A pitch glide activates an intermediate response between auditory N1 and mismatch negativity.

Pitch glides of a continuous tone elicit auditory N1-like responses. However, their characteristics have not well been investigated, and it remained unclear whether the response is an auditory true N1 or the mismatch negativity (MMN). We found here that a rapid pitch glide activates almost the same response as a true N1. On the contrary, as the rate of the pitch glide decreases, the response continuously varies the characteristics from true N1 to MMN. This suggests that there would exist intermediate responses between auditory N1 and MMN.

Auditory evoked off-response: its source distribution is different from that of on-response.

Offset auditory responses were investigated by electroencephalography mainly in the 1970s, but since then no particular attention has been paid to them. Among the studies using magnetoencephalography (MEG) devices there are, to our knowledge, only three studies of the auditory off-response, and no significant variance has ever been observed between the source locations of on- and off-responses elicited from pure tones. We measured auditory evoked magnetic fields (AEFs) to various frequency pure tone stimulation in 5 healthy subjects with a 122-channel helmet-shaped magnetometer, and compared the distributions of the source locations of auditory N100m-Off (magnetic off-response around 100 ms) with those of N100m-On. Their spatial distributions were quite close to each other, and yet they were significantly different.

In vivo 31P NMR studies on experimental cerebral infarction.

Sequential metabolic changes in rat brain were monitored by in vivo measurements of 31P NMR spectra using a topical magnetic resonance (TMR) spectrometer, during the course of experimentally induced cerebral infarction and also during recovery produced by restoration of circulation. The experimental cerebral infarction was rendered by a slightly modified version of the method of Pulsinelli and Brierley (1979). The bilateral coagulation of the vertebral arteries at the level of alar foramina of the first cervical vertebra (preinfarction) did not show any change in NMR spectrum, but the subsequent bilateral ligation of internal carotid arteries produced a decrease in the peaks of ATP and phosphocreatine and a concomitant increase in the peak of inorganic phosphate within a few minutes. Intracellular pH, calculated from the chemical shift of inorganic phosphate, declined. These changes became maximal at approximately 30 min after the infarction. Reinstatement of blood flow to the cerebrum, produced by untying the ligature of internal carotid arteries, resulted in an immediate restoration of the peaks of ATP and phosphocreatine, which was followed by a reduction in the peak of inorganic phosphate within a few minutes. The spectrum recovered to its preinfarction pattern about 30 min after the restoration of the circulation. These experiments demonstrate that phosphorus compounds change very rapidly during infarction, and that these changes were reversible at least during a 30 min period.