Exposure to high concentrations of CO2 is a common means of stunning and killing laboratory rodents. However, there is concern regarding the potential for animals to have aversive experiences, such as pain or breathlessness, prior to loss of awareness. This preliminary study evaluated the electroencephalographic (EEG) responses of rats (Rattus norvegicus) to CO2 inhalation, using a method based on a minimal anaesthesia model previously used to assess nociception in mammals. Fifteen adult female Sprague-Dawley rats were anaesthetised with halothane in oxygen and maintained at a minimal plane of anaesthesia. EEG was continuously recorded throughout a 10-min baseline period followed by sequential exposure to 5, 15, 30 and 50% CO2. The EEG summary variables median frequency (F50), 95% spectral edge frequency (F95) and total power (PTOT) were derived from the raw EEG. The F50 of the EEG, a sensitive indicator of nociception, increased significantly above baseline during exposure to 15% CO2, suggesting this concentration was noxious to rats. This is consistent with behavioural aversion in rats at around the same CO2 concentration. Stimulation of the rat mucosal nociceptors only occurs at CO2 concentrations of 37% or greater; therefore, it is hypothesised that the observed response was a result of what would have been CO2-induced aversive respiratory sensation in conscious animals, rather than pain. This study provides some evidence that an anaesthesia model may be utilised to study the nocuous effects of low-moderate CO2 exposure in rodents.

Despite decades of publications attesting to the role of the clinical EEG in diagnosing and managing psychiatric disorders, the procedure remains highly underutilized in the practice of psychiatry. The visually inspected EEG (vEEG) can detect various forms of abnormalities, each with its own clinical significance. Abnormalities can be paroxysmal (i.e., suggestive of an epileptic-like process) or stationary. The most important unanswered question remains the value of detecting epileptiform activity in a nonepileptic psychiatric patient in predicting favorable responses to anticonvulsant treatment. Despite the many shortcomings of vEEG, the available evidence suggests that in the presence of paroxysmal activity in a nonepileptic psychiatric patient a trial of a psychotropic anticonvulsant may be warranted if standard treatment has failed. More research on the contribution of paroxysmal EEG abnormalities to the problem of episodic psychiatric symptoms (e.g., panic attacks, dissociative episodes, repeated violence) is sorely needed. It is postulated that at least some of these conditions may represent an epilepsy spectrum disorder. Similarly, the significance of the presence of a slow-wave activity (whether focal or generalized) also deserves further well-designed research to ascertain the exact clinical significance. Nonetheless, the available data suggest that further medical workup is necessary to ascertain the nature and degree of the pathology when present.

First graders (aged 7-8) in a public elementary school served as subjects for this study. The structural components of their speech were analyzed to determine speech maturity level; total EEG activity was analyzed to assess the functional maturity of brain structures. Results showed that children with levels of speech below the age norm exhibited abnormal EEG patterns suggesting immaturity of the cerebral cortex and fronto-thalamic regulatory system, as well as impairments in the functioning of the mesodiencephalic structures and nonspecific activation systems. Abnormalities in the functioning of brain regulatory systems and the presence of local abnormalities in EEG activity of deep origin are important factors in determining the severity of functional speech impairments.

The laterality effects in 10 symmetrical EEG derivations in twins (20 MZ and 20 DZ pairs with a mean age of 20.5 years) were examined. The quantitative and qualitative analyses gave the following results: (1) cotwins in the MZ and DZ pairs differed particularly in the intensity of asymmetry for EEG parameters — one was more asymmetrical than the other; (2) among the MZ twins there were no “mirror” pairs (opposite asymmetry of the EEG), even where opposite-handedness existed. For example, a right-handed twin had an asymmetrical EEG, while the other, a left-hander, had a symmetrical one; (3) the most asymmetrical EEG was in the temporal derivations showing a more active left hemisphere; and, (4) there was no evidence of genetic influence in the intensity of EEG asymmetry.