Biomedical subjects

Louis R. Caplan

Publications and source records attributed to Louis R. Caplan.

5 recordsLinked to original sources

PubMed2004

Cardiac Encephalopathy.

Many patients develop confusion, lethargy, and cognitive and behavioral abnormalities during or after cardiac decompensation. Congestive heart failure and the accompanying elevation in systemic venous pressure and decrease in cardiac output can lead to changes within the cranial cavity that cause an encephalopathy. At times, excess cerebrospinal fluid accumulates within the cranium causing an apathetic state identical to that seen in patients with other causes of hydrocephalus. Awareness of the syndrome of cardiac encephalopathy and optimal management of congestive heart failure and body fluids can reverse the neurologic dysfunction. In some patients with excess cerebrospinal fluid, lumbar puncture with removal of cerebrospinal fluid can reverse the apathetic state.

Journal Article↗

PubMed2004

Cerebrovascular Complications of Fibromuscular Dysplasia.

Patients with cerebral ischemia or hemorrhage due to fibromuscular dysplasia (FMD) should be admitted to a monitored hospital bed and receive supportive stroke care. Based on our personal clinical experience, we recommend antiplatelet agents for future stroke prevention in patients with symptomatic FMD. In patients with watershed stroke due to hemodynamically significant FMD, our opinion is that hypertensive, hypervolemic therapy should be initiated immediately. Additionally, we suggest that potential revascularization therapies, such as intraoperative or primary percutaneous angioplasty, should be discussed.

Journal Article↗

PubMed2004

Carotid Artery Dissection.

Dissection of the carotid artery in the neck is a relatively common condition. Most dissections are spontaneous, likely related to activities that cause sudden stretch of the pharyngeal portion of the carotid artery. Many patients do not develop brain ischemia but have a triad of neck and head pain, Horner's syndrome, and pulsatile tinnitus. Others present with transient or persistent brain ischemia. Strokes are due to the embolization of thrombus material from the lumen of the dissected artery to the intracranial arteries, most often the middle cerebral artery. Although there have been no randomized therapeutic trials in patients with carotid artery dissection, experience shows that standard anticoagulants in the form of heparin followed by Coumadin (Du Pont Pharma, Wilmington, DE) are effective in preventing further artery-to-artery emboli.

Journal Article↗

PubMed2003

Thrombolytic Therapy in Acute Ischemic Stroke.

The use of intravenous thrombolytic therapy for the treatment of patients with acute ischemic stroke is now approved in the United States, Canada, Germany, and the European Union. Guidelines published in 1996 from the American Heart Association and American Academy of Neurology committees recommended intravenous administration of recombinant tissue-plasminogen activator (rt-PA) (0.9 mg/kg; maximum of 90 mg) given in a 10% bolus, followed by an infusion lasting 60 minutes, to patients within 3 hours of onset of ischemic stroke. The recommendations stipulate that a computed tomography scan before the infusion should not show major infarction, mass effect, edema, or hemorrhage. Yet, only a small fraction of eligible patients (< 5%) have received rt-PA during the 7 years since its approval in the United States. Although effective, thrombolysis carries an important risk (5% to 10%) of brain hemorrhage and edema that can prove fatal. Many physicians and medical centers are not presently equipped or willing to give thrombolytic drugs for stroke treatment.

Journal Article↗

PubMed2003

Atherosclerotic Vertebral Artery Disease in the Neck.

Atherosclerotic lesions are very common at the origin and first few centimeters of the vertebral artery in the neck. These lesions are often missed when using noninvasive diagnostic strategies. These lesions cause transient hypoperfusion and transient ischemic attacks, characterized mostly by vestibulocerebellar symptoms. Strokes are caused by embolism from these lesions. Patients with nonstenosing vertebral artery plaques should be treated with statins and antiplatelet agents. Symptomatic patients who have had embolism from an occluded vertebral artery should be treated with heparin followed by warfarin for a period of 4 to 12 weeks. Antiplatelet agents can then be given. The optimal treatment of asymptomatic and symptomatic patients with severe vertebral artery stenosis is unclear. Statins and warfarin are recommended for patients with concurrent stenotic lesions of the contralateral extracranial vertebral artery, the intracranial vertebral or basilar arteries, or the anterior circulation arteries. Balloon angioplasty or stenting will likely prove superior to surgery in those patients with severe stenosis who do not respond to medical treatment.

Journal Article↗