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D P Becker

Publications and source records attributed to D P Becker.

At least 109 records · Page 6Linked to original sources
PubMed1986

Effects of fluid-percussion brain injury on regional cerebral blood flow and pial arteriolar diameter.

The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 +/- 0.11 atm, mean +/- standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 +/- 0.19 atm) resulted in larger, statistically significant (p less than 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p less than 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

Animals↗
PubMed1986

Prognostic significance of ventricular CSF lactic acidosis in severe head injury.

Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 +/- 5.0 mm Hg and PaO2 at 122 +/- 18 mm Hg (mean +/- standard deviation). The mean Glasgow Coma Scale score on admission was 5.73 +/- 2.42. The first CSF sample was drawn within 18 hours after head injury. Over the first 4 days postinjury, patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing favorable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Arterial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. At that time, the ventricular CSF lactate concentration was still above normal in patients with a poor outcome but had decreased to normal in patients with moderate disabilities or a good outcome. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation; however, in a few patients close to death or with ventricular infection, a correlation was noted. Ventricular CSF lactate levels were not related to cerebral blood flow. In this study, profiles of ventricular CSF lactate concentration are defined in relation to the patients' clinical course and outcome. High ventricular CSF lactate concentration is present within 18 hours after severe head injury. Its decrease to normal in the following 48 hours is a reliable sign of clinical improvement; however, ventricular CSF lactate levels that are persistently high or that increase over time indicate the patient's deterioration. Serial assessment of ventricular CSF for acid-base status and metabolites in head-injured patients with a ventricular catheter already placed for ICP monitoring is useful in the evaluation of prognosis and clinical course.

Acidosis, Lactic↗
PubMed1986

CSF brain creatine kinase levels and lactic acidosis in severe head injury.

The posttraumatic creatine kinase-BB isoenzyme (CKBB) activity and lactate concentration in ventricular cerebrospinal fluid (CSF) have been studied in 29 patients with severe head injuries. The CKBB activity reaches its maximum a few hours after trauma, and has a monoexponential drop with a half-time of approximately 10 hours. Ventricular CSF lactate concentration continues to rise in patients with a poor outcome, and decreases only slowly and inconsistently in most of the other patients. Thus, increase of lactate in the ventricular CSF is not, like CKBB, a direct one-stage consequence of the trauma but is due to continuous production from a derangement of metabolism caused by the trauma. Since even higher ventricular CSF lactate levels can be survived when not caused by head injury, and since no significant pH changes were related to the ventricular CSF lactic acidosis in these artificially ventilated patients, it is concluded that ventricular CSF lactic acidosis is indicative of a severe, although not necessarily intractable, disturbance of brain function associated with intracellular lactate production and acidosis.

Acidosis, Lactic↗
PubMed1986

Pituitary tumors secreting growth hormone and prolactin.

The pathophysiology of functional adenomas of the anterior pituitary gland can be understood in the context of the central neural control of anterior pituitary secretion and by the fact that the cell types of the anterior pituitary gland generally express a single polypeptide hormone. Functional pituitary adenomas arise de novo from one or more of these cell types, but a defect in hypothalamic regulation can contribute to tumorigenesis and sometimes result in persistent tumor recurrence despite local surgical cure. The recent advances in molecular biology, radioimmunoassay, neuroradiology, and transsphenoidal microneurosurgery techniques have greatly improved our understanding of the pathophysiology of these tumors, enhanced diagnostic accuracy, and led to newer medical and surgical therapeutic approaches. This conference reviews the molecular and cellular pathophysiology, causes, diagnosis, clinical features, and medical and surgical management of the two common functional pituitary adenomas, prolactinoma and somatotropinoma.

Adenoma↗
PubMed1985

Depression of afferent-induced primary afferent depolarization at the lumbar spinal cord following concussive head injury.

Afferent-induced primary afferent depolarization (PAD) was depressed for 2-5 min following concussive head injury in the cat, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. These changes in PAD were abolished by spinal cord transection but not affected by midpontine transection. Spontaneous dorsal root potentials, resting amplitudes of antidromic dorsal root potentials and reductions of antidromic dorsal root potentials following tetanic root stimulation were not substantially altered by injury. These findings suggest that concussive head injury depresses spinal interneuronal transmission by neurally mediated processes involving the bulbar brainstem.

Animals↗
PubMed1985

Dissociation of endogenous components of auditory evoked potentials following carbachol microinjection into the cholinoceptive pontine inhibitory area.

Microinjections of the cholinergic agonist, carbachol, into an area ventromedial to the principal nucleus of the locus coeruleus produce pronounced suppression of postural somatomotor and sympathetic visceromotor functions, and profound unresponsiveness to external stimuli. In order to clarify whether this unresponsiveness is due exclusively to disruption of motor components of various behavioral responses, we examined changes in the endogenous components of auditory evoked potentials recorded in conjunction with a tone discrimination task. Concomitant with carbachol-induced behavioral unresponsiveness, the late positive component (LPC) at 250-350 ms disappeared, while the early positive component at 80-150 ms was enhanced. This result suggests that, after the onset of carbachol-induced behavioral unresponsiveness, external stimuli enter the brain but are not integrated in neural processes reflected in LPC which has previously been implicated in processes mediating orienting responses, selective attention, and/or cognitive evaluation.

Animals↗
PubMed1985

Early decision in clinical trials when the treatment differences are small. Experience of a controlled trial in head trauma.

In a long-term clinical trial, it is customary to review the results of the data periodically. Two possible situations suggesting a possible early decision in hypothesis testing may arise. First, the difference in outcome may be sufficiently convincing without further evidence from additional data. Second, the difference may be such that it is not likely to be significant even if additional data are collected. This article is mainly concerned with a method for reaching a decision under the second situation, in particular when inadequate patient acquisition has occurred. A predicted distribution of likely future outcomes on the basis of data already accumulated is used to evaluate what might happen if the trial were carried on to the designed end. The method is intended for the case where the outcome variable is dichotomous and the two groups are compared for the difference in proportions.

Adult↗
PubMed1985

Papilledema after acute head injury.

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.

Acute Disease↗
PubMed1985

Severe hypophosphatemia after head injury.

Hypophosphatemia occurs in a variety of clinical conditions. It develops in parallel with phosphate depletion from body losses or more commonly as a sequel to the redistribution of phosphate from the extracellular to the intracellular compartment. Hypophosphatemia is a multisystem disturbance capable of involving the neurological, immunological, and muscular systems, among others. In this report, we describe five patients with severe head injury who developed marked hypophosphatemia (less than 1 mg/dl) within 24 hours of hospitalization. This fall in serum phosphate coincided with the induction of respiratory alkalosis consequent to mechanical ventilation. In four of the five patients, as acid-base parameters returned to normal, serum phosphate values rose, in all instances reaching values greater than 2.5 mg/dl. Urinary phosphorus excretion, ordinarily negligible after hypophosphatemia induced by hypocapnia, was still present in Cases 1 and 4 (greater than 600 mg/24 hours). This is unexplained by any of the known hormonal or fluid alterations that accompany head injury. These five patients developed severe, yet transient, hypophosphatemia that resolved upon correction of hyperventilation-induced acid-base abnormalities. We discuss the pathophysiology of this entity and the implications for the head trauma patient.

Adolescent↗
PubMed1985

Computed tomography in the prediction of outcome in head injury.

To determine the prognostic significance of computed tomographic (CT) findings in head injury, retrospective analysis was performed in 128 randomly selected severe head-injury patients managed with a standardized protocol. The minimal criterion for entry into this study was that the patients were unable to obey simple commands or utter formed words. Serial CT was performed on admission and 3-5 days, 2 weeks, 3 months, and 1 year after injury. A scale of severity of abnormalities was devised taking into account the size of the traumatic lesions on CT. The CT findings using the proposed scale were correlated with the clinical outcome and analyzed using linear logistic regression. Other characteristics such as midline shift, multiplicity, and corpus callosum and brainstem lesions were not included in the analysis either because they did not affect the prognosis or because too few of these lesions were present for statistical analysis. The correct prediction rate of outcome using the proposed scale for CT findings alone was found to be 69.7%. When CT findings were combined with the Glasgow Coma Scale score this rate was increased to 75.8%.

Cerebral Hemorrhage↗
PubMed1985

Failure of prophylactic barbiturate coma in the treatment of severe head injury.

In certain subgroups of severely head-injured patients, the mortality rate remains unacceptably high. The authors describe a randomized, controlled trial of prophylactic pentobarbital therapy in a group of these patients. Pentobarbital was started as soon as possible after the head injury, regardless of the intracranial pressure (ICP), and was continued for a prescribed period of time. The study included 53 consecutive head-injured patients over the age of 12 years, who had either an acute intradural hematoma (subdural and/or intracerebral, large enough to warrant surgical decompression), or no mass lesion but whose best motor response was abnormal flexion or extension. All patients in the study were randomly assigned to a control group (26 cases) or a pentobarbital-treated group (27 cases) once the diagnosis had been made and informed consent obtained. All patients were treated with the same protocol of aggressive resuscitation, prompt diagnosis and treatment of mass lesions, and intensive care, with close follow-up monitoring. The randomization was effective in producing a close match between the control and treated groups with respect to age, sex distribution, cause of injury, neurological status, intracranial lesions, prevalence of early systemic insults, midline shift, and initial ICP. Outcome was essentially the same in each group. There was no difference between groups in the incidence of elevated ICP, the duration of ICP elevation, or the response of ICP elevations to treatment. Arterial hypotension occurred in 14 patients (54%) in the treated group and only two patients (7%) in the untreated group. Based on these data the authors cannot recommend the prophylactic use of pentobarbital coma in the treatment of patients with severe head injury. They also believe that its use is accompanied by significant side effects which can potentially worsen the condition of a patient with severe head injury.

Adolescent↗
PubMed1985

Pain suppression induced by electrical stimulation of the pontine parabrachial region. Experimental study in cats.

Cholinergic stimulation by microinjection of drugs into a region surrounding the lateral half of the brachium conjunctivum selectively produces a non-opiate form of pain suppression in the cat. Since this suppression does not appear to involve neural systems that mediate morphine analgesia, stimulation of this pontine parabrachial region (PBR) may potentially be useful for control of human pain resistant or tolerant to opiate treatment. Because of technical problems associated with the clinical use of microinjection techniques in the human brain, we investigated whether electrical stimulation of the PBR can produce pain suppression similar to pain suppression produced by cholinergic stimulation. The results indicate that electrical stimulation of an area generally corresponding to the PBR can also produce significant pain suppression. Although the PBR is a region previously implicated in a variety of behavioral and physiological functions, the stimulation parameters that produce maximal pain suppressive effects (namely, low frequency and relatively low intensity) were not associated with noticeable changes in such functions. The prolonged onset period and persistent analgesic effects outlasting the period of stimulation--features that have been reported in other studies of brain stimulation-produced pain suppression--were observed in the present study. The time course of pain suppression did not parallel other changes in behavioral and physiological functions. These data indicate that electrical stimulation of the PBR, under certain stimulation parameters, can activate previously demonstrated neural populations related to pain suppression without affecting neural elements contributing to other behavioral or physiological functions. The authors suggest that electrical stimulation of the PBR may be clinically applicable for treatment of human pain.

Acetylcholine↗
PubMed1985

Concussive head injury producing suppression of sensory transmission within the lumbar spinal cord in cats.

This study examines the effects of concussive levels of a fluid-percussion head injury on sensory transmission within the lumbar spinal cord of the cat. Primary afferent depolarization (PAD) was suppressed for 2 to 5 minutes following injury, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. Polysynaptic reflex discharges in ventral root potentials evoked by dorsal root stimulation were also profoundly suppressed during this same period, even when spontaneous and monosynaptic reflex discharges were facilitated. Changes in PAD produced by injury were abolished by spinal cord transection, but were not affected by midpontine transection. These findings suggest that concussive head injury can produce suppression of segmental sensory transmission by neurally mediated processes involving the bulbar brain stem. Recordings of dorsal root resting potentials, antidromic dorsal root potentials, and reductions of antidromic dorsal root potentials induced by tetanic root stimulation indicated that depressed segmental sensory function produced by injury was due to suppression of postsynaptic interneuronal transmission rather than to excitability changes in primary afferent fibers. Somatosensory cortical potentials evoked by dorsal root stimulation were profoundly depressed at the same time as segmental sensory transmission was suppressed, suggesting that suppressed segmental sensory transmission may also contribute to suppression of ascending sensory transmission. It is hypothesized that transmission failure of interneuronal systems in the initial period following insult may be a general response occurring in wide areas of the central nervous system, and not restricted to areas to which mechanical stress is directly applied. This response pattern may result from indiscriminate activation of interconnected excitatory and inhibitory elements of interneuronal systems.

Animals↗
PubMed1985

Regional brain metabolite levels following mild experimental head injury in the cat.

Glucose, adenosine triphosphate, phosphocreatine, and lactate levels in the cortex, striatum, diencephalon, hippocampus, cerebellum, and brain stem were measured in cats 1 hour after they were subjected to low-level (2 atm) fluid-percussion injury. Following injury, there was a mild but significant increase in lactate levels in the majority of regions studied. The hippocampus exhibited the highest percentage increase in lactate (fourfold). The cortical area directly under the trauma device showed a threefold lactate increase, while there was a twofold increase in other brain regions studied. Although there were consistent decreases in phosphocreatine levels, these decreases were significant only in the hippocampus (p less than 0.05). Glucose levels in all brain regions studied were no different from control levels at the time of study. The unchanged glucose levels, together with previous studies of identically injured cats showing that cerebral blood flow was unimpaired, suggest that excess lactate was not a consequence of cerebral ischemia. Rather, the increase in lactate levels may indicate that concussive injury can produce a mild derangement of brain energy metabolism in the absence of substrate limitations. This derangement may reflect altered mitochondrial function.

Adenosine Triphosphate↗
PubMed1985

Fate of reactive axonal swellings induced by head injury.

The fate of those reactive axonal swellings seen following head injury was assessed in cats subjected to mild to moderate fluid-percussion head injury. To allow for the ready visualization of any traumatically induced reactive axonal change at both the light and electron microscopic level, the anterograde axonal transport of wheat germ agglutinin conjugated to horseradish peroxidase was employed over a 21-day posttraumatic period in selected cerebral and cerebellar efferents coursing through the brain stem. At the designated posttraumatic survival time, the animals were perfused with aldehydes, processed for the light and electron microscopic visualization of the peroxidase reaction product, and examined for any evidence of reactive axonal change. At the 3rd and 4th posttraumatic days, peroxidase-laden swellings could be identified. Some reactive swellings were packed with organelles and were either encompassed by a distended myelin sheath or lacked myelin investment. Other reactive swellings demonstrated either lobulation or increased electron density with macrophage accumulation, all of which indicated degeneration. Wallerian change occurred distal to the reactive swellings; however, with the exception of these changes the related brain parenchyma and vasculature demonstrated no significant abnormality. With continued survival, reactive swellings comparable to those just described were consistently observed; however, now regenerative responses were also seen. At the 5th and 7th days, reactive sprouts were observed originating from reactive swellings which displayed a reduction both in size and in organelle content. By the 9th and 14th posttraumatic days, some sprout-containing swellings demonstrated several robust extensions. These regenerative changes were seen in both myelin- and nonmyelin-invested swellings and persisted through the 21st day, occurring in concert with lobulated, electron dense, and unchanged, swollen reactive axons. This study suggests that head injury elicits axonal swelling that may persist unchanged, degenerate, or undergo a regenerative response. The sustained regenerative responses are considered intriguing and may have relevance both for head-injured humans and for future studies of central nervous system regeneration.

Animals↗
PubMed1984

Bilateral lesions of the dorsolateral funiculus of the cat spinal cord: effects on basal nociceptive reflexes and nociceptive suppression produced by cholinergic activation of the pontine parabrachial region.

In cats, bilateral microinjections of the cholinergic agonist, carbachol (0.6 micrograms in 0.2 microliter), into an area surrounding the lateral half of the brachium conjunctivum (BC) produces a non-narcotic suppression of nociceptive responses, as assessed by flexion reflexes (tail-flick and calibrated pinch tests). Bilateral lesions of the dorsolateral funiculi (DLF) of the thoracic spina cord (T2) significantly reduced the magnitude of this nociceptive suppression. Nociceptive suppression following carbachol microinjections into sites along the dorsal aspect of BC was reduced by DLF lesions to a greater degree than nociceptive suppression following injections into sites within or ventral to BC. Relatively superficial DLF lesions produced reductions in nociceptive suppression which were equivalent to reductions induced by deeper lesions. DLF lesions, either superficial or deep, produced equivalent, reliable decreases in tail-flick test assessments of baseline nociceptive thresholds. The magnitude of decreases in baseline nociceptive thresholds produced by DLF lesions was not correlated with the magnitude of reduction of carbachol-induced suppression of nociceptive responses, indicating that DLF lesions suppress anti-nociception independent of baseline alterations. These data suggest that non-narcotic analgesia produced by cholinergic activation of cells along the dorsal aspect of BC may be predominantly mediated by fibers descending within the DLF. However, results of the retrograde horseradish peroxidase (HRP) tracing studies reported in the present investigation indicate that this pain suppression is probably mediated by polysynaptic pathways since this region dorsal to BC projects neither through DLF nor extra-DLF pathways. Retrograde HRP data show that areas ventral to and including BC projects to the cord via both DLF and extra-DLF pathways. Since DLF lesions were less effective in reducing analgesia attained from ventral compared to dorsal sites, spinal pathways other than DLF may mediate reflex suppression following carbachol microinjection into these more ventral sites. Possible cholinergic contributions to endogenous, non-opiate forms of analgesia are discussed.

Acetylcholine↗