Periodic lateralized epileptiform discharges (PLEDs) are typically associated with encephalitis, cerebral abscess, cerebral infarct, and status epilepticus. There is considerable debate as to whether this pattern is ictal or interictal when seen in association with status epilepticus. We present a patient with complex partial status epilepticus who developed PLEDs and remained comatose despite optimal drug therapy. Technetium 99m single-photon emission computed tomography (SPECT) showed hyperperfusion that resolved with further aggressive antiepileptic drug therapy, indicating that this pattern may indeed be ictal. Further studies are needed to define the significance of PLEDs in patients with status epilepticus. The role of SPECT in differentiating PLEDs as an interictal or ictal pattern also requires further study.
"LPDs is more controversial, as both focal hypo-and hyper-perfusion and metabolism have been described [Lee & Schauwecker, 1988; Ali et al., 2001; Assal et al., 2001; Bozkurt et al., 2002; Cury et al., 2004; Ergun et al., 2006; Kim et al., 2012]. This discrepancy between studies is likely attributable to the lack of control for the presence of seizures during or immediately before imaging, and to the presence and variable extent of an acute brain injury. "
[Show abstract][Hide abstract] ABSTRACT: Lateralized period discharges (LPDs,a.k.a PLEDs) in conjunction with acute brain injuries are known to be associated with worse prognosis but little is known about their importance in absence of such acute injuries. We studied the clinical correlates and outcome of patients with LPDs in the absence of acute or progressive brain injury.
This is a case-control study of 74 patients with no acute brain injury undergoing continuous EEG monitoring (CEEG), half with LPDs and half without, matched for age and etiology of remote brain injury, if any or history of epilepsy.
LPDs were found in 145/1785 (8.1%) of subjects; 37/145 (26%) had no radiological evidence of acute or progressive brain injury. Those with LPDs were more likely to have abnormal consciousness (86% vs. 57%; p= 0.005), seizures (70% vs 24%; p=0.0002), and functional decline (62% vs 27%; p =0.005), and were less likely to be discharged home (24% vs 62%; p=0.002). On multivariate analysis, LPDs and status epilepticus were associated with abnormal consciousness (p=0.009; OR= 5.2, 95% CI 1.60-20.00 and p=0.017; OR=5.0, 95% CI 1.4-21.4); and LPDs were independently associated with functional decline (p=0.001; OR= 4.8, 95% CI 1.6-15.4) and lower likelihood of being discharged home (p=0.009; OR= 0.2, 95% CI 0.04-0.6).
Despite absence of acute or progressive brain injury, LPDs were independently associated with abnormal consciousness and worse outcome at hospital discharge.
Journal of clinical neurophysiology: official publication of the American Electroencephalographic Society 07/2015; DOI:10.1097/WNP.0000000000000206 · 1.43 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The pathophysiological relation between periodic lateralized epileptiform discharges (PLEDs) and epileptic seizures is not known and the exact causative mechanism of PLEDs still remains unclear. In this report, the authors present a case in which the EEG displayed PLEDs after a complex partial seizure. This patient, with a long history of complex partial seizures, had previously undergone right standard anterior temporal lobectomy with hippocampectomy, with a diagnosis of mesial temporal sclerosis. She had one complex partial seizure 72 days after operation and was admitted to hospital. Her brain MRI revealed changes due to temporal lobectomy and small residual posterior hippocampic anomalies. PLEDs over the right temporal lobe were seen in postictal EEGs and persisted for 4 days despite the patient's normal mental status and normal neurologic examination. Brain perfusion scintigraphy with Tc-99m-HMPAO during PLEDs was performed on the second day after the seizure, and right temporal hyperperfusion was detected. EEGs and scintigraphic imaging were repeated after cessation of PLEDs. The repeated brain scan displayed right temporal hypoperfusion. PLEDs during the postictal period may actually be an ictal pattern, and if hyperperfusion in the brain SPECT studies during PLEDs is seen, further aggressive antiepileptic drug therapy may be necessary in some cases.
[Show abstract][Hide abstract] ABSTRACT: 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.
To describe the first Korean family with autosomal dominant nocturnal frontal lobe epilepsy.
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.
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.
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.
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