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Biomedical subjects

L R Caplan

Publications and source records attributed to L R Caplan.

At least 73 records · Page 4Linked to original sources
PubMed1997

Intracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry.

We studied 75 patients with severe intracranial vertebral artery (ICVA) occlusive disease from the New England Medical Center Posterior Circulation Registry to learn the etiologies and locations of the vascular lesions, the location and patterns of related ischemia and infarctions, and the outcomes. All patients had neuroimaging and vascular studies. Thirty-nine percent of patients had bilateral ICVA lesions. Twenty-four percent also had basilar artery disease and 36% had associated extracranial disease. The most common site of lesions was the distal ICVA after the origin of the posterior inferior cerebellar artery (PICA). Twenty-five percent of patients had only proximal intracranial posterior circulation territory infarcts (medullary and PICA cerebellar); 32% had infarcts that involved other intracranial territories in addition to the proximal territory. We found more distal intracranial territory infarcts resulting mainly from embolism from ICVA lesions than reported previously; this occurred in 17% of all patients. The ICVA was a recipient site for emboli in 8% of patients. Thirteen percent of patients died during follow-up. The outcome was favorable in most surviving patients. Three-fourths of them had no deficit or only slight disability. The patients with distal territory infarcts due to emboli from the ICVA had the worst outcome.

Adult↗
PubMed1997

Proximal intracranial territory posterior circulation infarcts in the New England Medical Center Posterior Circulation Registry.

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and longterm outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemimedullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extracranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.

Adult↗
PubMed1997

Intracranial angioplasty: experience and complications.

PURPOSE: To review our experience with intracranial angioplasty, including the complications we encountered. METHODS: During a 3-year period, from 1993 to 1996, 10 patients had intracranial percutaneous transluminal angioplasty (PTA). The stenosed vessels included three internal carotid arteries, one middle cerebral artery, one basilar artery, and five vertebral arteries. Stenosis in all patients was 75%, or greater. PTA was technically successful in eight patients; in two patients it could not be performed owing to inability to traverse the stenosed area. RESULTS: Two patients had successful and uneventful PTA. Five patients had vasospasm, which resolved with local vasodilators in two and with repeat PTA in one. Vasospasm led to stroke in two patients. Compromise of perforating vessels and arterial dissection were associated with stroke in two patients. CONCLUSION: Intracranial PTA is technically feasible but associated with risks related to vasospasm, arterial trauma, and compromise of perforating vessels.

Adult↗
PubMed1996

Management issues in asymptomatic carotid stenosis.

In the absence of symptoms, management is not clear-cut; indeed, are symptoms truly absent or merely unacknowledged? The workup must carefully balance risks associated with carotid endarterectomy against risks of nonsurgical treatment. Psychosocial factors are an important part of the balance; some patients prefer to live with the risk of stroke from essentially untreated disease.

Aged↗
PubMed1996

A reversible posterior leukoencephalopathy syndrome.

BACKGROUND AND METHODS: In some patients who are hospitalized for acute illness, we have noted a reversible syndrome of headache, altered mental functioning, seizures, and loss of vision associated with findings indicating predominantly posterior leukoencephalopathy on imaging studies. To elucidate this syndrome, we searched the log books listing computed tomographic (CT) and magnetic resonance imaging (MRI) studies performed at the New England Medical Center in Boston and Hôpital Sainte Anne in Paris; we found 15 such patients who were evaluated from 1988 through 1994. RESULTS: Of the 15 patients, 7 were receiving immunosuppressive therapy after transplantation or as treatment for aplastic anemia, 1 was receiving interferon for melanoma, 3 had eclampsia, and 4 had acute hypertensive encephalopathy associated with renal disease (2 with lupus nephritis, 1 with acute glomerulonephritis, and 1 with acetaminophen-induced hepatorenal failure). Altogether, 12 patients had abrupt increases in blood pressure, and 8 had some impairment of renal function. The clinical findings included headaches, vomiting, confusion, seizures, cortical blindness and other visual abnormalities, and motor signs. CT and MRI studies showed extensive bilateral white-matter abnormalities suggestive of edema in the posterior regions of the cerebral hemispheres, but the changes often involved other cerebral areas, the brain stem, or the cerebellum. The patients were treated with antihypertensive medications, and immunosuppressive therapy was withdrawn or the dose was reduced. In all 15 patients, the neurologic deficits resolved within two weeks. CONCLUSIONS: Reversible, predominantly posterior leukoencephalopathy may develop in patients who have renal insufficiency or hypertension or who are immunosuppressed. The findings on neuroimaging are characteristic of subcortical edema without infarction.

Adolescent↗
PubMed1996

Surgical treatment of systemic atheroembolism from the thoracic aorta.

BACKGROUND: Surgical procedures performed exclusively for atheroembolic events arising from the thoracic aorta rarely have been reported. Presented here are 2 patients who underwent successful operation for these problems. METHODS: The clinical presentation, diagnostic evaluation and surgical approach to 2 patients with different embolic sources in the thoracic aorta are presented. One patient had experienced three strokes and was noted by multiplane transesophageal echocardiography to have protruding atheromas with ulcerations in the transverse arch and origin of the brachiocephalic vessels. The transverse arch was replaced using hypothermic circulatory arrest with individual reimplantation of the brachiocephalic vessels. The second patient presented with "blue toe" syndrome from mobile atheromas in the mid-descending thoracic aorta defined by transesophageal echocardiography. A localized debridement was performed using simple aortic cross-clamping. RESULTS: Both patients had uneventful postoperative courses and had no further atheroembolic events. CONCLUSIONS: When standard diagnostic modalities do not delineate an embolic source for either stroke or peripheral embolization, transesophageal echocardiography is recommended as an excellent means of identifying atheromas in the thoracic aorta that could be the source for emboli. Once these lesions are identified, a surgical procedure should be performed to prevent further embolization.

Aorta↗
PubMed1996

Thalamic haemorrhage.

Thalamic haemorrhage is usually considered a single entity although the thalamus is composed of anatomically as well as functionally discrete subregions receiving blood from different arteries. The clinical features vary according to the intrathalamic location of the haematomas and the bleeding artery. We investigated the impact of haematoma location and vascular territory on the clinical symptoms and signs, neuro-imaging findings and clinical courses of patients with thalamic haemorrhages by a retrospective analysis of 175 consecutive patients with thalamic haemorrhage. Based on the neuro-imaging findings we classified thalamic haematomas into four regional types and one global type according to the primary bleeding sites: (i) anterior type occurring in the territory of the tuberothalamic arteries, (ii) posteromedial type occurring in the territory of the thalamic-subthalamic paramedian arteries, (iii) posterolateral type occurring in the territory of the thalamogeniculate arteries. (iv) dorsal type occurring in the territory of the posterior choroidal arteries and (v) global type occupying the entire area of the thalamus. We studied the clinical and neuroimaging characteristics of each type. Eleven patients (7%) had the anterior type: these were the smallest haematomas and often ruptured into the anterior horn of the lateral ventricle. The major clinical signs were acute behavioural abnormalities: the clinical course was usually benign. Twenty-four patients (14%) had the posteromedial type in which haematomas often ruptured into the third ventricle, causing marked hydrocephalus, and often extended mediocaudally, involving the mesencephalon. The prognoses of this type depended on the presence of mesencephalic involvement which was associated with the worst outcome among the types even if the size of the haematoma itself was not large. The posterolateral type was most frequent (77 patients, 44%) and was characterized by large haematomas, rupture into the posterior horn of the lateral ventricle and frequent extension into the posterior limb of the internal capsule. Clinical signs included marked sensory and motor signs, hemineglect in right-side haematomas and language abnormalities with left-side haematomas. The case fatality with this type was relatively high (35%) and permanent neurologic sequelae frequently resulted. In the dorsal type (32 patients, 18%) haematomas were best visualized at the level of the body of the lateral ventricle on CT scans. The size was moderate and haematomas often extended posterolaterally into the adjacent subcortical white matter. Sensory and motor signs were common and about one third of the patients were first misdiagnosed as having lacunar infarcts. The prognoses were excellent. The global type (31 patients, 18%) of thalamic haemorrhage was clinically and radiologically very similar to the posterolateral type except that the haematomas were too large to define the bleeding focus. Severe sensory and motor signs were almost always present. In this type 25 patients died (the case fatality was 81%).

Adolescent↗
PubMed1996

Brain edema after carotid surgery.

The postoperative hyperperfusion syndrome describes an abrupt increase in blood flow with loss of autoregulation in surgically reperfused brain. Reports described a spectrum of findings, including severe headache, transient ischemia, seizures, and intracerebral hemorrhage. Hypertension is common after carotid artery surgery and often plays a role in the pathophysiology. We now report five patients with severe white matter edema after carotid surgery, a finding not previously included in the hyperperfusion syndrome. Five to 8 days after carotid surgery and after hospital discharge, each patient developed hypertension, headache, hemiparesis, seizures, and aphasia or neglect due to severe white matter edema ipsilateral to the carotid surgery. One patient had a small hemorrhage within the edematous area. Hypertension was severe in four patients and moderate in one. The carotid artery was patent by ultrasound or angiography in each patient after surgery. Transcranial Doppler showed increased velocities ipsilateral to surgery in two patients and bilaterally in one. Computed tomographic abnormalities and neurologic signs resolved within 3 weeks in four of the five patients treated with antihypertensives and anticonvulsants. The fifth patient died from herniation secondary to massive edema. Brain edema with focal neurologic signs should be included as a serious but potentially reversible component of the postoperative hyperperfusion syndrome.

Aged↗
PubMed1996

Cerebellar hemorrhagic infarction.

We investigated 17 patients with 26 cerebellar hemorrhagic infarcts for their vascular anatomy, stroke mechanisms, and clinical course. Sixteen infarcts involved the superior cerebellar artery, nine the posterior inferior cerebellar artery, and one the anterior inferior cerebellar artery territories. The infarcts involved the full territory of the supplying arteries in 19 of 26 infarcts (73%). Sixteen of 17 patients were stable or improving when the hemorrhagic infarction was detected. All but one patient had an imaging study at the time of presentation that was negative for blood; hemorrhagic infarction was detected on routine serial scans performed during the first 15 days. Nine of the 17 patients were on anticoagulants when the cerebellar hemorrhagic infarct was detected; anticoagulation was maintained in eight of them with no clinical worsening. The stroke mechanism in all patients was considered embolic from cardiac and intra-arterial sources. The causes, imaging findings, and consequences of hemorrhagic infarcts in the posterior circulation are similar to those in the anterior circulation.

Anticoagulants↗
PubMed1996

Stroke with sensory symptoms mimicking myocardial ischemia.

OBJECTIVE: To report five stroke patients with sensory deficits including prominent chest discomfort mimicking angina. BACKGROUND: Chest wall sensory discomfort, as a part of unilateral sensory dysfunction, has seldom been recognized as a potential imitator of cardiac ischemia. METHODS: A retrospective review of stroke patients with sensory symptoms from the New England Medical Center Stroke Registry. RESULTS: As a part of an acute stroke that included unilateral sensory symptoms and signs, five patients had chest pain or discomfort, which prompted cardiac evaluation for potential coronary artery disease. In two patients, the primary presentation was chest discomfort. In the other three, chest discomfort was part of a more extensive stroke syndrome. The symptoms were described as "burning," "hot feeling," "flashes," "tightness," and "cold." In three patients, an MRI or CT scan showed an infarct in the thalamus, corona radiata, or lateral medulla. Cardiac evaluation was negative in all but one patient who had single vessel percutaneous transluminal coronary angioplasty without resolution of sensory symptoms. Chest discomfort fluctuated but persisted for months or years after presentation. CONCLUSION: Chest discomfort mimicking cardiac ischemia may be a prominent sensory symptom in acute stroke.

Aged↗
PubMed1996

Diabetes and brain ischemia.

Diabetes influences brain ischemia in a number of different ways. Diabetes causes and exacerbates macroangiopathies, increases the severity of ischemia, and increases stroke mortality. Unfortunately, few studies have examined in sufficient depth the influence of diabetes on the various vascular lesions that cause brain ischemia. These can be divided into: 1) cardiac-origin brain embolism; 2) atherosclerosis of the aorta and the large extracranial arteries--the internal carotid arteries (ICAs) and the vertebral arteries (VAs); 3) atherosclerosis of the large intracranial arteries--ICAs, anterior, middle, and posterior cerebral arteries, the VAs, and the basilar artery; 4) intracranial atheromatous branch disease of macroscopically visible branches of the intracranial arteries enumerated in 3; and 5) degenerative abnormalities such as lipohyalinosis and fibrinoid changes within penetrating artery branches visible only microscopically. The last three types of disorders all can cause deep subcortical brain infarcts, the predominant type of brain infarction found in Japan.

Brain↗
PubMed1995

Guidelines for carotid endarterectomy. A multidisciplinary consensus statement from the Ad Hoc Committee, American Heart Association.

BACKGROUND AND PURPOSE: Indications for carotid endarterectomy have engendered considerable debate among experts and have resulted in publication of retrospective reviews, natural history studies, audits of community practice, position papers, expert opinion statements, and finally prospective randomized trials. The American Heart Association assembled a group of experts in a multidisciplinary consensus conference to develop this statement. METHODS: A conference was held July 16-18, 1993, in Park City, Utah, that included recognized experts in neurology, neurosurgery, vascular surgery, and healthcare planning. A program of critical topics was developed, and each expert presented a talk and provided the chairman with a summary statement. From these summary statements a document was developed and edited onsite to achieve consensus before final revision. RESULTS: The first section of this document reviews the natural history, methods of patient evaluation, options for medical management, results of surgical management, data from position statements, and results to date of prospective randomized trials for symptomatic and asymptomatic patients with carotid artery disease. The second section divides 96 potential indications for carotid endarterectomy, based on surgical risk, into four categories: (1) Proven: This is the strongest indication for carotid endarterectomy; data are supported by results of prospective contemporary randomized trials. (2) Acceptable but not proven: a good indication for operation; supported by promising but not scientifically certain data. (3) Uncertain: Data are insufficient to define the risk/benefit ratio. (4) Proven inappropriate: Current data are adequate to show that the risk of surgery outweighs any benefit. CONCLUSIONS: Indications for carotid endarterectomy in symptomatic good-risk patients with a surgeon whose surgical morbidity and mortality rate is less than 6% are as follows. (1) Proven: one or more TIAs in the past 6 months and carotid stenosis > or = 70% or mild stroke within 6 months and a carotid stenosis > or = 70%; (2) acceptable but not proven: TIAs within the past 6 months and a stenosis 50% to 69%, progressive stroke and a stenosis > or = 70%, mild or moderate stroke in the past 6 months and a stenosis 50% to 69%, or carotid endarterectomy ipsilateral to TIAs and a stenosis > or = 70% combined with required coronary artery bypass grafting; (3) uncertain: TIAs with a stenosis < 50%, mild stroke and stenosis < 50%, TIAs with a stenosis < 70% combined with coronary artery bypass grafting, or symptomatic, acute carotid thrombosis; (4) proven inappropriate: moderate stroke with stenosis < 50%, not on aspirin; single TIA, < 50% stenosis, not on aspirin; high-risk patient with multiple TIAs, not on aspirin, stenosis < 50%; high-risk patient, mild or moderate stroke, stenosis < 50%, not on aspirin; global ischemic symptoms with stenosis < 50%; acute dissection, asymptomatic on heparin. Indications for carotid endarterectomy in asymptomatic good-risk patients performed by a surgeon whose surgical morbidity and mortality rate is less than 3% are as follows. (1) Proven: none. As this statement went to press, the National Institute of Neurological Disorders and Stroke issued a clinical advisory stating that the Institute has halted the Asymptomatic Carotid Atherosclerosis Study (ACAS) because of a clear benefit in favor of surgery for patients with carotid stenosis > or = 60% as measured by diameter reduction. When the ACAS report is published, this indication will be recategorized as proven. (2) acceptable but not proven: stenosis > 75% by linear diameter; (3) uncertain: stenosis > 75% in a high-risk patient/surgeon (surgical morbidity and mortality rate > 3%), combined carotid/coronary operations, or ulcerative lesions without hemodynamically significant stenosis; (4) proven inappropriate: operations with a combined stroke morbidity and mortality > 5%.

Arterial Occlusive Diseases↗
PubMed1995

Extinction during time controlled direct retinal stimulation after recovery from right hemispheric stroke.

The temporal variables of extinction in two patients with right hemispheric stroke and two normal controls were studied using a scanning laser ophthalmoscope (SLO). This instrument enabled eye movements to be controlled for by projecting time controlled stimuli directly on to the retina. Both patients had recovered from their stroke (four months and five years) and seemed clinically normal. At 50 ms, patient 1 extinguished one of two stimuli on seven of 40 double simultaneous stimulation (DSS) trials (five left, two right) and patient 2 extinguished the left stimulus on every DSS trial. At 100 ms, patient 1 performed almost perfectly, whereas patient 2 extinguished on 30% of the DSS trials (10 left, two right). At 200 ms, patient 2 performed perfectly. Neither of the controls showed extinction to DSS at any presentation time. Thus detecting DSS was time dependent in the patients but not the normal subjects. These data support the theory that recovery from neglect after right hemispheric damage may be mediated by the left hemisphere.

Adult↗