Paroxysmal Theta Research Articles

Ambulatory video-EEG-EMG monitoring and analysis during cataplexy in narcolepsy

Objective To comprehensively analyze the clinical and electroneurophysiological characteristics during the process of cataplexy by dynamic video?EEG?EMG monitoring. Methods Six narcolepsy type 1 patients with typical cataplexy were enrolled and 2 of them were diagnosed as status cataplecticus. All patients underwent polysomnography (PSG) and daytime Multiple Sleep Latency Test (MSLT) to clarify the diagnosis. Cataplexy was triggered by emotional stimulus and recorded under dynamic video-EEG-EMG monitoring. EEG characteristics during cataplexy were further compared and analyzed. Objective To comprehensively analyze the clinical and electroneurophysiological characteristics during the process of cataplexy by dynamic video-EEG-EMG monitoring. Methods Six narcolepsy type 1 patients with typical cataplexy were enrolled and 2 of them were diagnosed as status cataplecticus. All patients underwent polysomnography (PSG) and daytime Multiple Sleep Latency Test (MSLT) to clarify the diagnosis. Cataplexy was triggered by emotional stimulus and recorded under dynamic video-EEG-EMG monitoring. EEG characteristics during cataplexy were further compared and analyzed. Results Fourteen cataplectic attacks in 6 patients were recorded. According to the clinical and video- EMG characteristics, cataplectic attack was divided into 4 stages, including triggering phase (CA1), resisting phase (CA2), atonic phase (CA3) and recovering phase (CA4). EEG frequency and amplitude varied from one stage to another and hypersynchronous paroxysmal theta (HSPT) was observed in early resisting phase (CA2), which was supposed to be a distinctive EEG characteristic during the onset of cataplexy. Conclusions Generalized cataplectic ttack contain 4 stages, which indicate a complicated and dynamic process in clinical and electroneurophysiology. Moreover, it's highly possible that HSPT during resisting phase (CA2) is critical in the mechanism of cataplexy. DOI: 10.3969/j.issn.1672-6731.2017.09.006

Electroencephalogram paroxysmal theta characterizes cataplexy in mice and children

Astute control of brain activity states is critical for adaptive behaviours and survival. In mammals and birds, electroencephalographic recordings reveal alternating states of wakefulness, slow wave sleep and paradoxical sleep (or rapid eye movement sleep). This control is profoundly impaired in narcolepsy with cataplexy, a disease resulting from the loss of orexin/hypocretin neurotransmitter signalling in the brain. Narcolepsy with cataplexy is characterized by irresistible bouts of sleep during the day, sleep fragmentation during the night and episodes of cataplexy, a sudden loss of muscle tone while awake and experiencing emotions. The neural mechanisms underlying cataplexy are unknown, but commonly thought to involve those of rapid eye movement-sleep atonia, and cataplexy typically is considered as a rapid eye movement sleep disorder. Here we reassess cataplexy in hypocretin (Hcrt, also known as orexin) gene knockout mice. Using a novel video/electroencephalogram double-blind scoring method, we show that cataplexy is not a state per se, as believed previously, but a dynamic, multi-phased process involving a reproducible progression of states. A knockout-specific state and a stereotypical paroxysmal event were introduced to account for signals and electroencephalogram spectral characteristics not seen in wild-type littermates. Cataplexy almost invariably started with a brief phase of wake-like electroencephalogram, followed by a phase featuring high-amplitude irregular theta oscillations, defining an activity profile distinct from paradoxical sleep, referred to as cataplexy-associated state and in the course of which 1.5-2 s high-amplitude, highly regular, hypersynchronous paroxysmal theta bursts (∼7 Hz) occurred. In contrast to cataplexy onset, exit from cataplexy did not show a predictable sequence of activities. Altogether, these data contradict the hypothesis that cataplexy is a state similar to paradoxical sleep, even if long cataplexies may evolve into paradoxical sleep. Although not exclusive to overt cataplexy, cataplexy-associated state and hypersynchronous paroxysmal theta activities are highly enriched during cataplexy in hypocretin/orexin knockout mice. Their occurrence in an independent narcolepsy mouse model, the orexin/ataxin 3 transgenic mouse, undergoing loss of orexin neurons, was confirmed. Importantly, we document for the first time similar paroxysmal theta hypersynchronies (∼4 Hz) during cataplexy in narcoleptic children. Lastly, we show by deep recordings in mice that the cataplexy-associated state and hypersynchronous paroxysmal theta activities are independent of hippocampal theta and involve the frontal cortex. Cataplexy hypersynchronous paroxysmal theta bursts may represent medial prefrontal activity, associated in humans and rodents with reward-driven motor impulse, planning and conflict monitoring.

Theta Bursts, Closed Head Injury, and Partial Seizure-Like Symptoms: A Retrospective Study

The purpose of this retrospective, chart-review study was to provide additional information on the clinical correlates of paroxysmal theta activity on EEG and to further examine the previously proposed relation (Varney, Hines, Bailey, & Roberts, 1992) between episodic symptoms in the context of prior closed-head injury and theta bursts. All participants were veterans receiving their health care at a single, tertiary-care, Veterans Affairs medical center. Compared with patients with normal EEGs (comparison group, n = 30) and nonparoxysmal theta-delta slowing (comparison group, n = 30), consecutive patients with theta bursts (n = 38) were found to have significantly more episodic (i.e., partial seizure-like) symptoms documented in their medical records. History of closed-head trauma was also associated with increased reporting of episodic symptoms across all three clinical groups. These findings suggest that, in the presence of theta bursts on EEG, clinicians may wish to interview systematically for episodic, partial seizure-like phenomena, especially when paroxysmal theta activity occurs in the context of prior closed head injury.

Misdiagnosis and treatment in juvenile myoclonic epilepsy

Of 1300 epileptic patients 76 (5.8%) were found to have juvenile myoclonic epilepsy (JME). These 76 patients were examined at the epilepsy outpatient clinic of Bakirkoy State Hospital for Neurological and Psychiatric Diseases between 1991 and 1996 and data obtained were analysed retrospectively. Clinically typical absence seizures were reported in 40.8%, myoclonic jerks in 100%, and generalized tonic-clonic seizures in 82.9% of the patients. Neurological and mental examination was normal for all patients with the exception of three cases; two with essential tremor and one with minimal dysarthria. Precipitating factors were noted in 85.5% of cases. Abnormal EEG was recorded in 73 (6.1%) patients. Abnormalities mainly consisted of generalized discharges of spike/polyspike and slow-wave (86.6%) and generalized paroxysmal theta or delta (9.2%). Fifteen (19.7%) had focal abnormalities and 20 (26.4%) had photoconvulsive discharges. Of the 76 patients, 40 (52.6%) were not diagnosed at the initial interview; definite diagnosis was delayed by a mean of 5.9 years. As a result of misdiagnosis at the initial interview 40 patients had been administered AED except for valproate. After reassessment of clinical and EEG findings, the medication was changed to valproate therapy. As a result, 65 of our WE patients (85.5%) were seizure free after a one-year follow-up period.

Clinical and electroencephalographic features of simple partial seizures.

The clinical and electroencephalographic features of 87 simple partial seizures in 14 patients were studied with video-EEG telemetry. The patients were able to respond to verbal stimuli during all seizures and, later, could clearly recall ictal events. To determine whether the EEG changes in simple partial seizures could be reliably observed, a reader blindly reviewed four EEGs of equal duration for each seizure. These EEGs consisted of one ictal and three nonictal recordings obtained at predetermined times before the seizure. There were 27 motor seizures (mean duration, 86 seconds; range, 2 to 250 seconds), all involving clonic movements of the head and/or upper extremities; 8 (30%) of these had a sensory component (pain in 6, paresthesia in 2). An EEG change, usually localized spikes or sharp waves over the contralateral or both rolandic regions, was identifiable in nine (33%) of the motor seizures. The 60 nonmotor seizures (mean duration, 63 seconds; range, 8 to 375 seconds) involved a variety of symptoms, including somatosensory/special sensory (3 seizures), autonomic (26 seizures), cognitive (1 seizure), affective (14 seizures), and mixed, or more than one category of nonmotor symptoms (16 seizures). In only nine (15%) of the nonmotor seizures was there an ictal EEG change, usually localized spikes or paroxysmal theta activity over the temporal region. Overall, among the 87 simple partial seizures, only 18 (21%) revealed ictal EEG changes. Thus, a normal EEG is common during simple partial seizures and does not exclude the diagnosis.

Electroencephalographic findings in urea-cycle disorders

Eleven electroencephalograms in 4 infants with urea-cycle disorders were reviewed. All infants had one or more abnormal EEGs. The abnormalities consisted mainly of multiareal spikes, spike-waves, or sharp-and-slow-wave activity. In addition, one patient, a term infant, exhibited exaggerated spindle-delta bursts. This infant, and also one other at a similar age, had monorhythmic paroxysmal theta activity. Clinically, all patients had seizures shortly preceding abnormal EEGs. EEG alterations were encountered over a wide range of elevated serum ammonia levels. Normal EEGs occurred in the face of slightly elevated levels. It is concluded that epileptiform EEG alterations may be a characteristic manifestation of urea-cycle disorders.