Nobuo Moriyasu

Assessment of brainstem damage by the auditory brainstem response in acute severe head injury.

In 64 cases suffering from severe head injury (Glasgow coma scale: less than seven- the auditory brainstem responses (FARs) recorded at the vertex, which are thought to be volumet conducted far-field potentials reflecting the sequential electrical activities of the auditory afferen) system in the brainstem, were recorded in the neurosurgical intensive care room immediately after admission. The alterations in the responses were compared with the types of primary injury, neurological signs., CT findings and outcome following treatment. Based on the results obtained, it is concluded that the FAR is a useful indicator for predicting the effects of treatment on brainstem damage in patients with severe head injury, and that it provides more reliable information about the function of the brainstem than the neurological signs or CT findings. Moreover, it also offers a diagnostic method for primary brainstem injury. Three cases or primary brainstem injury without lesions in the supratentorial region were diagnosed by means of combined CT and FAR recording.

Evidence for involvement of the frontal cortex in pain-related cerebral events in cats: increase in local cerebral blood flow by noxious stimuli.

Noxious stimuli were shown to induce a remarkable increase in local cerebral blood flow restricted to the forepart of the cerebral hemispheres bilaterally anterior to the posterior sigmoid gyrus in cats. This increase in local cerebral blood flow was averted by lesions in the bilateral ventromedial thalamus and attenuated by pretreatment with an intraventricular injection of 6-hydroxydopamine.

Changes in local cerebral blood flow and neuronal activity during sensory stimulation in normal and sympathectomized cats

Activities of neurons of the thalamic relay nucleus and cortical somatosensory area which are capable of producing excitatory potentials in response to stimulation of the sciatic nerve were recorded, and local cerebral blood flow was measured simultaneously using a double microelectrode under local anesthesia in both non-pretreated cats and cats undergoing chemical denervation of the vasoadrenergic nerves by intraventricular injection of 6-hydroxydopamine (6-OHDA), in order to unmask the neural control on the cerebral vessels during increase of local metabolic rate. The results obtained may be summarized as follows. (1) A positive correlation was found between an increase in firing rate of a single neuron in the thalamic relay nucleus and somatosensory area and an increase in local cerebral blood flow following stimulation of the sciatic nerve. A distinct spatial and quantitative correlation was thus observed between neural activity and cerebral blood flow. (2) In 6-OHDA-pretreated cats, an increase in neuronal firing rate was observed following stimulation of the sciatic nerve, as it was in non-pretreated cats, but the concurrent response of local cerebral blood flow was seriously impaired. All these findings indicate that the increase in local cerebral blood flow occurring in association with increased neural activity does not result solely from increased local metabolism and a consequent increase in CO2 production, but requires for its occurrence that certain basic conditions be satisfied and maintained by the vasoadrenergic innervation.

Diencephalic modulation of activities of raphe-spinal neurons in the cat

Abstract The modulatory effects of diencephalic stimulation on the activities of raphe-spinal neurons were studied extracellularly in cats. Among 240 raphe neurons recorded, 57 neurons were activated antidromically by stimulation of the cervical dorsolateral funiculus. These raphe-spinal neurons were found in the caudal raphe nuclei, i.e., the raphe magnus (43 neurons), raphe obscurus (11), raphe pallidus (2), and raphe pontis (1). All of them responded to innocuous and/or noxious peripheral mechanical stimuli with a broad receptive field. The activities of the majority of these neurons were facilitated by trains of pulse stimulation of the rostral periaqueductal gray and the thalamic relay nucleus but not of the thalamic center median nucleus. The facilitation of firing persisted for more than 3 min after the cessation of train pulse stimulation when the stimulation was applied at 20 Hz for 5 to 30 s. This facilitation was not affected by decortication of the sensorimotor area bilaterally. The facilitatory response to periaqueductal gray stimulation was markedly suppressed by systemic administration of naloxone. On the other hand, that of the thalamic relay nucleus stimulation was found to be unaffected. Based on these findings, the mechanisms of pain relief by stimulation of the rostral periaqueductal gray and thalamic relay nucleus reported in human intractable pain appear to relate, at least partly, to the activation of raphe-spinal neurons. However, the paths to raphe-spinal neurons of stimuli from the periaqueductal gray and the thalamic relay nucleus are thought to be independent from each other based on the different effects of naloxone.

Slow rhythmic activity of caudate neurons in the cat: statistical analysis of caudate neuronal spike trains.

Spike trains of caudate neurons initially having mean interspike intervals of less than 4 ms were analyzed with progressive administration of pentobarbital (5 to 20 mg/kg). Among the neurons investigated, 77% (N = 79) showed evidence of a rhythmic basis of their activity in first-order interspike interval histograms and/or autocorrelation histograms in the course of becoming silent due to progressive administration of pentobarbital. Although the rhythmicies of given units varied depending on the level of anesthesia the most prominent cycle was almost always within the range of 200 to 320 ms; the majority were not discernable on visual inspection of the spike trains. Cortical stimuli reset the cycle. Cross-correlation histograms constructed from pairs of caudate neurons provided some evidence that their spontaneous firing was mutually inhibited. The possibility that the rhythmicities might arise from such mutual inhibition of spontaneously firing caudate neurons is discussed.

Motivational slow negative potential shift (CNV) related to thalamotomy.

The alteration of cortical electrical activity induced by imperative stimulation following warning stimulation, contigent negative variation (CNV), and psychological changes following thalamotomy for relief of intractable pain (CM) and tremor (VL) are studied, since CNV has a close relationship with the degree of psychological activity. Ventrolateral thalamotomy does not have any effect on the amplitude of cortical CNV, but the ventromedioposterior part of the centre median has a generating action of CNV in itself and it has facilitatory effects upon cortical CNV. According to these results, the effective mechanism of centre median thalamotomy for relief of intractable pain is caused by suppression of attention and expectancy for exogenous stimuli following lesions of the centre median.

Sacral Epidermoid Cyst Communicating with the Spinal CSF Canal

A 6-year-old girl was found to show a presacral epidermoid cyst which had a communication with the spinal canal. The patient was admitted as a case of meningitis, but squamous cells and cholesterin crystals were observed in the cerebrospinal fluid (CSF), and the CSF cholesterol level was very high. Diagnosis was established by myelography, and a cyst measuring 4.5 x 6.0 x 4.0 cm wide was totally excised surgically. A comparative discussion of this case and other reported cases of dermoid and epidermoid cysts in the central nervous system is given.

Emotional Slow Negative Potential Shift (CNV) in the Thalamus

In order to know the functional relationship between CNV recorded at the vertex and activity of the thalamic nucleus, the CNV at the vertex and the intrathalamic slow potentials responding to an S1-S2-R paradigm were recorded during thalamotomy under local anesthesia. It might be concluded that the activity of the medial thalamus and medial parts of the subthalamic area not only generate slow potential shifts corresponding to S1-S2-R, but also play an important role in controlling the CNV at the vertex.

Fatal Brainstem Damage Caused by Linear Acceleration Impact

The present experiment was undertaken to clarify the correlation between pathological findings of primary brainstem damage and alteration of the far field acoustic response of the rhesus monkey by linear acceleration head impact using a HYGE sled and slider impactor system. Brainstem damage was produced by the impact upon the frontal or occipital part of the head, at an linear acceleration in parallel to orbito-meatal line, 1, 000 1, 500 G and duration 3 ?? 5 msec. In 4 out of 12 monkeys, the electron microscopic cellular changes and disturbance of microcirculation at the lower brainstem were observed and they died within one hour after the impact. The far field acoustic response disappears just after the impact without any relation to cortical EEG. In the 6 monkeys that survived following the impact, the far field acoustic response did not disappear even just after the impact. Normal microcirculation and slight electron microscopic cellular changes were observed at the brainstem. Monkeys that died of cervical cord injury or intrathoracic bleeding by the impact, had slight electron microscopic changes with normal microcirculation at the brainstem as in survival group. The far field acoustic responses did not disappear just after the impact but disappeared when EEG became flat by death. According to these results, it is concluded that: 1) The primary brainstem damage consists of electron microscopic changes and disturbances of microcirculation is induced by pure linear acceleration head impact without any cranial fracture, intracranial hematoma or cerebral contusion; and 2) This primary brainstem damage is fatal in monkeys whenever all waves of the far field acoustic responses disappear.

Cerebral Venous Circulation Mechanism During Intracranial Hypertension

The main cause of acute brain swelling under increase of intracranial pressure is arterial vasoparalysis, in spite of no-attention about the cerebral venous circulation. The aim of this experiment is to find out the role of venous circulation and its mechanism to include the acute brain swelling under the increase of intracranial pressure.