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Biomedical subjects

L H Pitts

Publications and source records attributed to L H Pitts.

At least 73 records · Page 4Linked to original sources
PubMed1989

Brain shift, level of consciousness, and restoration of consciousness in patients with acute intracranial hematoma.

Recently, Ropper reported that horizontal brain shift caused by acute unilateral mass lesions correlated closely with consciousness, and suggested that recovery of consciousness was unlikely to occur after surgical evacuation if the shift was insufficient to explain the observed diminution of consciousness. The authors have sought to confirm the correlation of pineal shift with level of consciousness and to assess the prognostic value of brain shift measurements in a prospective study. Forty-six patients (19 with subdural hematoma, 14 with intracerebral hematoma, and 13 with epidural hematoma) were accrued to the study group consecutively. A correlation was found between a decrease in the level of consciousness and a significant increase in the mean lateral brain displacement at the pineal gland (from 3.8 to 7.0 mm) and septum (5.4 to 12.2 mm). When outcome was examined in patients who were stuporous or comatose on admission, a significant increase in septal shift was found among patients with a poor outcome, but there was no significant relationship between outcome and degree of pineal or aqueductal shift. A poor outcome was more likely with effacement of both perimesencephalic cisterns or the ipsilateral cistern, but not the contralateral cistern, although this difference did not reach statistical significance. These results do not substantiate the value of brain shift as an independent prognostic factor after evacuation of an acute unilateral mass lesion. The decision to operate and the determination of prognosis should be based rather on established criteria such as the clinical examination, age of the patient, and the mechanism of injury.

Acute Disease↗
PubMed1988

Proliferative potential of brain metastases.

Thirteen patients with metastatic brain tumors received an intravenous infusion of bromodeoxyuridine (BUdR) 200 mg/m2 at craniotomy) to label S-phase tumor cells. Excised tumors were stained immunohistochemically for BUdR. The percentage of BUdR-positive cells was calculated to determine the BUdR labeling index (LI) (or fraction of S-phase cells), which provides an estimate of the proliferative potential. Histologically, 11 patients had adenocarcinoma (four well-differentiated, three moderately differentiated, and four poorly differentiated), one had a large cell carcinoma, and one had a small cell carcinoma. All tumors had a BUdR LI greater than 5% (mean, 13.3 +/- 7% standard deviation). Moderately and poorly differentiated adenocarcinomas had a higher LI than well-differentiated adenocarcinomas (median, 15.3% versus 8.2%). These LI values are considerably higher than those reported for primary tumors with comparable histologic features. Thus, metastatic tumors in the brain may grow faster than the primary tumors from which they originate.

Adenocarcinoma↗
PubMed1988

Radiation therapy for the treatment of non-eight nerve intracranial neurilemmoma.

The records of 19 patients treated for intracranial neurilemmomas, other than of the eighth nerve, at the University of California, San Francisco from 1945 through 1983 were reviewed. One patient who died within 30 days following surgery was excluded from the analysis. The 5th and the 9/10/11th nerve complex were the most common sites of tumor origin. Patients were classified by the extent of surgical resection: total (90-99% resection, NTR), subtotal (less than 90% resection, STR) and biopsy. Five patients had total excision of their tumor without post-operative irradiation and none had recurred. One of the 2 patients who had STR and did not receive post-operative irradiation recurred, while 2 of the 3 patients who received post-operative irradiation following STR recurred. One of the 2 patients who had NTR and did not receive post-operative irradiation recurred, while 1 of the 3 patients who received post-operative irradiation following NTR recurred. Two patients were treated with post-operative irradiation following biopsy and one recurred. One patient was treated with planned preoperative irradiation to reduce tumor vascularity, followed by total resection. Because of the small number of patients, no firm conclusion regarding the efficacy of irradiation for non-eighth nerve intracranial neurilemmoma can be made.

Adolescent↗
PubMed1988

High energy phosphate metabolism in experimental permanent focal cerebral ischemia: an in vivo 31P magnetic resonance spectroscopy study.

Relative levels of phosphate metabolites in the brain were examined in vivo by 31P magnetic resonance spectroscopy (MRS) in 50 Sprague-Dawley rats before, during, and after induction of focal permanent cerebral ischemia. After acquisition of baseline spectra, rats were subjected to injury within the core of the MR spectrometer, and 31P spectra were collected for 60 min after injury: in 7 rats, permanent, acute focal cerebral ischemia was induced (ischemia group); in 6 rats, mild hypoxia (FiO2 14%) was induced at the time of the ischemic insult and was maintained for 20 min (ischemia-hypoxia group); in 6 rats, mild hypoxia (FiO2 14%) only was induced for 20 min (hypoxia group). Control studies were performed in 25 rats. Cerebral intracellular pH, calculated from the chemical shift of inorganic phosphate (Pi), decreased immediately after injury in the ischemia and ischemia-hypoxia groups. The first 31P spectrum obtained after injury was characterized by an increase in Pi and a decrease in phosphocreatine (PCr) in the ischemia and ischemia-hypoxia groups; these changes in spectra were significantly greater in the ischemia-hypoxia group. No significant changes in adenosine triphosphate (ATP) were found in either group. Within 60 min of occlusion, 31P spectra returned toward baseline spectra in both ischemia-hypoxia and ischemia groups. No significant changes were seen in spectra of rats subjected to hypoxia alone. These results confirm that 31P MRS is a sensitive measure of early changes of high energy metabolites in focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

An epidural intracranial pressure monitor for experimental use in the rat.

We described the construction and use of a simple and reliable catheter system that can be used to monitor intracranial pressure (ICP) from the epidural space in rats in an experimental setting. The catheter system is easily fabricated in the laboratory from readily available materials. The monitor is fitted flush with the inner table through a burr hole in the temporal squama. A side port is used to fill the system with saline and to irrigate the system should be catheter become obstructed. The distal end of the catheter is fitted to a pressure transducer that is connected to a graphic display and recording system. This system was used to record ICP in 30 anaesthetized adult rats. Seven were subjected to baseline ICP recording only and 23 were subjected to baseline recordings followed by epidural balloon compression of the contralateral hemisphere. Baseline ICP varied between 0 and 8 mmHg and respiratory variation could be detected on the tracings for 24 rats (75%). ICP responded directly and sensitively to epidural balloon inflation in all 23 rats tested. In 5 rats that died during balloon inflation, the decrease in ICP after death followed closely the loss of arterial blood pressure. There was a close correlation of numerical values obtained in two rats in which ICP was recorded simultaneously from the epidural catheter and from a catheter in the subarachnoid space at the cisterna magna. In one rat in which ICP increased to more than 70 mmHg, the epidural catheter continued to record ICP accurately while the cisternal catheter became obstructed with herniated brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Presentation of type I Chiari malformation after head trauma.

An unusual case of Type I Chiari malformation that became symptomatic after closed head injury is reported. The patient manifested transient upper extremity weakness, persistent lower cranial nerve dysfunction, and cerebellar signs that slowly resolved. Magnetic resonance images showed tonsillar ectopia but no displacement of the brain stem or syringomyelia. Type I Chiari malformation should be included in the differential diagnosis of patients who present with upper extremity weakness, lower cranial nerve palsies, or cerebellar signs after trauma.

Adolescent↗
PubMed1988

The effects of hypovolemic hypotension on high-energy phosphate metabolism of traumatized brain in rats.

To clarify the effect of hypovolemic hypotension on high-energy phosphate metabolism in head injury, sequential changes in in vivo phosphorus-31 magnetic resonance (31P MR) spectra were compared in 35 rats after impact injury with and without hypotension. Fourteen rats were subjected to hypotension alone (mean arterial blood pressure (MABP) of either 40 or 30 mm Hg for 60 minutes), seven to fluid-percussion impact injury (4 to 5 atm) alone, and 14 to impact injury and hypotension (MABP of 40 to 30 mm Hg). Impact injury alone caused a transient decrease in the phosphocreatine (PCr) level and an increase in the inorganic phosphate (Pi) value. While hypotension alone produced only small changes on 31P MR spectra, impact injury plus hypotension caused pronounced changes. Impact injury and an MABP of 40 mm Hg caused a 50% decrease in PCr concentration and an approximately twofold increase in Pi level, which were significantly greater than values in rats with impact injury alone. Impact injury and an MABP of 30 mm Hg also caused a significant decrease in adenosine triphosphate value, which was not observed in rats with impact injury alone or with an MABP of 30 mm Hg alone. Decreases in intracellular pH were greater in rats with impact injury and hypotension. After traumatic injury, the brain is extremely vulnerable to hypovolemic hypotension, as reflected in the loss of high-energy phosphates in brain.

Animals↗
PubMed1988

Effect of opiate antagonists on middle cerebral artery occlusion infarct in the rat.

The authors examined the effect of the opiate antagonists naloxone and thyrotropin-releasing hormone (TRH) on neurological outcome and the size of areas of cerebral infarction in a rat model of focal cerebral ischemia. The middle cerebral artery (MCA) was permanently occluded in 66 adult Sprague-Dawley rats. The rats were randomly divided into three groups. In 20 Group I rats, TRH in normal saline was administered initially as a 2-mg/kg bolus followed by continuous infusion of 2 mg/kg/hr for 4 hours. In 20 Group II rats, naloxone in normal saline was administered initially as a 2-mg/kg bolus followed by continuous infusion of 2-mg/kg/hr for 4 hours. In 26 Group III rats, physiological saline was administered as an initial 0.5-cc bolus followed by continuous infusion of 0.5 cc/hr for 4 hours. All solutions were given in volumes of 0.5 cc for the bolus and 0.5 cc/hr for continuous infusion, and all infusions were begun within 10 minutes of MCA occlusion. Twenty-four hours after treatment, the rats underwent a careful neurological examination and were then sacrificed immediately. The size of areas of cerebral infarction was evaluated using 2,3,5-triphenyltetrazolium chloride staining techniques. The neurological grade of the rats correlated with the size of infarcted areas among all grades, irrespective of treatment (p less than 0.01). Neither naloxone nor TRH improved neurological function or reduced the size of infarction compared to saline-treated control rats. Treatment with TRH caused a significant increase in mean arterial blood pressure during infusion, but naloxone had no effect. These results suggest that neither TRH nor naloxone are effective in the treatment of acute focal cerebral ischemia.

Animals↗
PubMed1988

The effect of intracerebral hematoma location on the risk of brain-stem compression and on clinical outcome.

The clinical findings and computerized tomography (CT) brain scans of 45 patients with supratentorial intracerebral hematomas were evaluated to determine the effect of hematoma location on the clinical course and outcome of the disease. The lesions were frontal in 18 patients, temporal or temporoparietal in 17, and parieto-occipital in 10. No patient with a frontal or parieto-occipital hematoma had clinical signs of transtentorial herniation at admission or subsequently, whereas seven (41%) of those with temporal or temporoparietal lesions had signs of herniation (p less than 0.05); three of these seven patients had an abnormal mental status, ipsilateral anisocoria, and lateralizing motor findings at admission, and four developed these signs within 12 hours after admission, necessitating urgent surgical intervention. The mean volume of the lesions estimated from the CT scans was similar in the three groups (frontal 47 +/- 28 cc; parieto-occipital 53 +/- 26 cc; temporal/temporoparietal 41 +/- 21 cc). None of the six patients with temporal or temporoparietal hematomas smaller than 30 cc had signs of tentorial herniation, compared with seven (64%) of 11 patients with larger hematomas (p less than 0.05); in six of these seven cases, the hematoma was caused by head injury. Patients with a temporal or temporoparietal hematoma had a worse outcome than those in the other two groups, and no patient with signs of tentorial herniation had a good outcome. Patients with temporal or temporoparietal hematomas appear to be at greater risk of brain-stem compression, especially if the lesion is larger than 30 cc and caused by head injury, than are those with hematomas in other sites. In such cases, prompt surgical intervention should be considered.

Adolescent↗
PubMed1987

Kynurenate inhibition of cell excitation decreases stroke size and deficits.

Pharmacological inhibition of excitatory neurotransmission attenuates cell death in models of global ischemia/reperfusion and hypoglycemia. The current investigations extend these observations to a model of focal ischemia. Kynurenic acid, a broad-spectrum antagonist at excitatory amino acid receptors, was used as treatment (300 mg/kg; 3 doses at 4-hour intervals) before and after focal cerebral ischemia in rats (n = 54). Preischemia but not 1 hour postischemia treatment with kynurenate attenuated infarction size (p less than 0.001) and improved neurological outcome (p less than 0.001) studied at 24 hours after injury. These data support the role of excitatory neurotransmission in acute neuronal injury and support pharmacological inhibition of cell excitation as a potential therapy for stroke.

Animals↗
PubMed1987

Implications of systemic hypotension for the neurological examination in patients with severe head injury.

Thirty-six patients admitted with severe head injury and various degrees of systemic hypotension were studied to determine the effect of hypotension on the validity of the neurological examination in reflecting mechanical brain compression. All patients had clinical signs of transtentorial herniation or upper brainstem compression and underwent immediate bilateral placement of exploratory burr holes for the diagnosis and removal of intracranial hematomas. All patients were initially hypotensive: 10 were in cardiac arrest, 7 had a systolic blood pressure (SBP) less than 60 torr, and 19 had SBP of 60-90 torr. The median score on the Glascow coma scale was 3 (range 3-8). Although 4 of the 10 cardiac arrest patients had anisocoria, only one (10%) had an intracranial hematoma. Among the seven patients with severe hypotension, only two had anisocoria and neither had and intracranial hematoma; one patient in this group (14%) had a hematoma that was diagnosed at autopsy. In contrast, intracranial hematomas were discovered by burr-hole placement and evacuated in 13 (68%) of 19 patients with initially moderate hypotension, including seven (78%) of nine patients with anisocoria. Anisocoria was associated with mechanical brain compression from an intracranial hematoma significantly more often in patients with an initial SBP of 60-90 torr than in those with initial cardiac arrest or SBP less than 60 torr (chi-square p less than 0.05). Intracranial hematomas were significantly more frequent among patients with SBP of 60-90 torr than among those with a lower SBP or initial cardiac arrest (P less than 0.01). Thirty-three of 36 patients died; each of the three survivors had an initial SBP of 60-90 torr, and hematomas were removed in two. In head-injured patients with SBP greater than 60 torr, clinical signs of tentorial herniation or upper brainstem dysfunction remain valid indicators of possible mechanical compression; the high percentage of patients with acute intracranial hematomas in this group warrants immediate diagnostic burr-hole exploration. In patients with severe initial hypotension (SBP less than 60 torr) or cardiac arrest, clinical findings of brainstem dysfunction cannot be relied upon to indicate mechanical compression, and computed tomography scanning should be done immediately after resuscitation to determine the need for surgical exploration.

Adolescent↗
PubMed1987

The effect of hypoxia on traumatic head injury in rats: alterations in neurologic function, brain edema, and cerebral blood flow.

We evaluated the effects of early posttraumatic hypoxia on neurologic function, magnetic resonance images (MRI), brain tissue specific gravities, and cerebral blood flow (CBF) in head-injured rats. By itself, an hypoxic insult (PaO2 40 mm Hg for 30 min) had little effect on any measure of cerebral function. After temporal fluid-percussion impact injury, however, hypoxia significantly increased morbidity. Of rats subjected to impact (4.9 +/- 0.3 atm) plus hypoxia, 71% had motor weakness contralateral to the impact side 24 h after injury, while only 29% of rats subjected to impact alone had demonstrable weakness (p less than 0.05). Lesions observed on MR images 24 h after injury were restricted to the impact site in rats with impact injury alone, but extensive areas with longer T1 relaxation times were observed throughout the ipsilateral cortex in rats with impact injury and hypoxic insult. Brain tissue specific gravity measurements indicated that much more widespread and severe edema developed in rats with impact injury and hypoxia. [14C]Iodoantipyrine autoradiography performed 24 h after injury showed that there was extensive hypoperfusion of the entire ipsilateral cortex in rats with impact injury and hypoxia. These results show that large areas of impact-injured brain are extremely vulnerable to secondary insults that can irreparably damage neural tissue, and provide experimental evidence for the observed adverse effects of hypoxia on outcome after human head injury.

Animals↗
PubMed1987

Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology.

The effect of hypoxia on neurological function, compressed spectral array electroencephalography, and histopathology in head-injured rats was evaluated. By itself, an hypoxic insult (PaO2, 40 mm Hg for 30 minutes) caused no neurological deficit. Twenty per cent of rats injured by a 5-atmosphere temporal fluid percussion impact were hemiparetic contralateral to the side of impact, whereas 80% had no deficit 24 hours after injury. Seventy per cent of rats with both fluid impact injury and hypoxic insult, however, either had a definite hemiparesis, showed no spontaneous movement, or died (P less than 0.02). Impact alone produced an initial depression in electroencephalogram power that was prolonged in rats with hypoxic insult; the most dramatic effect was found in the injured hemisphere, with shorter and less profound effects in the contralateral hemisphere. Perfusion staining of injured cerebral tissue in vivo with 2,3,5-triphenyltetrazolium chloride showed an area of extensive ischemia around the impact site in rats with hypoxic insult. This ischemic area was not present in rats with either impact injury or hypoxia alone. We conclude that posttraumatic hypoxia clearly increases the severity of impact injury in this rat model. These findings suggest that hypoxia, which is common in head-injured patients, very likely worsens the effect of impact injury and may account for much of the diffuse neurological dysfunction in patients with severe craniocerebral trauma.

Animals↗