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Biomedical subjects

L F Marshall

Publications and source records attributed to L F Marshall.

At least 109 records · Page 6Linked to original sources
PubMed1979

Teratocarcinoma of the brain -- a treatable disease?

Teratocarcinoma of the brain is a rare teratoid tumor. Less than 100 cases have been previously reported and only 4 were patients with tumors in the lateral ventricular system. At the Children's Hospital of Philadelphia, 2 patients with teratocarcinoma of the lateral ventricle of the brain have been treated in the past 5 years and both are long-term survivors. A third patient with a recurrence at University Hospital is now receiving chemotherapy. Our experience suggests that a combination of radical surgery, supervoltage radiotherapy and chemotherapy may be successful in controlling these neoplasms. Furthermore, since there is increasing evidence that they have a strong histologic relationship to the embryonal carcinomas that arise in the testes and elsewhere, it appears logical to apply chemotherapeutic strategies to these intracranial neoplasms based on experience with such tumors located in other regions of the body.

Adolescent↗
PubMed1979

Acute therapeutic modalities for experimental vasogenic edema.

Experimental vasogenic cerebral edema was created in rabbits with a cold-induced left occipital cortical lesions. Intracranial pressure (ICP), intracranial elastance (Em), water content, hemispheric brain tissue volume, electrolytes, electroencephalograms, behavior, and gross pathology were studied. Various therapeutic modalities were employed alone or in combination to reduce ICP acutely: acetazolamide, furosemide, mannitol, pentobarbital, lorazepam, and dexamethasone. All therapies except dexamethasone were effective in reducing ICP. Peak ICP reduction occurred at 27 +/- 9.8 (SD) minutes with mannitol and at 71.4 +/- 15.5 minutes with acetazolamide, with the remaining agents and combinations falling between these two extreme values. Em improved by 31.7 +/- 17.02% in all therapuetic trials except those employing acetazolamide and lorazepam. With therapy, there was a reduction in the water content of the hemispheres, but the difference from that in the untreated, lesioned animals was not statistically significant. In the lesioned left hemisphere, sodium content was increased by acetazolamide (p less than 0.005), furosemide (p less than 0.025), pentobarbital (p less than 0.05), and the combination of dexamethasone, pentobarbital, and mannitol (p less than 0.005). Significant reduction was noted in the lesioned group for the potassium content of the left hemisphere in the dexamethasone (p less than 0.05), pentobarbital (p less than 0.025), and combination groups containing these agents (p less than 0.005 to 0.025). (Neurosurgery, 5: 656--665, 1979).

Acetazolamide↗
PubMed1978

Intracranial pressure responses to PEEP in head-injured patients.

PEEP (positive end-expiratory pressure) was required in 12 head-injured patients in whom intracranial pressure (ICP) monitoring had been previously established. In six, ICP increased by 10 mm Hg or more as 4-8 cm H2O of PEEP were administered. In 10 patients the mean arterial pressure decreased during PEEP. Before PEEP, the mean cerebral perfusion pressure (CPP = BP-ICP) was above 50 mm Hg in all patients. The CPP was less than 50 mm Hg in six patients given PEEP. Neurological deterioration occurred in two patients during PEEP therapy. In head-injured patients, optimal titration of PEEP therapy should include ICP measurement and/or continuous evaluation of neurologic status.

Brain Injuries↗
PubMed1978

Mannitol dose requirements in brain-injured patients.

There is little information as to the optimal use of mannitol. To determine the dose-response relationship, the osmotic gradient required, and the time course of intracranial pressure (ICP) reduction produced by mannitol, eight patients with acute head injury were studied in whom ICP was monitored with a ventriculostomy and found to be elevated. Ventilation was controlled to a pCO2 of 25 +/- 3 mm Hg and all were paralyzed with Pavulon. None had received barbiturates. Before mannitol administration the intracranial volume-pressure response was determined. Mannitol was administered as a bolus of 0.25 gm/kg, 0.5 gm/kg, and in six patients, 1 gm/kg, separated by at least 8 hours. In all patients the ICP reduction with 0.25 gm/kg (41.3 +/- 10.2 mm Hg leads to 16.4 +/- 5.6, p less than 0.01) was equivalent to that achieved with the larger doses. Serum osmolality rises of 10 mOsm or more were associated with a reduction in ICP. Much smaller doses than those previously recommended were effective in reducing the ICP acutely, although at 5 hours there was a trend toward persistent reduction when the larger dose is used. This trend was small and indicates that smaller and more frequent doses are as effective in reducing the ICP while avoiding the risk of osmotic disequilibrium and severe dehydration.

Brain Injuries↗
PubMed1978

Vertebrobasilar spasm: a significant cause of neurological deficit in head injury.

Cerebral vasospasm in the anterior circulation has been recognized as a significant factor in the sequelae of head injury; however, vertebrobasilar spasm resulting from trauma has received much less attention. In the past year we have observed six patients where spasm in the major vessels of the posterior circulation was primarily or in part responsible for the neurological deficit. In such cases, the neurological examination may suggest a supratentorial mass with herniation and, in three of our cases, burr holes or carotid angiography were performed first. However, in every instance neurological signs present on admission indicated primary brain-stem dysfunction. In each of the six cases vertebral angiography demonstrated significant spasm in either the vertebral or basilar arteries. Intracranial pressure was monitored in each of the six patients and did not exceed 25 mm Hg in any. In cases of head injury where the neurological examination indicates brain-stem dysfunction inconsistent with or after a supratentorial mass has been excluded, vertebral angiography may aid in the diagnosis and subsequent management of such patients.

Adolescent↗
PubMed1977

Post-irradiation pituitary sarcoma.

A fibrosarcoma developed in the pituitary fossa of a patient who had been irradiated 13 years previously for treatment of pituitary adenoma. The tumor was a large aggressively growing spindle cell neoplasm which eroded adjacent structures, causing increased intracranial pressure, and eventual cerebellar tonsillar herniation. In common with previously described post-irradiation sarcoma of the pituitary, this lesion developed in the path of irradiation after a long latent period, did not metastasize, and contained histologically recognizable benign appearing pituitary adenoma interspersed among the spindle cell tumor. The dose of radiation (5000 rads) also lay within the range associated with sarcomatous transformation.

Aged↗
PubMed1977

Combined therapy for metastatic extradural tumors of the spine.

The effectiveness of combined modality therapy was studied in 29 patients with metastatic extradural spinal tumor who had had a previous diagnosis of malignancy. Dexamethasone was begun upon suspicion of the diagnosis in a dose of 40 mg daily. Following emergency myelography, in all patients without rapid progression, dexamethasone in combination with radiotherapy and chemotherapy, when appropriate, was instituted. If deterioration occurred, decompressive laminectomy was performed. Five ambulatory patients had neurological function preserved and the condition of seven nonambulatory patients was improved to ambulation at discharge with a combination of dexamethasone, radiation therapy, and chemotherapy. These were patients with prostatic carcinoma, Hodgkin's disease, or breast carcinoma. In five patients who failed medical therapy decompressive laminectomy was successful. In patients with metastatic bronchogenic carcinoma, nonsurgical therapy failed and all underwent surgical decompression with a favorable outcome in only two of 10 patients.

Adult↗
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↗