Ventricular fibrillation (VF) is the most serious variety of arrhythmia which requires quick and accurate detection to save lives. In this paper, we propose a new time domain algorithm, called threshold crossing sample count (TCSC), which is an improved version of the threshold crossing interval (TCI) algorithm for VF detection. The algorithm is based on an important feature of the VF signal which relies on the random behavior of the electrical heart vector. By two simple operations: comparison and count, the technique calculates an effective measure which is used to separate lifethreatening VF from other heart rhythms. For assessment of the performance of the algorithm, the method is applied on the complete MIT-BIH arrhythmia and CU databases, and a promising good performance is observed. Seven other classical and new VF detection algorithms, including TCI, have been simulated and comparative performance results in terms of different quality parameters are presented. The TCSC algorithm yields the highest value of the area under the receiver operating characteristic curve (AUC). The new algorithm shows strong potential to be applied in clinical applications for faster and accurate detection of VF.

Objective: Recent research suggests that obstructive laryngospasm and consequent respiratory arrest may be a mechanism in sudden unexpected death in epilepsy. We sought to test a new hypothesis that this laryngospasm is caused by seizures driving reflux of stomach acid into the larynx, rather than spontaneous pathological activity in the recurrent laryngeal nerve. Approach: We used an acute kainic acid model under urethane anesthesia to observe seizure activity in Long-Evans rats. We measured the pH in the esophagus and respiratory activity. In a subset of experiments, we blocked acid movement up the esophagus with a balloon catheter. Main Results: In all cases of sudden death, terminal apnea was preceded by a large pH drop from 7 to 2 in the esophagus. In several animals we observed acidic fluid exiting the mouth, sometimes in large quantities. In animals where acid movement was blocked, sudden deaths did not occur. No acid was detected in controls. Significance: The results suggest that acid movement up the esophagus is a trigger for sudden death in KA induced seizures. The fact that blocking acid also eliminates sudden death implies causation. These results may provide insight to the mechanism of SUDEP in humans.

Objective: To investigate how prolonged seizure activity affects cardiorespiratory function and activity of pre-Bötzinger complex, leading to sudden death. Methods: Urethane-anesthetized female Long-Evans rats were implanted with nasal thermocouple; venous and arterial cannulae; and electrodes for electrocardiography (ECG) and hippocampal, cortical, and brainstem recording. Kainic acid injection into the ventral hippocampus induced status epilepticus. Results: Seizures caused hypertension, tachycardia, and tachypnea punctuated by recurrent transient apneas. Salivation increased considerably: in 11 of 12 rats, liquid with alkaline pH consistent with saliva was expelled from the mouth. Most transient apneas were obstructive: nasal airflow ceased, while, in 83%, efforts to breathe persisted as continued rhythmic activity of respiratory pre-Bötzinger neurons, inspiratory electromyography (EMG), and excursions of the chest wall and abdomen. Blood pressure oscillated in time with respiratory efforts. This pattern also occurred in a minority of cases (16%) of incomplete apnea, but not in rare cases (1%) of transient central apneas. During transient obstructive apneas, the frequency of all inspiratory efforts decreased abruptly by ~30%, suggesting a resetting of the central respiratory rhythm generator. Twenty-two of thirty-one rats died, due either to obstructive apnea (12) or central apnea following progressive slowing of respiration (10). Most rats dying of central apnea had experienced several transient obstructive apneas.Negative DC field potential shifts of the brainstem followed the final breath, consistent with previous reports on spreading depolarization in mouse models. Timing suggests that the DC shift is a consequence rather than cause of respiratory collapse.Cardiac activity continued for tens of seconds. Significance: Seizure activity in forebrain induces pronounced autonomic activation and disrupts activity in medullary respiratory centers, resulting in death from either obstructive or central apnea. These results directly inform mechanisms of death in status epilepticus, and indirectly provide clues to mechanisms of sudden unexpected death in epilepsy (SUDEP). K E Y W O R D SHeart rate, obstructive apnea, status epilepticus, SUDEP | 2347 JEFFERYS Et al.

No abstract

Reliable chronic neural recording from focal deep brain structures is impeded by insertion injury and foreign body response, the magnitude of which is correlated with the mechanical mismatch between the electrode and tissue. Thin and flexible electrodes cause less glial scarring and record longer than stiff electrodes. However, insertion of flexible microelectrodes into the brain has been a challenge. Here, a novel insertion method is proposed, and demonstrated, for precise targeting deep brain structures using flexible micro-wire electrodes. The microelectrode is spun and slowly inserted in the brain through an appropriate electrode guide. The electrode guide does not penetrate into cortex. Based on two new mechanisms, namely spinning and guided insertion, we have demonstrated successful insertion of 25 micron platinum flexible electrodes about 10 millimeter deep in rat brain without buckling. We present an electrode insertion device based on the proposed method and demonstrate its use to implant flexible microelectrodes in rat brains. The step-by-step insertion process is described. Microelectrodes were inserted in the Bötzinger complex of 11 rat brains and chronic respiratory neural activity was recorded from 2 rats for 50 days.