Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion.

PURPOSE: This prospective study evaluated the possible prevention of postoperative neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms (TAAA), types I and II, by use of perioperative cerebrospinal fluid drainage and distal aortic perfusion. METHODS: Between September 18, 1992, and August 8, 1993, 45 consecutive patients underwent TAAA repair (14 type I, 31 type II). Thirty-six were men and nine were women. The median age was 63 years (range 28 to 88). Twenty-four of 45 patients (53%) had dissection and 17 of 45 (38%) had prior proximal aortic replacement. All patients underwent perioperative cerebrospinal fluid drainage and distal aortic perfusion. Median aortic clamping time was 42 minutes. Thirty-five of 45 patients (78%) underwent intercostal artery reattachment. RESULTS: The 30-day survival rate was 96% (43 of 45 patients). Early neurologic deficit occurred in two of 45 patients (4%), and late neurologic deficit also occurred in two of 45 patients (4%). We compared the neurologic deficit of our current group of 45 patients with the data of a previously unpublished study of 112 patients also from this center. Total neurologic deficit for the current group was four of 45 (9%) versus the previous group of 35 of 112 (31%) with a p value of 0.0034 (Pearson chi-square test). Neurologic deficit for patients with type I TAAA was 0 of 14 (0%) versus 15 of 73 (21%) (p = 0.062); for patients with type II TAAA 4 of 31 (13%) versus 20 of 39 (51%) (p = 0.0008). In patients with aortic dissection, neurologic deficit was 3 of 24 (12%) versus 9 of 32 (28%) (p = 0.0304); no dissection was 1 of 21 (5%) versus 26 of 80 (32%) (p = 0.011). For aortic clamp times less than 45 minutes, neurologic deficit was 1 of 24 (4%) versus 14 of 68 (21%) (p = 0.061); for aortic clamp times equal to or greater than 45 minutes, neurologic deficit was 3 of 21 (14%) versus 21 of 44 (48%) (p = 0.0090). CONCLUSION: Neurologic deficit in patients treated for types I and II TAAA was reduced significantly by perioperative cerebral spinal fluid drainage and distal aortic perfusion.

Brain protection via cerebral retrograde perfusion during aortic arch aneurysm repair.

Eleven patients underwent resection and graft replacement of ascending and aortic arch aneurysms. Retrograde cerebral perfusion was used during the procedures to minimize cerebral ischemia. Retrograde cerebral perfusion (15 degrees to 24 degrees C) was administered through the superior vena cava. The mean cerebral ischemic time was .35 minutes (range, 11 to 71 minutes). Throughout retrograde cerebral perfusion, blood samples were drawn from the innominate and left carotid arteries at 1, 5, and every 10 minutes thereafter for analysis of arterial oxygen content, total creatine kinase level, and creatine kinase BB fraction. All patients survived. All except 1 awoke neurologically intact. In this patient, electroencephalogram and transcranial Doppler studies conducted before circulatory arrest were consistent with embolic phenomena. There was no significant difference between the current group's intraoperative electroencephalograms and those of a similar historical group. Postoperative complications included transient renal failure, myasthenia gravis, cholecystitis, premature atrial contractions, atrial fibrillation, and vocal cord paralysis. The creatine kinase BB fraction range was 1.8 to 13.4. The increase of total creatine kinase level was due to MM fraction. Retrograde cerebral perfusion during circulatory arrest is a valuable adjunct for protecting the brain. The creatine kinase BB band was not a good marker to detect brain injury. With continued use of this technique and accumulation of a larger series, we may better define the role of retrograde cerebral perfusion in brain protection.

How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms.

This paper reviews the literature on the EEG effects of hyperventilation, with particular emphasis on the literature concerning the mechanism of EEG slowing with hyperventilation. We suggest that there is no definite evidence to support the theory that the EEG slowing and "activation" are caused by hypoxia secondary to cerebral vasoconstriction induced by hypocapnia during voluntary hyperventilation. Since it is known that hypocapnia produces decreased activity in the mesencephalic reticular formation and that lesions of the thalamus abolish the hyperventilation response, we propose a strong, albeit speculative, analogy between awake-sleep transitory states and the mechanism of EEG "activation" by hyperventilation. Furthermore, it is proposed that both the EEG changes and the associated clinical symptomatology (as well as changes in level of anesthesia, which vary with arterial PCO2) may be explained by altered arousal, and that the vasoconstriction observed during hyperventilation is a central neurogenic response to hypocapnia at a brainstem level.

Improved wave V resolution by dual-channel brain stem auditory evoked potential recording.

Brain stem auditory evoked potentials were recorded simultaneously from the vertex and ear contralateral to stimulation (Ac-Cz) and from the vertex and ear ipsilateral to stimulation (A1-Cz). There was clearer definition of wave V and less latency variability between trials in Ac-Cz channel recordings, resulting in enhanced wave form stability and greater reproducibility of wave I-V interpeak latencies. The clinical interpretation of dual-channel recordings is currently limited by the complexity of the auditory pathways, but the technique itself shows promise as a routine clinical procedure.

Prognostic value of EEG in acute vascular aphasia: a long term clinical-EEG study of 53 patients.

A group of 53 patients rendered acutely aphasic by occlusive cerebrovascular disease were studied by serial EEG's, repeated neurologic examinations and speech evaluations (Porch Index of Communicative Ability) over a period of eight to twenty-four months, in order to correlate EEG findings with the degree of language disorder and prognosis for language recovery. Normal and mildly abnormal EEG's, posterior slow foci, focal slowing of semirhythmic type and higher alpha frequencies over the intact hemisphere correlated with good language recovery. In the majority of the patients, the curves of "EEG Improvement" and "Language Recovery" closely paralleled each other. These data indicate that the EEG is of prognostic value as to recovery from aphasia in patients suffering from acute occlusive cerebrovascular disease. Despite the advent of newer diagnostic tests, such as CAT scan, which has established its value in evaluation of the anatomy of aphasia, (9) EEG remains to be useful as a tool that could predict the outcome of aphasia in stroke patients.