New horizons (Baltimore, Md.)最新文献

Spontaneous subarachnoid hemorrhage is usually caused by a ruptured cerebral aneurysm. Aneurysmal rupture classically presents with sudden severe headache, often accompanied by an altered mental status. Diagnosis is made with computed tomography or lumbar puncture. Patients with ruptured cerebral aneurysms are at risk for rebleeding, cerebral artery vasospasm (and subsequent ischemia or stroke), and hydrocephalus. Early surgical clipping of the aneurysm under the microscope is usually the initial treatment of choice. This surgery prevents rebleeding and allows for safe use of pressors in the event that clinical vasospasm develops. Factors that would favor delayed surgery, "coiling" procedures, or conservative management include poor patient condition, basilar artery aneurysms, and unusually large or irregular aneurysms. Patients with ruptured aneurysms are treated with nimodipine, a calcium-channel blocker, to help prevent vasospasm-related ischemia. The degree of vasospasm that develops in the first 2 wks after aneurysmal rupture is assessed by transcranial Doppler sonography and cerebral angiography, in addition to the clinical examination. Patients with symptomatic vasospasm are kept well hydrated and treated with pressors (provided the aneurysm has been successfully clipped).

Cerebellar hemorrhage may present with a spectrum of clinical manifestations, from a benign course with little to no neurologic deficit to a rapidly fatal course with hydrocephalus and brainstem compression. In patients with clinical deterioration, ventricular drainage and surgical evacuation of clot may be life-saving. Several retrospective studies have attempted to define radiographic indicators of the need for surgery with moderate success. A rational approach to the management of the patient with cerebellar hemorrhage is presented.

Intraventricular hemorrhage (IVH) frequently occurs in the setting of intracerebral and subarachnoid hemorrhage, and is an independent and significant contributor to morbidity and mortality in both conditions. Present therapy of IVH is directed at treating the associated complications of obstructive and communicating hydrocephalus. These therapies are often inadequate to treat the complications and do not remedy the underlying IVH. Intraventricular thrombolysis is a promising but unproven new therapy that directly addresses the IVH and may reduce the incidence of obstructive and communicating hydrocephalus.

Neuroprotective therapy for acute ischemic stroke is the focus of considerable animal and human research. Several agents have progressed through human clinical trials and hold great promise both as single agents and adjuncts to thrombolytic therapy. Cytoprotective therapy is aimed at interfering with the ischemic cascade in penumbral tissue in regions of reduced cerebral blood flow. The ischemic cascade involves failure of adenosine triphosphate-driven ion pumps and consequent cell swelling and lactate accumulation. The cascade continues to involve excitatory amino acid-mediated injury which involves calcium dysregulation. Human studies which have progressed from previous animal work have focused on inhibiting excitatory amino acid-mediated injury, preventing free-radical effects, and blocking intracellular accumulation of calcium. The clinical use of these neuroprotective agents is definitely on the horizon, while active research continues.

Advances in stroke treatment are discussed in the context of vertebrobasilar ischemia. The anatomy of the vertebral and basilar arteries and the pathophysiology of posterior circulation stroke are reviewed. The diagnosis and management of patients with vertebrobasilar occlusion is emphasized and the controversies surrounding the use of intra-arterial and intravenous thrombolytic therapy in posterior circulation disease are addressed.

Cerebral venous thrombosis (CVT) is less frequent than arterial thrombosis, however, it is still frequently overlooked. Pathophysiologically it is characterized by a disturbance of the equilibrium between endogenous thrombogenic and fibrinolytic factors. In addition, the time course depends on the presence or absence of efficient venous collaterals. A wide variety of clinical symptoms do occur, however, they may be grouped into at least four relatively typical syndromes: a) the pseudotumor cerebri syndrome, b) the combination of headache and focal neurologic deficit, c) the combination of focal epileptic seizure (with or without Todd's paresis) and headache, and d) deep CVT characterized by headache, nausea, bilateral long-tract symptoms and usually a rapidly progressing decline in the level of consciousness. Two diagnostic routes are generally accepted, the one consisting of cranial computed tomography plus radiographic angiography, the other one consisting of magnetic resonance imaging and magnetic resonance angiography. The mainstay of therapy is partial thromboplastin time-effective anticoagulation (PTT at least doubled, target PTT between 80 and 100 secs). Anticoagulation should be performed even if intracranial hemorrhage is present. In cases where deterioration occurs despite effective heparin treatment and in subjects presenting with stupor or coma, more aggressive therapy, e.g., local fibrinolysis during venous angiography, may be considered.

The medical management of the subarachnoid hemorrhage patient has changed considerably over the past two decades. The widespread acceptance of early aneurysm obliteration allows the aggressive prophylaxis and treatment of many of the serious complications of this condition. Recognition of cerebral vasospasm and the prevention of the delayed ischemic deficits it can produce are the cornerstones of critical care for these patients. Analysis of their fluid and electrolyte disturbances is complex, but important for the optimization of intravascular volume and consequent cerebral blood flow. Recognition of the numerous infectious and other medical complications that can befall these patients aids in the attempt to restore them to as normal a functional capacity as is possible.

Spontaneous hemorrhage into the cerebral parenchyma accounts for 8% to 13% of all strokes. It is more common in males, in blacks, and in the elderly. Fifty percent of cases are due to the effects of chronic hypertension on intracranial perforating arteries. The basal ganglia are the most frequent site of bleeding. Lobar hematomas tend to occur in younger patients, and may be due to specific causes such as vascular malformations. Many patients will have increased intracranial pressure and will require treatment in an intensive care unit. If surgery is necessary, stereotactic aspiration and pharmaceutical clot lysis are recent developments that may be advantageous. Prognosis is related to the patient's age and neurologic condition, and to the size, location, and rapidity of formation of the hematoma.