Y. Katayama

Corticospinal direct response in humans: identification of the motor cortex during intracranial surgery under general anaesthesia.

The corticospinal direct (D) response to stimulation of the motor cortex exposed for intracranial surgery was recorded in 20 cases from wire electrodes inserted into the spinal epidural space. The D response was obtained from stimulation of restricted areas of the cerebral cortex, that is, the hand, trunk and thigh areas of the motor cortex. The D response was resistant to anaesthesia and unaffected by muscle relaxants. Thus, recordings of the D response are useful for identifying the location of the motor cortex during intracranial surgery under general anaesthesia.

Increase in focal concentration of deoxyhaemoglobin during neuronal activity in cerebral ischaemic patients

Background and Purpose: Blood oxygenation level dependent contrast functional magnetic resonance imaging (BOLD-fMRI) has been applied to functional mapping in brain disorders, based on the assumption that normal adults and patients with brain disorders exhibit similar evoked cerebral blood oxygenation (CBO) changes. This study compared evoked CBO changes measured by near infrared spectroscopy (NIRS) with the activation mapping obtained by BOLD-fMRI in patients with cerebral ischaemia. Methods: The study involved six normal adults and six patients with cerebral ischaemia. Hand grasping was performed as a motor task. All patients could perform the task similarly to the controls at the time of examination, but single photon emission computed tomography demonstrated low baseline cerebral blood flow and a decreased haemodynamic reserve in the primary sensorimotor cortex on the lesion side. Using NIRS, concentration changes of deoxyhaemoglobin (Deoxy-Hb), oxyhaemoglobin (Oxy-Hb), and total haemoglobin (Total-Hb) were measured in the primary sensorimotor cortex contralateral to the task. BOLD-fMRI signals were measured by 1.5 T magnetic resonance imaging using an echo-planar technique. Activation maps were calculated by statistical parametric mapping. Results: In the controls, Deoxy-Hb decreased in association with increases of Oxy-Hb and Total-Hb in the primary sensorimotor cortex during the task. However, in the patients, Deoxy-Hb increased significantly from baseline, while Oxy-Hb and Total-Hb also increased, indicating the presence of rCBF increases in response to neuronal activation. BOLD-fMRI demonstrated only limited activation areas in the primary sensorimotor cortex on the lesion side. Conclusion: The CBO changes in patients with cerebral ischaemia differed from those of normal adults; Deoxy-Hb was increased in activation areas of the patients. This implies that BOLD-fMRI may overlook activation areas in the patients unless both increases and decreases of signal are taken into consideration.

Heterogeneous Mechanisms of Early Edema Formation in Cerebral Contusion: Diffusion MRI and ADC Mapping Study

Severe cerebral contusion is sometimes associated with early edema formation within 24-48 hours post-trauma, and this frequently results in progressive ICP elevation and clinical deterioration. To investigate the underlying mechanisms of such severe contusion edema, diffusion imaging and ADC mapping were performed in 20 patients with cerebral contusion, employing 1.5 T echo planar MRI. Within 24 hours post-trauma, the diffusion images demonstrated a low intensity core in the central area and a high intensity rim in the peripheral area of contusion. The ADC value increased in the central area (ADC ratio (contusion/normal brain) = 1.13 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.83 +/- 0.13). This suggested that intra- and extracellular components underwent disintegration and homogenization within the central area, whereas cellular swelling was predominant in the peripheral area. A crescent-shaped zone of very high ADC value (ADC ratio = 1.38-1.61) was observed at the border between these two areas during the period of 24-48 hours post-trauma in some cases, apparently indicating that edema fluid was accumulated within a space formed by homogenization. The ADC values in the peripheral area shifted to an increase after 48-72 hours post-trauma. These findings imply that multiple mechanisms operate in early edema formation in cerebral contusion. It appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that a combination of such events facilitates edema fluid accumulation in the central area and contributes, together with the cellular swelling in the peripheral area, to the mass effect of contusion edema. Diffusion MRI and ADC mapping represent powerful tools for investigating spatially as well as temporally heterogeneous mechanisms of contusion edema.

Oedema Fluid Formation Within Contused Brain Tissue as a Cause of Medically Uncontrollable Elevation of Intracranial Pressure: The Role of Surgical Therapy

In patients with focal cerebral contusions, medical therapies have generally been advocated unless haemorrhages significantly contributing to the elevated intracranial pressure (ICP) exist. We report here several lines of clinical evidence which indicate that (1) enormous amount of extracellular oedema fluid is formed within contused brain tissue, (2) the formation of extracellular oedema fluid within contused brain tissue alone can be a cause of medically uncontrollable elevation of ICP and (3) surgical excision of the contused brain tissue provides excellent control of the elevated ICP in such patients. The excision of contused brain tissue appears to be the only therapy currently available to alleviate the formation of extracellular oedema fluid in cerebral contusions. We believe that, if ICP is elevated primarily by extracellular oedema due to cerebral contusions and the elevated ICP is medically uncontrollable, surgical excision of contused brain tissue should be carried out without delay regardless of the size of associated haemorrhages.

Gadolinium DTPA-Enhanced Magnetic Resonance Imaging of Cerebral Contusions

The morphological characteristics of cerebral contusions in head trauma patients suggest that an increase in cerebrovascular permeability is responsible for the contusion edema which develops within 1-3 days posttrauma. In the present study, 10 patients with cerebral contusions (mean age, 38 years old; 8 males and 2 females) were examined by gadolinium (Gd)-DTPA enhanced magnetic resonance imaging (MRI) at 1-2 days after trauma. Gd-DTPA (0.3 mmol/kg) was infused intravenously over a period of 30 min. MRIs were taken before, and at 2 and 4 hours after initiation of the Gd-DTPA administration. It was found that contusion edema areas were frequently enhanced by Gd-DTPA at 2 hours. The enhancement diminished at 4 hours. These findings appear to be inconsistent with the results of previously reported similar studies in which enhancement was detected at 6-9 days posttrauma but not during the period earlier than 6 days. This discrepancy may be attributable to the presence of a high blood concentration of Gd-DTPA for a longer period of time and a delay in the time at which MRIs were taken in the present study. The present data indicate that an increased cerebrovascular permeability occurs at as early as 1-2 days posttrauma, and suggest that contusion edema which progresses during the initial 1-3 days may be at least partially vasogenic in nature.

Excitatory Amino Acid Release from Contused Brain Tissue into Surrounding Brain Areas

The EAA release from contused brain tissue and its effect on the extracellular EAA levels in brain areas surrounding the contusion were investigated with microdialysis technique in the rat. A significant increase in extracellular EAA levels was observed in the contused brain tissue. The EAA increase was significantly greater in the contused brain tissue than in the isolated but non-contused brain tissue. It was further demonstrated that EAAs were released from non-contused brain areas 1-2 mm distant from contused brain tissue. No such EAA release from surrounding brain areas was demonstrated when the cavity was filled with isolated but non-contused brain tissue. The increase in EAAs was attenuated by KYN administered through microdialysis, suggesting that the EAA release from the surrounding brain areas appears to be a consequence that is secondary to the EAA release from the contused brain tissue. Such a diffusion-reaction process is probably mediated by the neurotransmitter actions of EAAs. The results of the present study are of clinical importance, since surgical removal of contused brain tissue and administration of EAA antagonists may serve to protect the surrounding brain areas from EAA neurotoxicity.

Preoperative determination of the level of spinal cord lesions from the killed end potential

To determine preoperatively the level of lesions in acute cervical cord injury, the killed end potential of the spinal cord was recorded with a pair of electrodes placed in the spinal epidural space, one initially being placed rostrally to the lesions for obtaining recordings and the other placed caudally to the lesions for stimulation. The level associated with the largest killed end potential was clearly determined without much difficulty, with sequential recordings on stepwise withdrawal of the recording electrode, in four of five cases investigated. In two cases subjected to surgery, the recording electrode left in place at the level associated with the largest killed end potential was found to be located at, or a few millimeters below, the center of the lesions. This demonstrates the preoperative localizing value of the killed end potential for determining the level of lesions responsible for myelopathy.

Cerebral blood oxygenation changes induced by bypass blood flow in moyamoya disease and non-moyamoya cerebral ischaemic disease

SummaryBackground. Superficial temporal artery–middle cerebral artery (STA–MCA) anastomosis has been used to prevent stroke in patients with moyamoya disease (MD) and non-moyamoya ischaemic disease (non-MD). However, little is yet known regarding the difference between these groups of patients in the extent to which the bypass contributes to maintaining adequate cerebral blood oxygenation (CBO), or the temporal changes after surgery. In the present study, we evaluated the CBO changes induced by bypass blood flow in patients with MD and non-MD during the peri-operative periods employing optical spectroscopy.Methods. We investigated 13 patients who underwent STA–MCA anastomosis, including 5 MD and 8 non-MD patients. We evaluated the effects of STA blood flow on the CBO in the MCA territory on the anastomosis side, employing visual light spectroscopy during surgery and near infrared spectroscopy (NIRS) at one week after surgery.Findings. In 4 MD patients and one non-MD patient, the STA blood flow increased the oxyhaemoglobin and cortical oxygen saturation (CoSO2), indicating that the bypass supplied blood flow to the ischaemic brain; the CBO changes were observed more frequently in MD than in non-MD patients (p < 0.02). The pre-anastomosis CoSO2 (65.4 ± 5.4%) in MD was significantly lower than that (72.8 ± 7.6%) in non-MD (p < 0.05). Postoperative NIRS demonstrated that the bypass began to supply blood flow to the brain in 5 non-MD patients whose bypass did not supply blood flow during surgery.Conclusions. Although MD has vessels of small diameter as compared to non-MD, the bypass begins to supply blood flow to the ischaemic brain earlier in MD than in non-MD after anastomosis. The fact that the CoSO2 in MD was lower than that in non-MD suggested that the perfusion pressure in MD was lower than that in non-MD, and this might account for the difference in the bypass blood supply after anastomosis between MD and non-MD. Our data suggest that, even if the bypass does not supply blood to the brain during surgery in non-MD, the bypass blood flow gradually increases after surgery.

Responses of Raphe-Spinal Neurons to Stimulation of the Pontine Parabrachial Region Producing Behavioral Nociceptive Suppression in the Cat

Cholinergic stimulation of the pontine parabrachial region (PBR) produces behavioral nociceptive suppression in the awake cat. This report shows that electrical stimulation of both PBR sites (verified to be associated with behavioral nociceptive suppression on cholinergic stimulation) and the periaqueductal gray (PAG) excites raphe-spinal neurons which have been implicated in descending nociceptive suppression. Although several lines of evidence have strongly indicated that pathways from the PBR and PAG for nociceptive suppression are anatomically as well as neurochemically distinct, the results of the present study appear to suggest that certain components of the pathways from the PBR may be synergic in function with those from the PAG with regard to the activity of raphe-spinal neurons.

Ultra-early study of edema formation in cerebral contusion using diffusion MRI and ADC mapping

OBJECTIVE Our previous studies have reported that heterogeneous mechanisms exist in early edema formation in cerebral contusion, and cytotoxic edema plays an important role within 48 hours post-trauma. It is remains unclear, when edema begins to develop following injury. In order to determine the time course of edema development, diffusion imaging and ADC (apparent diffusion co-efficient) mapping was performed in 10 patients within 24 hours post-trauma with cerebral contusion. METHODS Diffusion imaging and ADC mapping were performed employing 1.0 T echo planar MRI. ADC values were indicated as a ration relative to the values of intact brain areas. RESULTS Within 3 hours post-trauma, diffusion MRI showed no remarkable changes, and the ADC values were within normal limit (ADC ratio (=contused/normal brain) = 1.00 +/- 0.21, (mean +/- SD)). At 6 hours post-trauma, diffusion images demonstrated a low intensity core in the contusion proper and a high intensity rim in the peripheral area of contusion. The ADC value increased in the contusion proper (ADC ratio = 1.26 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.58 +/- 0.19). CONCLUSIONS These findings indicated that early cellular swelling in the peripheral area of contusion begins within 6 hours following injury. This delayed occurrence of contusion-induced cellular swelling suggests that the CBF does not decrease to ischemic level immediately following injury.