoflurane concentration and hyperventilation affected the frequency and the extent of electrocorticogram spike activity in epileptic patients.

Furosemide and Mannitol Suppression of Epileptic Activity in the Human Brain

Most research on basic mechanisms of epilepsy and the design of new antiepileptic drugs has focused on synaptic transmission or action potential generation. However, a number of laboratory studies have suggested that nonsynaptic mechanisms, such as modulation of electric field interactions via the extracellular space (ECS), might also contribute to neuronal hypersynchrony and epileptogenicity. To date, a role for nonsynaptic modulation of epileptic activity in the human brain has not been investigated. Here we studied the effects of molecules that modulate the volume and water content of the ECS on epileptic activity in patients suffering from neocortical and mesial temporal lobe epilepsy. Electrophysiological and optical imaging data were acquired from the exposed cortices of anesthetized patients undergoing surgical treatment for intractable epilepsy. Patients were given a single intravenous injection containing either 20 mg furosemide (a cation-chloride cotransporter antagonist) or 50 g mannitol (an osmolyte). Furosemide and mannitol both significantly suppressed spontaneous epileptic spikes and electrical stimulation-evoked epileptiform discharges in all subjects, completely blocking all epileptic activity in some patients without suppressing normal electroencephalographic activity. Optical imaging suggested that the spread of electrical stimulation-evoked activity over the cortex was significantly reduced by these treatments, but the magnitude of neuronal activation near the stimulating electrode was not diminished. These results suggest that nonsynaptic mechanisms play a critical role in modulating the epileptogenicity of the human brain. Furosemide and other drugs that modulate the ECS might possess clinically useful antiepileptic properties, while avoiding the side effects associated with the suppression of neuronal excitability.

Stress Impairs α1A Adrenoceptor-Mediated Noradrenergic Facilitation of GABAergic Transmission in the Basolateral Amygdala

Intense or chronic stress can produce pathophysiological alterations in the systems involved in the stress response. The amygdala is a key component of the brain's neuronal network that processes and assigns emotional value to life's experiences, consolidates the memory of emotionally significant events, and organizes the behavioral response to these events. Clinical evidence indicates that certain stress-related affective disorders are associated with changes in the amygdala's excitability, implicating a possible dysfunction of the GABAergic system. An important modulator of the GABAergic synaptic transmission, and one that is also central to the stress response is norepinephrine (NE). In the present study, we examined the hypothesis that stress impairs the noradrenergic modulation of GABAergic transmission in the basolateral amygdala (BLA). In control rats, NE (10 microM) facilitated spontaneous, evoked, and miniature IPSCs in the presence of beta and alpha(2) adrenoceptor antagonists. The effects of NE were not blocked by alpha(1D) and alpha(1B) adrenoceptor antagonists, and were mimicked by the alpha(1A) agonist, A61603 (1 microM). In restrain/tail-shock stressed rats, NE or A61603 had no significant effects on GABAergic transmission. Thus, in the BLA, NE acting via presynaptic alpha(1A) adrenoceptors facilitates GABAergic inhibition, and this effect is severely impaired by stress. This is the first direct evidence of stress-induced impairment in the modulation of GABAergic synaptic transmission. The present findings provide an insight into possible mechanisms underlying the antiepileptogenic effects of NE in temporal lobe epilepsy, the hyperexcitability and hyper-responsiveness of the amygdala in certain stress-related affective disorders, and the stress-induced exacerbation of seizure activity in epileptic patients.

Heart rate variability during sleep in children with partial epilepsy.

Alterations in autonomic control of cardiac activity in epileptic patients have been reported by several studies in the past, and both ictal and interictal modifications of heart rate regulation have been described. Alterations of autonomic control of cardiac activity can play an important role in sudden unexplained death in patients with epilepsy (SUDEP). However, the presence of specific changes in heart rate variability (HRV) during sleep, not correlated with seizures, has not been assessed in children with epilepsy; for this reason, we evaluated features of cardiac autonomic function during sleep without ictal epileptiform electroencephalogram (EEG) activity in a group of children with partial epilepsy. Eleven patients (five males and six females; mean age 11.5 years, SD: 3.65 years) affected by partial epilepsy were admitted to this study; 11 normal subjects (five males and six females; mean age 12.9 years, SD: 2.72 years) served as a control group. All subjects slept in the laboratory for two consecutive nights. The data were analyzed during the second night. Sleep was polygraphically recorded [including one electrocardiography (ECG) channel] and signals were digitally stored. A series of 5-min ECG epochs were chosen from each sleep stage, during periods without evident ictal epileptiform activity in the EEG. Electrocardiography signals were analyzed for automatic detection of R-waves and, subsequently, a series of time- and frequency-domain measures were calculated. Epileptic subjects tended to show an overall lower HRV in both time- and frequency-domain parameters, principally during rapid eye movement (REM) sleep and, to a lesser extent, during sleep stage 2. Among the different bands, this decrease was most evident for the high-frequency band (HF) absolute power. For this reason, the ratio between the low-frequency band (LF) and HF was always higher in epileptic patients than in normal controls and the difference was statistically significant during sleep stages 3 and/or 4 and REM sleep. Our results indicate that during sleep, a particular condition of basal modification in autonomic characteristics occurs (mostly during REM sleep) in partial epilepsy patients. This finding might represent an important factor contributing to the complex mechanism of SUDEP which takes place most often during sleep and supports the need of studying HRV specifically during this state in subjects with seizures.

Planned Ictal FDG PET Imaging for Localization of Extratemporal Epileptic Foci

This work demonstrates the feasibility of planned ictal positron emission tomography (PET) with [18F]fluoro-2-deoxy-glucose (FDG) for localization of epileptic activity in patients with frequent partial seizures of extratemporal origin. Ictal PET imaging was performed in four patients (two men and two women, ages 28-61) with continuous or very frequent (every 3-15 min) partial seizures. All patients had abnormalities apparent on magnetic resonance (MR) or computed tomographic (CT) imaging, two with extensive brain lesions that precluded precise localization of the seizure focus with interictal PET or single-photon emission tomography (SPECT) imaging. Ictal PET imaging demonstrated a restricted area of focal hypermetabolism concordant with surface electroencephalographic (EEG) recording in all cases. The PET images were registered to MR imaging data for further anatomic localization of hypermetabolic regions in three cases. The ictal PET data were used to guide neurosurgical intervention in one case. We conclude that planned ictal PET imaging may be a useful and potentially superior approach to ictal SPECT for identifying the epileptic focus in a selected group of patients with continuous or frequent simple partial seizures.

3-17-07 EEG background activity in epileptic patients in monotherapy with carbamazepine

3-17-07 EEG background activity in epileptic patients in monotherapy with carbamazepine

Epileptic seizures in patients with acute catatonic syndrome.

Acute catatonic syndrome is a condition that can be caused by a variety of metabolic, neurological, psychiatric, and toxic conditions, including neuroleptic malignant syndrome. Although ictal catatonia as a manifestation of non-convulsive status epilepticus has been described, reference to the occurrence of seizures in patients with acute catatonic syndrome is anecdotal. Twenty nine patients with acute catatonic syndrome were reviewed to identify patients with seizures after the onset of acute catatonic syndrome. Patients were divided into four diagnostic groups: affective (15), schizophrenic (eight), toxic (two), and organic (four). Seizures occurred in four patients (13.8%): two patients with dystonic seizures had viral encephalitis and schizophrenic disorder respectively; one patient with complex partial seizures had viral encephalitis and one patient with absence status had neuroleptic malignant syndrome. The results indicate the value of EEG in detection of epileptic activity in patients with acute catatonic syndrome, both at onset and in the course of such disturbance, particularly to provide a differential diagnosis between pseudo-seizures and neuroleptic-induced acute dystonia.

Anomia for Facial Expressions: Neuropsychological Mechanisms and Anatomical Correlates

We report a patient with a selective impairment in naming and pointing to emotional facial expressions following a circumscribed lesion of the right temporal lobe. Detailed investigation of this patient′s deficit revealed that the neuropsychological mechanism underlying his anomia for facial expressions is best understood as a category-specific bidirectional visual-verbal disconnection between intact visual semantic and verbal semantic representations for facial emotions. Magnetic resonance imaging findings from this case and from another patient previously described with this unique syndrome (Rapcsak, Kaszniak, & Rubens, 1989), together with the results of cortical electrical stimulation studies and microelectrode recordings of cortical neuronal activity in epileptic patients, provide converging evidence that the inferotemporal visual association cortex of the right middle temporal gyrus plays an important functional role in the verbal labeling of emotional facial expressions. The implications of these findings for cognitive and neural models of facial affect processing are discussed.

Selective changes in the microorganization of the human epileptogenic neocortex revealed by parvalbumin immunoreactivity.

The microanatomy of the human lateral temporal cortex removed from patients with intractable temporal lobe epilepsy was studied using correlative light and electron microscopic immunocytochemical methods for the localization of the calcium-binding protein parvalbumin (PV). PV immunostaining was mainly used to label a subpopulation of powerful cortical inhibitory interneurons that have been shown to be lost at epileptic foci in certain animal models of epilepsy. In the human neocortex with normal appearance, we identified the same local neuronal circuitry as in the normal monkey cortex, but in some regions of the same cortex, a fine disorganization of neuronal circuits (loss of inhibitory neurons and presumptive thalamocortical terminals) was found. This abnormal circuitry may interfere with normal cerebral activity in epileptic patients. These results also indicate that PV immunoreactivity can be a useful tool to study normal and abnormal synaptic circuits in the human cerebral cortex.

Concentration-dependent reduction in erythrocyte 5-aminolaevulinate dehydratase activity in epileptic patients on carbamazepine monotherapy

Conference Article| April 01 1985 Concentration-dependent reduction in erythrocyte 5-aminolaevulinate dehydratase activity in epileptic patients on carbamazepine monotherapy G. M. McGUIRE; G. M. McGUIRE *Departments of Medicine, Western Infirmary, Glasgow G11 6NT, U.K. Search for other works by this author on: This Site PubMed Google Scholar M. J. BRODIE; M. J. BRODIE †Departments of Clinical Pharmacology, Western Infirmary, Glasgow G11 6NT, U.K. Search for other works by this author on: This Site PubMed Google Scholar G. J. A. MACPHEE; G. J. A. MACPHEE *Departments of Medicine, Western Infirmary, Glasgow G11 6NT, U.K. Search for other works by this author on: This Site PubMed Google Scholar M. R. MOORE; M. R. MOORE *Departments of Medicine, Western Infirmary, Glasgow G11 6NT, U.K. Search for other works by this author on: This Site PubMed Google Scholar A. GOLDBERG A. GOLDBERG *Departments of Medicine, Western Infirmary, Glasgow G11 6NT, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1985) 13 (2): 376–377. https://doi.org/10.1042/bst0130376 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation G. M. McGUIRE, M. J. BRODIE, G. J. A. MACPHEE, M. R. MOORE, A. GOLDBERG; Concentration-dependent reduction in erythrocyte 5-aminolaevulinate dehydratase activity in epileptic patients on carbamazepine monotherapy. Biochem Soc Trans 1 April 1985; 13 (2): 376–377. doi: https://doi.org/10.1042/bst0130376 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search Keywords: CBZ, carbamazepine, ALA-D, 5-aminolaevulinate dehydratase, CBZ-E, carbamazepine-10,11-epoxide This content is only available as a PDF. © 1985 Biochemical Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.