Donald P. Becker
With an overview of CNS acidosis
Michael J. Rosner and Donald P. Becker
✓ The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p < 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p < 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.
Experimental observations and a theoretical model
Michael J. Rosner and Donald P. Becker
✓ Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg “A-waves” are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction.
Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.
Donald P. Becker and Frank E. Nulsen
Theodore G. Obenchain and Donald P. Becker
✓ An abscessed Rathke's cleft cyst was removed in a 50-year-old woman who had had headaches and episodic fever for 3 years and had been on intermittent methotrexate therapy for psoriasis for 4 years. There was clinical and laboratory evidence of panhypopituitarism. Erosion of the sella turcica was present. The patient has remained asymptomatic on replacement therapy. A brief review of abscess formation in the region of the pituitary gland is presented.
Theodore G. Obenchain and Donald P. Becker
✓ A woman with hydrocephalus and head bobbing presented with headaches and episodic loss of consciousness. Contrast studies revealed a cyst within the third ventricle. At craniotomy it occupied the entire third ventricle and its walls merged with the hypothalamus. This is considered to be a congenital suprasellar arachnoid cyst which expanded superiorly through the third ventricle. Similar cases are reviewed and therapy briefly discussed.
Stanley J. Goodman and Donald P. Becker
✓ The neurological status and supra- and infratentorial intracranial pressures were studied in awake unsedated cats during expansion of a supratentorial mass. The pontomesencephalic portion of the brain stem was removed, serially sectioned, stained with sodium nitroprusside benzidine, and microscopically examined. Three types of vascular abnormality were seen: macrocirculation hemorrhages, microcirculation hemorrhages, and vascular stasis. As the supratentorial mass expanded and the intracranial pressure rose, there was a progression of vascular lesions from stasis to microcirculation hemorrhages, and finally to macrocirculation hemorrhages. The microcirculation hemorrhages occurred in stuporous animals, and the macrocirculation hemorrhages in comatose animals. Microcirculation hemorrhages were distributed primarily in the tectum, and macrocirculation hemorrhages were mainly in the tegmentum. Microcirculation hemorrhages first appeared in association with moderate to severe intracranial hypertension; macrocirculation hemorrhages were seen mainly with extreme intracranial hypertension. The clinical implications of these brain-stem vascular lesions are discussed.
Frank E. Nulsen and Donald P. Becker
Correlation with human head-injury data
Richard P. Greenberg, Donald M. Stablein and Donald P. Becker
✓ Multimodality evoked potential (MEP) data from over 300 comatose head-injured patients suggest that central nervous system dysfunction of the brain stem and/or hemispheres can be localized with this noninvasive neuroelectric technique. Based on this work, decerebrate motor posturing and prolonged coma are not associated with brain-stem dysfunction but rather with dysfunction of the hemispheres, while absent pupillary and oculocephalic responses are correlated with brain-stem dysfunction alone. However, the accuracy with which MEP data localized human brain-stem or hemispheric dysfunction could not be confirmed by pathological correlation because of low mortality and the small number of autopsies obtained in the patients who died. Therefore, this study was undertaken in an animal model of brain-stem lesion.
Complete brain-stem transections were made at the cervicomedullary junction, the medulla just caudal to the eighth nerve, and at the intercollicular region. All cortical visual evoked potential (VEP) peaks were reduced in amplitude and delayed by each of the brain-stem transections, but none of the peaks was abolished. In spite of brain-stem transection, VEP's can be used to gain information about hemispheric function. Somatosensory (SEP) and auditory cortically generated evoked potentials (AEP) were abolished by these brain-stem transections, but early-latency brain-stem SEP and AEP data could accurately localize specific areas of brain-stem dysfunction caused by the lesions. Observations made on human MEP data seem to be confirmed by these animal experiments. Correlations between human and cat MEP data are discussed.
David J. Mayer, Donald D. Price, Donald P. Becker and Harold F. Young
✓ A sensitive quantitative index for predicting optimal electrode position in percutaneous anterolateral cordotomy was determined by electrical stimulation through the lesioning electrode. If the threshold for pain elicited by the stimulation electrode was less than 300 µA, a 5-sec radiofrequency lesion of 50 mA would produce complete contralateral analgesia with no weakness. When the pain threshold exceeded 300 µA, incomplete or no analgesia would result with the standard single lesion. The results further suggested that the fibers in the anterolateral quadrant that transmit pain are discretely rather than diffusely localized.