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Biomedical subjects

S E Kasner

Publications and source records attributed to S E Kasner.

17 recordsLinked to original sources
PubMed1999

Initial clinical experience with IV tissue plasminogen activator for acute ischemic stroke: a multicenter survey. The t-PA Stroke Survey Group.

We assessed initial clinical experience with IV tissue plasminogen activator (t-PA) treatment of acute ischemic stroke in a standardized retrospective survey of hospitals with experienced acute stroke treatment systems. The incidence of symptomatic intracerebral hemorrhage (ICH) was 6% (11 of 189 patients; 95% CI 3 to 11%), similar to that in the National Institute of Neurological Disorders and Stroke (NINDS) t-PA Stroke Study. Deviations from the NINDS protocol guidelines were identified in 30% of patients (56 of 189). The incidence of symptomatic ICH was 11% among patients with protocol deviations as compared with 4% in patients who were treated according to the NINDS protocol guidelines, suggesting that strict adherence to protocol guidelines is prudent.

Aged↗
PubMed1999

Early clinical and radiological predictors of fatal brain swelling in ischemic stroke.

BACKGROUND AND PURPOSE: Early identification of acute stroke patients at risk of fatal brain swelling is necessary to facilitate implementation of aggressive therapies. Initial clinical, laboratory, and CT characteristics that may be used as selection criteria were analyzed to determine predictors of herniation and neurological death. METHODS: Data from the placebo arm of the Lubeluzole-International-9 trial were reviewed to identify patients with fatal brain edema. Early clinical, laboratory, and radiographic parameters were evaluated in a case-control design. Initial CT scans were analyzed for early ischemic abnormalities by 2 blinded investigators. RESULTS: Twenty-three patients died from brain swelling, with minimum baseline National Institutes of Health Stroke Scale (NIHSS) scores of 20 (n=12; mean, 23.2+/-1.8) with left and 15 (n=11; mean, 17.6+/-2.2) with right hemispheric infarctions (P=0. 0001). A sample of 112 subjects with comparably severe strokes, but who did not die from brain swelling, was selected from the remaining population according to the same NIHSS scores. Among clinical and laboratory characteristics, nausea/vomiting within 24 hours after onset (odds ratio [OR], 5.1; 95% CI, 1.7 to 15.3; P=0.003) and 12-hour systolic blood pressure >/=180 mm Hg (OR, 4.2; 95% CI, 1.4 to 12.9; P=0.01) were independently associated with fatal brain swelling. Among radiographic factors, only hypodensity of >50% of the middle cerebral artery territory on initial CT scan was an independent predictor (OR, 6.1; 95% CI, 2.3 to 16.6; P=0.0004). CONCLUSIONS: Patients with baseline NIHSS score >/=20 with left or >/=15 with right hemispheric infarctions within 6 hours of symptom onset who also have nausea/vomiting or >50% middle cerebral artery territory hypodensity are at high risk for developing fatal brain swelling.

Acute Disease↗
PubMed1998

Ischemic stroke.

Acute ischemic stroke is a neurological emergency that requires ultra-rapid intervention. Stroke teams and stroke protocols can be devised to expediate evaluation and treatment. In carefully selected patients, thrombolytic therapy offers a significant benefit but must be initialized within 3 hours of stroke onset. Emerging alternative strategies for reperfusion and neuroprotection must also be initiated during the hyperacute period. The role of more traditional therapies, such as antiplatelet agents and anticoagulants, have been better defined through several recent major clinical trials.

Anticoagulants↗
PubMed1998

Intravenous tissue plasminogen activator for acute ischemic stroke: feasibility, safety, and efficacy in the first year of clinical practice.

BACKGROUND AND PURPOSE: The feasibility, safety, and efficacy of intravenous tissue plasminogen activator (t-PA) for patients with acute ischemic stroke in clinical practice need to be assessed. METHODS: We initiated a prospective open-label study at a university hospital and two community hospitals in Houston, Tex, immediately after the publication of the National Institute of Neurological Disorders and Stroke (NINDS) t-PA study. A total of 30 patients, age 32 to 90 years, were treated with 0.9 mg/kg of intravenous t-PA (maximum dose, 90 mg) within 3 hours of acute ischemic stroke between December 1995 and December 1996. RESULTS: Six percent (6%) of all patients hospitalized with ischemic stroke received intravenous t-PA at the university hospital and 1.1% at the community hospitals. The rates of total, symptomatic, and fatal intracerebral hemorrhage were 10%, 7%, and 3%. Thirty-seven percent (37%) of patients recovered to fully independent function. The average time from stroke onset to emergency department arrival was 57 minutes; emergency department arrival to computed tomography scan 41 minutes; and computed tomography scan to administration of treatment 59 minutes. CONCLUSIONS: When treatment guidelines are carefully followed in an urban hospital setting, intravenous t-PA for acute ischemic stroke is feasible and shows safety and efficacy comparable to the results of the NINDS study.

Activities of Daily Living↗
PubMed1998

Hemopericardium and cardiac tamponade after thrombolysis for acute ischemic stroke.

Hemorrhage is the major complication of IV recombinant tissue plasminogen activator (rt-PA) treatment for stroke. We report three patients with mild or indistinct cardiac symptoms prior to thrombolysis in whom hemodynamically significant cardiac tamponade occurred after treatment with rt-PA. Acute ischemic stroke patients may have undetected myocardial or pericardial disease that may pose a risk for hemopericardium and life-threatening tamponade after treatment with rt-PA.

Aged↗
PubMed1997

Emergency identification and treatment of acute ischemic stroke.

In this review we describe the pathophysiology of cerebral ischemia and its implications for potential therapy. We summarize the results of recently completed trials of acute stroke intervention and explore some of the controversy surrounding thrombolysis for acute stroke. We also introduce the key concepts of neuroprotection and its therapeutic possibilities. Finally, we discuss the delays that may occur in the emergency evaluation and management of acute ischemic stroke and suggest some methods to expedite the process.

Brain Ischemia↗
PubMed1997

Magnetic resonance angiography demonstrates vascular healing of carotid and vertebral artery dissections.

BACKGROUND AND PURPOSE: Dissection of the carotid and vertebral arteries is most accurately diagnosed with conventional angiography. MR techniques are sensitive for detecting the abnormalities associated with dissection but may lack specificity. We hypothesized that MR may be useful for serial monitoring of dissection and may therefore guide therapy. METHODS: All patients with angiographically proven carotid and/or vertebral artery dissection from July 1994 to June 1996 were followed for a median duration of 10.5 months. Of these 29 patients (44 vessels), 18 were concurrently evaluated with MR, and a target group of 9 patients (17 vessels) was prospectively followed with MR at 3-month intervals. RESULTS: In the 18 patients with both imaging studies at baseline, angiography revealed 30 dissected vessels while MR detected 27 (90%). In the target group of 9 patients, initial MR identified 15 of the 17 dissections diagnosed with angiography. Serial MR revealed complete healing in 5 vessels, improvement in 6 vessels, no change in 4 vessels, and worsening in 2 vessels. The radiographic features most likely to resolve were stenosis and mural hematoma, while occlusion and luminal irregularity tended to persist. Late ischemic events occurred in 2 patients, both with persistent MR evidence of dissection, one while subtherapeutic on warfarin therapy and the other occurring 1 week after warfarin was discontinued. CONCLUSIONS: MR is a reliable noninvasive method for following the vascular response to treatment and may guide the course of a clinical trial comparing medical therapies for carotid and vertebral artery dissection.

Adolescent↗
PubMed1997

Magnetization transfer imaging in progressive multifocal leukoencephalopathy.

We report a patient with biopsy-proven progressive multifocal leukoencephalopathy (PML) who was serially imaged with MRI and magnetization transfer imaging. The magnetization transfer ratio (MTR) was profoundly and significantly diminished when compared with normal control subjects. The pattern of MTR was distinct from that of MS and periventricular ischemic white matter disease. Magnetization transfer imaging techniques may aid in the differential diagnosis of PML.

Aged↗
PubMed1997

Neuro-ophthalmologic aspects of aneurysms.

The visual pathways and the ocular motor cranial nerves are frequently injured by expanding cerebral aneurysms. Neuro-ophthalmologic signs and symptoms may be the only indications of an aneurysm prior to rupture. Acute or chronic visual loss may herald an aneurysm prior to rupture. Acute or chronic visual loss may herald an aneurysm in the carotidophthalmic, supra clinoid carotid, internal carotid bifurcation, or anterior communicating artery distributions. Diplopia and retro-orbital pain may be warning signs that precede the discovery of a posterior communicating, basilar, or cavernous sinus aneurysm.

Acute Disease↗
PubMed1996

Nitric oxide relaxes rabbit corpus cavernosum smooth muscle via a potassium-conductive pathway.

We tested the hypothesis that acetylcholine-induced relaxation in cavernosal tissue is the result of nitric oxide production that alters K+ conductance. In the organ bath, acetylcholine- and sodium nitroprusside-induced relaxation of corpus cavernosum were significantly attenuated by tetraethylammonium. Basal [K+]i in cavernosal smooth muscle cells was 102 +/- 11 mM using a K+-sensitive fluorescent dye. Acetylcholine produced a decrease in [K+]i to 74 +/- 10 (n > 4, P < 0.05). Tetraethylammonium pretreatment blunted the acetylcholine- and sodium nitroprusside-induced decrease in [K+]i by 82%, (n > 5, P < 0.001), respectively. L-NMMA blunted the acetylcholine- and sodium nitroprusside-induced fall in [K+]i by 93% and 83% (n > 4, P < 0.001), respectively. These data suggest that acetylcholine-mediated cavernosal smooth muscle cells relaxation occurs through nitric oxide release with activation of K+ conductance.

Acetylcholine↗
PubMed1996

Cavernous sinus syndrome in Hodgkin's disease.

Hodgkin's disease has not been reported to produce an isolated cavernous sinus syndrome, although this phenomenon is well-described in non-Hodgkin's lymphoma. We review the 16 cases of cavernous sinus syndrome caused by non-Hodgkin's lymphoma and report two patients with Hodgkin's disease in clinical remission who developed recurrent disease in the cavernous sinus. MRI revealed a mass lesion in the left cavernous sinus in each patient. Corticosteroids and radiation therapy were effective palliative measures. In both patients, recurrence in the cavernous sinus preceded other systemic evidence of recurrent Hodgkin's disease.

Adult↗
PubMed1995

Spontaneous intracranial hypotension: headache with a reversible Arnold-Chiari malformation.

Spontaneous intracranial hypotension is characterized by severe postural headache in the setting of low CSF pressure, usually attributed to a cryptic CSF leak. We report a patient whose prolonged refractory headache was characterized by the clinical symptoms of occipital neuralgia, but was also associated with the radiographic appearance of an Arnold-Chiari malformation, type I and low CSF pressure. After extensive diagnostic evaluation, CT cisternomyelography ultimately demonstrated a CSF leak at the C2 vertebral level. Symptomatic relief was sustained only with long-term theophylline administration. The apparent Arnold-Chiari malformation resolved with treatment of the low CSF pressure.

Adult↗
PubMed1995

Nitric oxide alters cytosolic potassium in cultured glomerular mesangial cells.

Endothelium-derived relaxing factor is believed to be nitric oxide (NO). Evidence suggests that it has important functions in the regulation of mesangial cell (MC) tone and possibly in inflammation. As a vasodilator, its vasorelaxant effect depends, in part, on changes in cell membrane potential. We therefore tested the hypothesis that MCs in culture produce NO that results in cell relaxation through the opening of K+ conductance pathways. The K(+)-sensitive fluorescent dye, potassium-binding benzofuran isophthalate, was used to detect rapid changes in intracellular K+ concentration ([K+]i). The membrane potential-sensitive dye, 1,3-(sulfonatopropyl)-4-([beta-di-n- butylamino)-6-naphthyl]vinyl)pyridinium betaine (Di-4-AN-EPPS), was used to detect changes in membrane potential. Basal [K+]i was 92 +/- 9 mM (n = 46). In response to sodium nitroprusside (SNP), acetylcholine (ACh), and bradykinin (BK), [K+]i decreased to 72 +/- 7 (n = 5, P < 0.05), 70 +/- 8 (n = 7, P < 0.05), and to 69 +/- 13 mM (n = 6, P < 0.05), respectively. [K+]i rapidly returned to basal level in the continued presence of all three agonists. The SNP-, ACh-, and BK-induced decrease in [K+]i was significantly blunted by Ba2+ by 85, 92, and 89%, respectively (n > 4 for each agonist examined, P < 0.0001). NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P < 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Regulation of intracellular potassium in mesangial cells: a fluorescence analysis using the dye, PBFI.

We investigated the regulatory transport processes that maintain intracellular K+ homeostasis in cultured rat glomerular mesangial cells (MCs). Intracellular K+ concentration ([K+]i) of quiescent MCs, passages 3-8, grown to subconfluence on glass cover slips, was assessed by spectrofluorometry using the K(+)-sensitive dye, K(+)-binding benzofuran isophthalate (PBFI). Serum-starved MCs were incubated at 37 degrees C in 5 microM PBFI for 90 min. Excitation ratios of luminescences at 340 and 380 nm, measured at a constant emission at 500 nm, were used to determine [K+]i. Ionophores valinomycin and nigericin were used to clamp [K+]i to known [K+]o and thereby obtain an intracellular calibration of dye. Dependence of fluorescence ratio on [K+]i conformed to Michaelis-Menten behavior, with a Km of 113 mM (n = 40). PBFI retains its sensitivity to alterations in [K+]i with pH change (pHi from 6.5 to 7.5) but is relatively insensitive when intracellular Na+ is greater than 75 mM and cell osmolarity exceeds 500 mM. Normal resting [K+]i for all experiments was determined in MCs to be 102 +/- 7 mM (n = 81) in a HCO3(-)-free HEPES-buffered solution. When MCs were exposed to ouabain, [K+]i fell to 48 +/- 6 mM and did not recover, suggesting presence of Na(+)-K(+)-ATPase. When MCs were exposed to furosemide, [K+]i transiently declined to 58 +/- 11 mM, which was followed by a rapid recovery to near steady state, indicating additional presence of Na(+)-K(+)-Cl- cotransporter. Recovery was completely abolished when MCs were exposed to ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗