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Biomedical subjects

J F Rothrock

Publications and source records attributed to J F Rothrock.

At least 55 records · Page 3Linked to original sources
PubMed1988

Optic nerve head drusen and pseudotumor cerebri.

A 42-year-old woman presented with a history of headache. Results of funduscopic examination revealed elevated disc margins and bilateral optic nerve head drusen. Lumbar puncture, head computed tomography, and fluorescein fundus angiography results were consistent with the diagnosis of pseudotumor cerebri and coexistent disc drusen. Visual loss was demonstrated by formal perimetry. Headaches were unresponsive to a medical regimen that included prednisone, glycerol, acetazolamide, furosemide, and repeated lumbar punctures. A lumbar peritoneal shunt was performed, with immediate resolution of headache. Optic disc drusen can be associated with pseudotumor cerebri and can lead to diagnostic confusion.

Adult↗
PubMed1988

Migrainous stroke.

Twenty-two patients with acute migraine-associated stroke were prospectively evaluated; 91% were female, and 23% had a prior history of presumed migrainous stroke. The incidences of major stroke risk factors and mitral valve prolapse were no higher for the study group than for the general population of similar age. Computed tomography, magnetic resonance imaging, or radionucleotide scanning of the brain was performed on all patients, and demonstrated ischemic or hemorrhagic infarction in 12 (55%). Cerebral arteriography revealed abnormalities related to the acute stroke in five (42%) of 12 cases overall, and in four (67%) of six studies performed within 72 hours of stroke onset; one patient (8%) suffered significant complications from arteriography. Although a variety of processes, alone or in combination, may contribute to migrainous stroke, extracranial and/or intracranial vasospasm appears to play a major role in at least some cases.

Acute Disease↗
PubMed1988

Hemodilution with low-molecular-weight hydroxyethyl starch after experimental focal cerebral ischemia in rabbits.

Newly developed colloid volume-expanding agents with mean molecular weights lower than currently available agents may improve outcome after stroke with fewer allergic and coagulation system side effects. The smaller molecule, however, may exacerbate ischemic cerebral edema if it accumulates in areas where ischemia has damaged the blood-brain barrier. We administered low-molecular-weight hydroxyethyl starch to rabbits after embolic infarction and measured specific gravity and total water content. We found evidence of ischemic edema in the hemisphere ipsilateral to the embolic arterial occlusion, but the measures of edema were not different in treated and control groups. Of those rabbits suffering severe neurologic deficit, mortality was 2 of 13 in the treated compared with 7 of 12 in the control groups (p less than 0.01). Thus, hemodilution with low-molecular-weight hydroxyethyl starch did not exacerbate cerebral edema and may have improved survival in this model.

Animals↗
PubMed1988

'Crescendo' transient ischemic attacks: clinical and angiographic correlations.

Forty-seven consecutive patients presenting acutely with repetitive symptoms indicative of anterior circulation ischemia ("crescendo" transient ischemic attacks) were evaluated to identify clinical features that might reliably predict the presence of significant stenosis, ulceration, or both in the presumably symptomatic internal carotid artery. Angiographic or intraoperative correlation was obtained in all patients, and 26 (55%) were found to have anatomically significant disease. Of 20 patients with signs or symptoms suggestive of cortical ischemia, amaurosis fugax, or both, 17 (85%) had "positive" angiograms; of 18 with numbness/weakness only, 9 (50%) had positive angiograms; of 9 whose symptoms suggested lacunar ischemia, none had positive angiograms.

Aged↗
PubMed1988

MR and CT of lacunar infarcts.

Twenty-two patients with clinical signs and symptoms compatible with lacunar transient ischemic attack or stroke of varying chronicity were evaluated with MR imaging. CT was also performed in 21 of these patients. MR revealed small, deep cerebral lesions in locations appropriate to the clinical symptoms in 19 patients. Lacunar infarcts were imaged by CT in 11 patients; however, no lesions were identified on CT that were not detected with MR. Presumed lacunar infarcts were identified on MR images in 17 additional patients. Lacunae generally appeared as focal areas of decreased signal intensity on T1-weighted images and as focal areas of increased signal intensity on T2-weighted images. T2-weighted MR images detected a greater number of lacunar infarcts than did mixed T1-/T2-weighted images, which in turn detected more lacunae than did T1-weighted images. In general, acute lacunar infarcts (within 1 week of onset or recurrence of clinical symptoms) were seen only on T2-weighted images, while chronic lesions (more than 1 week) were seen on both T1- and T2-weighted images. Our results indicate that MR is superior to CT for evaluating lacunar infarcts, and second, that T2-weighted images are more sensitive than T1- and mixed T1-/T2-weighted images for detecting lacunar infarcts.

Adult↗
PubMed1987

Intracerebral hemorrhage after experimental embolic infarction. Anticoagulation.

Embolic stroke was induced in rabbits using autologous blood clot. One hour after stroke, animals received heparin anticoagulation (AC) for five hours (acute AC) or five days (chronic AC). Animals received excessive AC (partial thromboplastin time greater than 3.0 times control), adequate AC (partial thromboplastin time, 1.2 to 2.5 times control), or saline. After the animals were killed, the brains were examined for macroscopic evidence of intracerebral hemorrhage. There was no significant increase over control in the incidence or severity of hemorrhage in any of the four treatment groups. The data suggest that heparin AC does not promote intracerebral hemorrhage after experimental embolic stroke.

Animals↗
PubMed1987

Clinical evaluation and management of transient ischemic attacks.

Transient ischemic attack (TIA) is a common but poorly understood disorder. Although it rightfully has been classified as a major risk factor for stroke, the majority of patients with TIAs do not suffer subsequent stroke, and it is unclear whether aggressive evaluation and treatment of TIA will significantly lower stroke risk. To effectively treat this disorder, the implications of transient cerebral ischemia and the basic pathophysiologic process underlying this condition must be understood, as well as the myriad of specific clinical causes that must be considered in any patient. Any less sophisticated approach will only propagate the confusion that already exists and lead to the use of therapies that may be useless or even harmful.

Cerebrovascular Disorders↗
PubMed1986

Neurogenic bladder from occult herpes zoster.

Active infection with herpes zoster may cause acute urinary retention, especially when it involves sacral dermatomes. Although frank retention usually develops days to weeks after eruption of the typical rash, bladder incompetence infrequently develops first, raising concern over other, more ominous etiologies. In the case presented, rash appearance was delayed until six weeks after the initial onset of urinary retention, a much longer interval than previously reported. Occult herpes zoster infection should be considered in patients presenting with an acute neurogenic bladder of obscure cause.

Acyclovir↗
PubMed1986

Magnetic resonance imaging of hemorrhagic cerebral infarction.

A comparative study between magnetic resonance (MR) and computed tomography (CT) showed MR to be more sensitive than CT for detecting subacute and chronic hemorrhage into cerebral infarction. The hemorrhage appeared as either high signal on T1 weighted images or low signal on T2 weighted images, depending on the age of the hemorrhage. Cortical hemorrhagic infarction showed a characteristic gyral pattern. Methemoglobin and hemosiderin served as markers of previous hemorrhage into cerebral infarcts.

Adolescent↗
PubMed1984

Fulminant polyneuritis after overdose of disulfiram and ethanol.

A 39-year-old woman developed a severe sensorimotor polyneuritis after simultaneous ingestion of ethanol and disulfiram in high doses. The disorder was similar to other cases of disulfiram neuropathy, but was acute and more severe. Disulfiram can cause a fulminant polyneuropathy that is not always benign and reversible.

Adult↗
PubMed1981

Wernicke's disease complicating surgical therapy for morbid obesity.

A case of Wernicke's disease complicating surgical therapy for morbid obesity is presented. Features emphasized include the occurrence of the condition in a nonalcoholic patient and the persistence of neurological signs and symptoms despite prompt therapy. Prophylactic treatment in situations of potential thiamine depletion is essential if iatrogenic Wernicke's disease is to be avoided.

Adult↗