Biomedical subjects
Publications and source records attributed to T W Langfitt.
The Hospital of the University of Pennsylvania was the first university-owned teaching hospital in the nation. The author briefly reviews its history and association with the other faculties of the University.
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Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale. The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability. Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.
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A total of 159 head-injured patients were classified into four groups based on two acute categories of injury severity (minor-to-moderate and severe) and the subsequent presence or absence of visual field defects (VFDs). They were assessed neuropsychologically within ten to 19 months after injury. Within both minor-to-moderate and severe injury classifications, patients with VFDs were more impaired neuropsychologically and had more frequent acute secondary intracranial complications (brain swelling, intracranial hypertension, and cerebral hyperemia) than patients without VFDs. The findings suggest that the presence of VFDs during the long-term period may be residuals of acute secondary complications indicative of increased neuropsychological deficits after head injury.
Neuropsychological outcome within two years after injury was determined in 159 head injured patients who were classified into three groups according to the presence of either unilateral, bilateral, or no visual field defects (VFDs). The VFDs occurred irrespective of injury severity as determined by the Glasgow coma scale, or social outcome as determined by the Glasgow outcome scale. Differences among the three visual field groups were obtained for several neuropsychological functions: intelligence, memory, learning, acquired verbal skills, visuospatial skills, and visuomotor speed. Patients with bilateral VFDs were more severely impaired neuropsychologically than those with unilateral or no VFDs. Occurrences of secondary complications (brain swelling, intracranial hypertension, and hyperemia) were more prevalent among the bilateral VFD cases. The findings suggested that bilateral VFDs may be indicators of increased brain damage from secondary insults.
The relationship between severity of injury [as determined by the Glasgow Coma Scale (GCS)] and the quality of survival (as determined by neuropsychological measurements and work return) were investigated in 54 conscious survivors within 16 months following head injury. While severely head injured (GCS less than or equal to 8) patients had more neuropsychological impairments in areas of intelligence, attention, memory, visuomotor speed, and motor skills than those with mild injuries (GCS greater than 8), performances after both types of injury were below normative levels in areas of learning, memory, and visuomotor speed. Unemployment increased after both severe and mild injuries, while employment status changed more frequently after severe injuries. Age had a minimal effect on neuropsychological and employment outcomes after minor head injuries (GCS greater than 13). The findings suggest that regardless of acute severity, closed head injury influences long-term quality of survival.
Outcome at 6 months after severe head injury was determined in 117 patients whose computed tomographic (CT) examinations demonstrated diffuse axonal injury (DAI), diffuse swelling (DS), or focal injuries. Neuropsychological sequelae were ascertained from two examinations in 30 of the conscious survivors within the 1st year after injury. Outcome differences varied with the type of CT lesion. DS and focal injuries resulted in more favorable (good recovery) outcomes. Mortality was higher after DAI. Neuropsychological outcome varied with the type of CT lesion and the function measured. Overall differences in memory and learning were revealed among the three CT lesion categories, whereas differences in intelligence and visuomotor functions were not significant. Levels of memory, learning, and visuomotor speed were higher after DS injuries, but improvement was less. Greater improvement of memory, learning, and visuomotor speed occurred after DAI. After focal injuries, visuomotor speed improved, but not recall and learning. The results suggest that the type of injury incurred differentially influences the outcome and the neuropsychological aftermath of severely head-injured adults.
In order to study the metabolic events surrounding ischemia induced by the graded increase of cerebrospinal fluid (CSF) pressure, the technique of simultaneous phosphorus-31- and hydrogen-1-enhanced nuclear magnetic resonance spectroscopy was applied to five cats as intracranial pressure (ICP) was gradually raised by the instillation of mock CSF. Threshold lactate rose at an average cerebral perfusion pressure (CPP) of 49 torr, and, in general, preceded a threshold decrease in phosphocreatine, which was observed at an average CPP of 29 torr. There was considerable variation among cats in the CPP at which failure of brain energy metabolism occurred, however, suggesting differences in the autoregulatory curves. It is concluded that, with elevated ICP, there is no universally "safe" CPP at which brain energy metabolism may be assumed to be uncompromised.
Results of computerized tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), xenon-133 measurement of cerebral blood flow (CBF), and neuropsychological assessments are described in three head-injured patients. The patients were selected because they presented with intracranial hemorrhage diagnosed by CT. Two of the patients were studied acutely and again approximately 6 months later. In the acute stage, MRI was superior to CT in identifying the precise location and extent of intracranial hemorrhage and associated edema. Small subdural hematomas diagnosed on MRI were missed with CT scanning. The extent of apparent encephalomalacia in the chronic stages of injury was also better defined with MRI. Positron emission tomography showed disturbances of glucose metabolism that extended beyond the structural abnormalities demonstrated by MRI and CT; anterior temporal lobe dysfunction was particularly evident in all three patients. Regional CBF studies failed to detect a number of the abnormalities seen on MRI and CT, and even ignored the metabolic dysfunction evident on PET that should have been accompanied by changes in regional CBF. The neuropsychological studies localized frontal lesions, but did not reveal abnormalities attributable to the structural lesions and the reduced metabolism in the anterior temporal lobes.
Neuropsychological outcome within 1 year after severe head injury was examined in 42 conscious survivors and correlated with acute measurements of cerebral blood flow (CBF) and intracranial pressure (ICP). During acute coma, CBF was elevated in 23 patients, indicating hyperemia, and was reduced in the remaining 19 cases. Intracranial hypertension (ICP 20 mm Hg or greater) was present acutely in 15 patients and absent in 27. Occurrences of hyperemia and intracranial hypertension were significantly related. During chronic recovery, neuropsychological dysfunction was found in all cases. However, patients with hyperemia revealed greater impairment of overall intellectual and memory functions than did those with reduced flow, while patients with intracranial hypertension showed greater memory deficit than did those without ICP elevations. The results suggest that early pathophysiological events can influence subsequent neuropsychological outcome, and that chronic recovery is not homogeneous in young severely head-injured adults.
Cerebral blood flow (CBF) measurements were made in 75 adult patients with closed head injuries (mean Glasgow Coma Scale score 6.2) using the xenon-133 intravenous injection method with eight detectors over each hemisphere. All patients were studied acutely within 96 hours of trauma, and repeatedly observed until death or recovery (total of 361 examinations). Arteriojugular venous oxygen differences (AVDO2) were obtained in 55 of the patients, which permitted assessment of the balance between metabolism and blood flow, and provided estimates of cerebral metabolic rate for oxygen (CMRO2). Based on mean regional CBF, the patients were classified into two groups: those who exhibited hyperemia on one or more examinations, and those who had a consistently reduced flow during their acute illness. "Hyperemia" was defined as a normal or supernormal CBF in the presence of coma, a definition that was independently confirmed by narrow AVDO2's indicative of "luxury perfusion". During coma, all patients showed a significant depression in CMRO2. Forty-one patients (55%) developed an acute hyperemia with an average duration of 3 days, while 34 patients (45%) consistently had subnormal flows. Although more prevalent in younger patients, hyperemia was found at all age levels (15 to 85 years). There was a highly significant association between hyperemia and the occurrence of intracranial hypertension, defined as an intracranial pressure above 20 mm Hg. Patients with reduced flow showed little or no evidence of global cerebral ischemia, but instead revealed the expected coupling of CBF and metabolism. The CBF responses to hyperventilation were generally preserved, with the hyperemic patients being slightly more reactive. In 10 patients with reduced flow, hyperventilation resulted in wide AVDO2's suggestive of ischemia.
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In the past few years, considerable progress has been made in describing patients with head injuries in such a manner that comparisons in morbidity and mortality can be made among neurosurgical centers according to the seriousness of the injury. Less progress had been made in classifying the type of pathology, especially by computerized tomography. The authors have introduced a classification that includes both the type and the seriousness of the injury. There appear to be two principal causes of the brian damage produced by head injury: 1) mechanical damage to neurons and their processes, especially axons and 2) ischemia. Mechanical damage produces axonal degeneration. Although central regeneration generally is quite limited, perhaps many of the axons damaged by head injury degenerate in continuity, a circumstance in which functional regeneration by axoplasmic outgrowth is much more likely to occur than in most experimental situations where the axons are physically divided. The ischemic brain damage that is so common in head injury appears to be mass lesions and brain swelling that both cause intracranial hypertension. The more the brain swells, and the higher the intracranial pressure, the more difficult it is to control the swelling and the pressure. In patients with acute subdural hematoma in particular, the brian swelling and the high mortality appear to be due to ischemic brain damage. There is recent evidence that the mortality rate in patients with acute subdural hematoma is a function of the time from injury to evacuation of the hematoma. Therefore, outcome from head injury can be improved by the earliest possible removal of space-occupying hematomas and by early, vigorous management of intracranial hypertension.