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Biomedical subjects

Gholam K Motamedi

Publications and source records attributed to Gholam K Motamedi.

7 recordsLinked to original sources
PubMed2006

Termination of epileptiform activity by cooling in rat hippocampal slice epilepsy models.

Cooling has been shown to terminate experimentally induced epileptiform activity in models of epilepsy without causing injury to the cooled brain, suggesting that cooling could represent an approach to seizure control in intractable focal epilepsies. Here we sought to determine the most effective way to apply cooling to abort spontaneous epileptiform discharges in in vitro brain slice models. We induced spontaneous epileptiform activity in rat brain slices by exposure to 4-aminopyridine (4-AP), 4-AP plus bicuculline, and Mg(2+)-free artificial CSF (aCSF) at 28-34 degrees C. Extracellular field recordings were made at hippocampal or neocortical sites. Slice temperature was reduced by perfusion with cold aCSF. Rapid cooling at rates of 2-5 degrees C/s was compared to cooling at slower rates of 0.1-1 degrees C/s. Cooling at both rates reversibly aborted epileptiform discharges in all three models and at all recording sites. With rapid cooling, small temperature drops were highly effective in terminating discharges, an effect that was sustained for as long as the reduced temperature level was maintained. In contrast, slow cooling required much larger temperature drops to inhibit discharges. With slow cooling, absolute temperature drops to 21-22 degrees C caused a 90% reduction in event frequency, but cooling to 14-15 degrees C was required to terminate discharges. We conclude that rapid cooling as effectively aborts discharges in in vitro epilepsy models as does slow cooling, but the magnitude of the temperature change required is less. Practical devices to inhibit seizure activity may only need to induce small temperature drops, if the cooling can be applied sufficiently rapidly.

4-Aminopyridine↗
PubMed2006

Antiepileptic drugs and neurodevelopment.

Clinical studies have documented the teratogenic potential of antiepileptic drugs (AEDs). More recent cohort studies have been trying to sort out which AEDs impose the highest risk of teratogenicity. Currently, there is evidence demonstrating an increased risk of major congenital malformations (MCMs) for valproate, phenobarbital, and polytherapy during pregnancy. Based on the current data from multiple studies, the risk for valproate is the highest. Additional studies are needed to fully delineate if differences exist for other AEDs, especially the newer AEDs. However, although MCMs are easy to recognize and have been shown to be more common after in utero exposure to AEDs, there are insufficient data regarding their long-term effects on cognition and behavior in exposed children. Although most children born to women with epilepsy are healthy, in recent years there has been increasing awareness of the long-term effects of in utero exposure to AEDs. Recent discovery of neuronal apoptosis following in utero AED exposure in animals during a period that corresponds to the third trimester and early infancy in humans raises further concerns. Prospective clinical studies seem necessary in order to better understand the long-term neurodevelopmental effects of in utero exposure to AEDs.

Abnormalities, Drug-Induced↗
PubMed2004

Antiepileptic drugs and memory.

Impaired memory is among the most common complaints of patients with epilepsy. Multiple factors contribute to memory impairment in patients with epilepsy. Thus, delineation of the effects of antiepileptic drugs (AEDs) on memory in clinical populations faces methodological difficulties. Further, subjective perception of memory problems by patients is influenced by mood. However, there is evidence from animal and healthy volunteer studies supporting an independent potential for AEDs to impair memory. Differential AED effects on memory have been observed, and AED effects may interact with focal brain lesions. Memory impairment from AEDs is a greater concern at the age extremes, although the effects of AEDs, especially the newer agents, have not been thoroughly studied in these populations. Well-controlled studies are needed to understand the underlying mechanisms and to further delineate the magnitude and relative effects of AEDs on memory.

Aged↗
PubMed2003

A Korean kindred with autosomal dominant nocturnal frontal lobe epilepsy and mental retardation.

BACKGROUND: A Korean family had distinctive clinical and neuroimaging features and carried the same genetic mutation that was found in a previously described Japanese kindred with autosomal dominant nocturnal frontal lobe epilepsy. OBJECTIVE: To describe the first Korean family with autosomal dominant nocturnal frontal lobe epilepsy. METHODS: Members of a large family, including 9 affected individuals from 3 generations, underwent a comprehensive genetic, clinical, electroencephalographic, neuropsychological, and neuroimaging evaluation. Affected members were tested for possible mutations in transmembrane regions 1 through 3 of the neuronal nicotinic acetylcholine receptor alpha4 subunit (CHRNA4) by direct sequencing and subsequent restriction analysis. RESULTS: Seizures began in childhood, presenting as nocturnal episodes of staring, confusion, shouting, perioral movements, unintelligible speech, and hand waving. Some patients had ictal or interictal epileptiform activity in the temporal and/or frontocentral areas. Neurological examination and brain magnetic resonance imaging results showed no abnormalities, except that all patients available for testing had mild to moderate mental retardation. Fluorodeoxyglucose F 18 with positron emission tomography showed mild decreased glucose uptake in the superior and middle frontal regions, more so on the left than on the right. Patient response to carbamazepine was poor. All affected members were heterozygous for the CHRNA4 Ser252Leu mutation. CONCLUSIONS: Disorders associated with mutations in the transmembrane region 2 of CHRNA4 are genetically and phenotypically heterogeneous. Distinctive features of this kindred include (1) mental retardation in all affected members available for testing, (2) abnormal brain findings on fluorodeoxyglucose F 18 with positron emission tomography, (3) poor response to carbamazepine, and (4) full penetrance.

Adolescent↗
PubMed2002

Wavelet-crosscorrelation analysis can help predict whether bursts of pulse stimulation will terminate afterdischarges.

OBJECTIVE: Extraoperative cortical localizing stimulation (LS) is a standard clinical tool used to assess brain function before epilepsy surgery. However, LS can produce unwanted afterdischarges (ADs). We previously have shown that brief pulses of electrical stimulation (BPS) can terminate ADs caused by cortical stimulation. Our objective was to assess whether wavelet-crosscorrelation analysis could help predict the conditions under which BPS would be most likely to terminate ADs. METHODS: We used wavelet-crosscorrelation analysis to get wavelet-correlation coefficients (WCC), and determine time lag (TL) and absolute value of TL (ATL) between two electrodes. For Analysis-1, we compared WCC and ATL in epoch 1 which was before LS, epoch 2 which was after LS but before BPS, and epoch 3 which was after BPS. For Analysis 2, we compared WCC and ATL during epoch 1 under 4 conditions: epochs when ADs subsequently terminated within 2 s after the end of BPS (1A), terminated within 2-5 s (1B), did not terminate within 5 s (1C), and when ADs did not appear (1D). RESULTS: We found that BPS efficacy in terminating ADs was predicted by (1) low correlation and (2) slow propagation speed between electrode pairs in the 2-10 s period before stimulation. CONCLUSIONS: Wavelet-crosscorrelation analysis can help predict conditions during which BPS can abort ADs. It is possible that similar analyses could help predict when BPS or other interventions could abort clinical seizures.

Adolescent↗
PubMed2002

Optimizing parameters for terminating cortical afterdischarges with pulse stimulation.

PURPOSE: We previously reported that brief pulses of electrical stimulation (BPSs) can terminate afterdischarges (ADs) during cortical stimulation. We investigated conditions under which BPS is more likely to suppress ADs. METHODS: We analyzed parameters altering BPS effectiveness on 200 ADs in seven patients with implanted subdural electrodes. RESULTS: The odds of BPSs stopping ADs was 8.6 times greater at primary sites (directly stimulated electrodes) than at secondary sites (adjacent electrodes) (p = 0.016). BPS applied within 4.5 s after onset of AD had 2 times greater odds of stopping ADs (p = 0.014). BPS applied when AD voltage was negative was 1.9 times more likely to stop ADs (p = 0.012). ADs with rhythmic pattern responded best (p < 0.0001). BPS stopped 100% of ADs not starting immediately after localization stimulus (LS) versus 29% of those starting immediately (p < 0.0001). CONCLUSIONS: BPS is more likely to terminate ADs at primary electrodes, if given early, if applied to the negative peak of the AD waveform, if AD has a rhythmic pattern, and if AD did not start immediately after LS.

Adolescent↗