A new model of focal axonal injury was reproduced by rapid and controlled elongation (uniaxial stretch) of the guinea pig optic nerve. Light microscopy study of optic nerve specimens after horseradish peroxidase injection into the vitreous of the animal's eye showed that axonal lesions were identical to those seen in human and primate post-traumatic diffuse axonal injury (DAI). The lesions were characterized by the formation of terminal clubs in severed axons and focal axonal enlargements in those axons that were lesioned-in-continuity. Visual-evoked potentials upon flash stimulation were recorded before and after injury. Mean amplitude and mean latency of occipital peaks were significantly elongated in the acute post-traumatic phase. Electron microscopy examination showed that the main axonal changes observed in this model were cytoskeleton disorganization, accumulation of axoplasm membrane-bound bodies at the site of terminal balls and dilatations-in-continuity and detachment of the axolemma from the myelin sheath. Such axonal alterations were similar to those found in many other biological models of central and peripheral axonal injuries in which the lesion was produced by invasive methods. This model is unique since it reproduces the same mechanism of injury and the identical lesions that have been demonstrated in humans and primates with post-traumatic (DAI).

EEGs and short-latency somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded during 151 carotid endarterectomies, performed under general anaesthesia. Carotid occlusion did not affect either EEG or SEP in 120 cases (group A). In 31 cases the EEG showed "ischaemic" abnormalities (group B). A temporary shunt was inserted only in 16 B patients showing also severely depressed cortical SEPs within 2 min after carotid occlusion (group B shunt). In 15 B patients in whom SEPs were less affected, the operation was completed without shunt (group B no shunt). One intraoperative stroke occurred in group A and two in group B shunt. No neurological complications occurred in group B no shunt. Overall stroke rate was 2%. On retrospective analysis, latency and amplitude of N20 and P25 waves proved to be uninfluenced by carotid occlusion in group A, but were significantly affected in group B shunt. P25 amplitude alone was reduced in B no shunt. An arbitrary index (need-for-shunt index, NSI) was made in order to rate changes of P25 latency and amplitude. Its mean values were significantly different in the 3 groups. A threshold value is suggested above which shunt is required, as a useful adjunct to EEG, in order to balance prevention of brain ischaemia against the risks of shunt.

We report our experiences with somatosensory evoked potential (SSEP) monitoring during cerebral aneurysm operations under hypotension. In the first part of this study the surgical technique was intentionally not changed as a result of SSEP monitoring; in this way, we established what changes in intraoperative SSEP were consistent with preservation of function during surgical manipulations. We recorded both short-latency SSEP to computer central conduction time (CCT) and long-latency cortical SSEP, with a timebase of 200 ms, on admission of the patients to the hospital and intraoperatively. We found that 54% (7 of 13) patients with preoperative signs of arterial spasm, i.e., increased rate of blood flow in the middle cerebral artery, had ipsilateral prolongation of CCT and depression of the cortical late waves. During the operation a CCT exceeding 9 ms for at least 10 minutes and an irreversible loss of the cortical late waves were the only parameters predictive of postoperative deterioration in function. In addition, the patients whose neurological status deteriorated postoperatively had preoperative CCT equal to or longer than 7.5 ms and depression of the cortical late waves over the affected hemisphere. These patients are not good candidates for operations under hypotension. On the basis of these results, patients in the second part of this study who were not candidates for operation under hypotension were operated upon with the technique of temporary clipping under normotension, with evoked potential monitoring. No patients operated upon according to this protocol showed postoperative deterioration in function. Brainstem auditory evoked potentials (BAEP) were recorded, in addition to SSEP, when aneurysms of the vertebral artery were operated upon. Prolongation of the wave I-V interval was caused by brainstem retraction, but even more severe BAEP changes developed when hypotension was induced. These changes soon reversed when blood pressure was raised after the aneurysm had been clipped.

Flash and pattern reversal visual evoked potentials were recorded in awake patients undergoing stereotactic procedures for severe dyskinetic disorders resistant to medical treatment. The nucleus ventralis lateralis thalami was reached via an occipital approach. VEPs were recorded on the scalp at the entrance of the intracerebral electrode, and serially from sites at different depths. A polarity reversal of the surface recorded wave form took place as the intracerebral electrode was advanced beneath the surface cortical layers. As concerns F-VEPs, most of the scalp activity mirrored the potentials recorded down to the depth of 70-65 mm from the thalamus. The largest amplitude of intracerebral F-VEPs was obtained from recording sites at 50-70 mm from the thalamus, i.e., in the depth of the calcarine fissure. A negative wave, peaking around 47-50 msec, became evident in recording sites at 30-40 mm from the thalamus but vanished as the electrode was advanced farther. In only one patient could we record a small negative wave, peaking at 33 msec, in the vicinity of the corpus geniculatum externum. Furthermore, the oscillatory activity recorded from the scalp appeared to be generated in the cortical layers. PR-VEPs also underwent polarity reversal as the electrode traversed the cortex. PR-VEPs disappeared more superficially than F-VEPs. No PR-evoked activity could be recorded in the vicinity of the corpus geniculatum externum. We conclude that slow and fast components of VEPs recorded from the scalp are entirely generated in cortical layers.

Deliberate arterial hypotension is currently used to operate upon cerebral aneurysms. However, it is not ascertained whether this practice is really safe for all patients, especially those presenting with preoperative vasospasm. 50 patients, requiring surgical treatment for cerebral aneurysm, have been submitted, during surgery, to the recording of Somatosensory Evoked Potentials (SEPs) on median nerve stimulation. This technique allows the functional evaluation of neural pathways mediating the somatosensory stimuli and of primary somatosensory cortex; it is known that a decrease of cerebral perfusion may affect the SEP waveforms in terms of reduced subcortical conduction velocity (i.e., increased central conduction time, CCT) and of reduced cortical response amplitude. These changes may be apparent before a permanent neurological damage is produced. Preoperative SEP recording demonstrated a prolonged CCT, possibly related to vasospasm, in 9 patients, a normal clinical evaluation notwithstanding (grade I and II).

A group of patients undergoing aortic replacement of thoracic and abdominal aneurysms were studied by intraoperative recording of Somatosensory Evoked Potentials (SEPs). Lower limb nerves were stimulated and SEPs recorded at spinal and cortical level. Progressive changes of cortical SEPs until their disappearance were observed. In operations on the thoracic aorta, the spinal response was essentially unmodified, so that the observed alterations reflected true dysfunction of the spinal cord. The only patient who developed an intraoperative anterior spinal infarct had the longest period of absent SEPs and a striking latency prolongation when they returned. Postoperative recordings were absolutely normal. When the abdominal aorta was occluded, SEP alterations involved both cortical and spinal responses, so that it is difficult to distinguish between the relative roles of peripheral nerve and spinal cord ischemia. These findings indicate that SEPs can be reliably applied to spinal cord monitoring in the course of aortic surgery, even though they are mainly conducted in the posterior cord tracts.

The pathogenesis of brain dysfunction in phenylketonuria (PKU) is still under investigation. Hyperphenylalaninaemia results in increased turnover of myelin. In order to demonstrate the derangement of myelinization in PKU we studied the visual evoked potentials (VEP) in 14 PKU patients and in 20 normal subjects. VEP findings were correlated with the metabolic control of the disease and with the electroencephalographic findings. VEP were more sensitive than the EEG in detecting a neurological dysfunction. VEP are influenced by dietary control and are normal only in children with good metabolic control.

Pattern-reversal visual evoked potentials (PR-VEPs) and EEG were recorded in 14 phenylketonuric (PKU) children on a low-phenylalanine (phe) diet; the data obtained were correlated with metabolic parameters, namely, the actual phe plasma level, the mean phe plasma level in the last year, an the beginning of the diet. PR-VEPs seem to be more sensitive than EEG in detecting neurophysiological derangements in these subjects; in fact PR-VEPs were pathological in six patients while EEG detected three; no significant alterations were found in the neurophysiological tests among the children with good metabolic control, and only one child was abnormal among the six on an early dietetic regimen; in contrast, six of the nine subjects presenting with high mean phe plasma levels (>10 mg/100 ml) and five of the eight whose diet started after the 2nd month of life showed pathological PR-VEPs.