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Biomedical subjects

T W Langfitt

Publications and source records attributed to T W Langfitt.

At least 55 records · Page 3Linked to original sources
PubMed1976

Methodology for intraventricular and subarachnoid continuous recording of intracranial pressure in clinical practice.

The methodology for continuous monitoring intracranial pressure (ICP) being presently employed in the Neurosurgery Service of the University of Pennsylvania is presented. The methods are intraventricular recording of ICP (IVP) and subarachnoid recording of ICP (SaP). The indications for employing either method are briefly presented. IVP is favored in those situations in which the lateral ventricles are enlarged and SaP is preferred in the cases of brain swelling or other situations in which there is a small ventricular system.

Cerebral Ventricles↗
PubMed1976

Analysis of the response to therapeutic measures to reduce intracranial pressure in head injured patients.

Five methods of therapy for increased ICP were used in the treatment of 32 head-injured patients. The effects of steroids could not be evaluated. Withdrawal of CSF was always effective because intracranial volume was reduced and pressure must follow, but because of brain swelling and collapse of the ventricular system in this group of patients, it was not an effective permanent form of therapy. Hypertonic Mannitol reduced ICP in nearly every case irrespective of the degree of brain damage or the height of ICP. Hyperventilation was least effective in the most severely ill patients, presumably due to the non-responsiveness of the cerebral vessels to changes in PaCO2. The poorest response of ICP seemed to be with hypothermia.

Adolescent↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function.

Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 +/- 4.2 ml/100 gm/min to 26.3 +/- 4.4 (p less than .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 2: Brain morphology.

The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism.

The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.

Adenosine Triphosphate↗