Poststroke depression: a review emphasizing the role of prophylactic treatment and synergy with treatment for motor recovery.

Neuropsychiatric manifestations are common post stroke. Depression has a prevalence rate of 9% to 34% in the initial 3 to 6 months following stroke and is the most common neuropsychiatric sequel of stroke. Poststroke depression (PSD) has a significant adverse impact on the course of rehabilitation following stroke, resulting in overall impaired functional outcome. An increased risk of suicide and increased mortality have been reported. The association of depression and stroke is well established, highly complex, and multifactorial in origin, and the etiology of PSD involves size, location and number of lesions, stroke subtype, stroke severity, social handicap, and family support. Additionally, depression itself is an independent risk factor for stroke. In this article, we review the complex pathogenesis of PSD and summarize pharmacological treatment options. Because of recent important results that may relate to underlying cellular restorative processes, we focus on early prophylactic treatment, particularly as it involves selective serotonin uptake inhibitors (SSRIs). There is a recently recognized synergy between functional recovery and depression prophylaxis. New evidence that antidepressants, and SSRIs in particular, can make a substantial contribution to stroke recovery is explored.

Central poststroke pain: current diagnosis and treatment.

Central post-stroke pain syndrome (CPSP) is a debilitating sequel that can follow thalamic sensory stroke. Less well recognized, CPSP follows lateral medullary stroke and parietal cortical stroke and may develop anywhere along the spinothalamic or trigemino-thalamic pathways. Patients describe sharp, stabbing, or burning pain and experience hyperpathia and especially allodynia. Although CPSP was first described over 100 years ago, CPSP is too frequently underrecognized. It is treatable disorder. Pharmacological therapy, magnetic stimulation, and invasive electrical stimulation are reviewed and recommendations made.

Pre-tissue plasminogen activator blood pressure levels and risk of symptomatic intracerebral hemorrhage.

BACKGROUND AND PURPOSE: From small pilot studies, uncontrolled pretreatment systolic blood pressure >185 mm Hg and diastolic blood pressure >110 mm Hg in patients with acute ischemic stroke were introduced in the National Institute of Neurological Diseases and Stroke rtPA Stroke Study as a contraindication for thrombolysis. We sought to determine if pretreatment blood pressure protocol violations in patients with acute ischemic stroke receiving intravenous tissue plasminogen activator are related to the subsequent risk of symptomatic intracranial hemorrhage (sICH). METHODS: We reviewed medical records of consecutive ischemic stroke admissions treated with intravenous thrombolysis over a 10-year period at our tertiary care hospital. The National Institutes of Health Stroke Scale score on admission was used to determine baseline stroke severity. The closest documented blood pressure values to the time of tissue plasminogen activator bolus (range, 0 to 10 minutes) were considered as pretreatment blood pressure. Pretreatment blood pressure protocol violations were identified as systolic blood pressure >185 or diastolic blood pressure >110 mm Hg prebolus. sICH was defined as brain imaging evidence of intracranial hemorrhage with clinical worsening by the National Institutes of Health Stroke Scale score increase of >or=4 points. RESULTS: Among 510 patients with ischemic stroke treated with intravenous tissue plasminogen activator (282 men; mean age, 65+/-15 years), sICH occurred in 31 patients (6.1%). Blood pressure protocol violations were present in 63 patients (12.4%) and they were more frequent in patients with sICH (26% versus 12%; P=0.019). After adjusting for demographic characteristics, onset-to-treatment time, baseline National Institutes of Health Stroke Scale, stroke risk factors and medications, pretreatment blood pressure protocol violations were independently associated with a higher likelihood of sICH (OR, 2.59; 95% CI, 1.07 to 6.25; P=0.034). CONCLUSIONS: These data support current guidelines advising not to use intravenous tissue plasminogen activator when pretreatment blood pressure exceeds the prespecified thresholds by showing that blood pressure protocol violations are independently associated with a higher likelihood of sICH.

Advances and controversies in the management of cerebral venous thrombosis.

Cerebral venous thrombosis (CVT) is a rare form of stroke found most often in young women of reproductive age, often associated with oral contraceptive use, genetic or acquired thrombophilia, pregnancy, dehydration, or infection. CVT should be considered in any young patient who presents with an unexplained headache in combination with known hypercoagulable state, focal neurologic deficits, seizure, lobar hemorrhage, or bilateral thalamic or basal ganglionic edema. Acute treatment is with unfractionated heparin or low-molecular-weight heparin. It is important to provide supportive treatment. Outcomes are good compared with other types of stroke. Pediatric patients, excluding neonates, have similar presentation, treatment, and outcomes as adults.

Commonly asked questions in transient ischemic attack.

With the advent of modern neuroimaging techniques, transient ischemic attack (TIA) has been redefined as, "a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction." If infarct is evident on neuroimaging, the event is a stroke. It is important to recognize and correctly diagnose TIA and minor stroke because of the substantial early risk of stroke. Much of the early stroke risk is attributable to large artery atherosclerosis. Stroke-risk stratification in TIA patients can be done based on clinical grounds using an ABCD(2) score. There is, however, abundant data to support inclusion of neuroimaging in stroke-risk determination, which can also be combined with a clinical risk assessment. The hybrid ABCDE⊕ score further refines early stroke risk. Rapid assessment and treatment in the emergency department or in specially designed 'TIA clinics' appear to reduce stroke rate.

Late onset CNS immune reconstitution inflammatory syndrome in an immunocompetent patient.

Immune reconstitution inflammatory syndrome (IRIS) refers to the presence of paradoxical clinical deterioration attributable to immune system recovery during highly active antiretroviral therapy (HAART). We present an immunocompetent patient with multifocal leukoencephalopathy on HAART, with central nervous system (CNS) IRIS pathology of unknown infectious etiology. CNS IRIS pathology should be suspected in patients on longstanding HAART without immune reconstitution, presenting with unexplained leukoencephalopathy.

Direct thrombin inhibitors and factor Xa inhibitors in patients with cerebrovascular disease.

Stroke is a leading cause of cardiovascular morbidity and mortality worldwide. Approximately, 795,000 strokes occur in the USA each year, 610,000 of which are first events, and 185,000 of which are recurrent events. Of all strokes, 87% are ischemic strokes. Novel anticoagulants serve as an alternative antithrombotic intervention in patients with ischemic cerebrovascular disease. This paper reviews the role of the novel anticoagulants, dabigatran, rivaroxaban and apixaban, in stroke prevention among patients with nonvalvular atrial fibrillation.

Central and extrapontine myelinolysis affecting the brain and spinal cord. An unusual presentation of pancreatic encephalopathy.

Pancreatic encephalopathy refers to a gamut of neuropsychiatric symptoms complicating acute pancreatitis. Osmotic myelinolysis is a known complication of pancreatic encephalopathy. We evaluated a 58-year-old woman with pancreatic encephalopathy associated to pontine and extrapontine myelinolysis involving the brain and spinal cord. To our knowledge, this is the first clinic pathological case report of pancreatic encephalopathy involving the spinal cord.

Stroke- and pregnancy-induced hypertensive syndromes.

Pregnancy-induced hypertensive syndromes are an important cause of cerebrovascular diseases during pregnancy. Women with pregnancy-induced hypertensive syndromes are at an increased risk of ischemic and hemorrhagic strokes. Posterior reversible encephalopathy and reversible vasoconstriction syndromes are common. Cerebral venous sinus thrombosis may also occur. Preeclampsia and eclampsia reflect generalized endothelial dysfunction. Prompt diagnosis and identification of patients at risk allows for early therapeutic interventions and improved clinical outcomes.

Statins in hemorrhagic stroke.

Statin therapy has a major impact on the treatment of coronary artery disease and also has an impact on the treatment of ischemic stroke. Both clinical and experimental studies support the concept of statin actions beyond those of lipid lowering per se (pleiotrophic effects). In this article, we briefly review the clinical, experimental and biological data on the actions of statins and then review the literature regarding the impact of statin use on the two major forms of hemorrhagic stroke: aneurysmal subarachnoid hemorrhage and intracranial hemorrhage (ICH). We make recommendations regarding acute statin therapy, statin withdrawal and chronic statin therapy, including a possibly negative impact - the increased incidence of ICH associated with the use of higher doses of statin in patients with a prior history of stroke. Epidemiological data on the association between low total cholesterol or low levels of low-density cholesterol, hypertension and the incidence of ICH appear relevant and are also discussed. We speculate on the relationship between data derived from randomized controlled trials employing statin and ICH epidemiology.

Intra-arterial thrombolysis for acute ischemic stroke: preliminary experience with platelet glycoprotein IIb/IIIa inhibitors as adjunctive therapy.

OBJECTIVE: To evaluate the safety profile of platelet glycoprotein IIb/IIIa inhibitors administered as adjunctive therapy to patients with large-vessel occlusion and acute ischemic stroke refractory to pharmacological thrombolysis with recombinant tissue plasminogen activator (rtPA) and mechanical disruption, balloon angioplasty, or both. METHODS: Twenty-one patients (mean age, 62 yr; range, 29-88 yr) met the following criteria: 1) large-vessel occlusion and acute ischemic stroke syndrome at presentation, 2) failure to recanalize after administration of rtPA (intra-arterial and/or intravenous) with or without mechanical thrombolysis, and 3) subsequent treatment with IIb/IIIa inhibitors (intra-arterial or intravenous). RESULTS: Eleven patients had ischemia in the dominant hemisphere, 8 in the vertebrobasilar system, and 2 in the nondominant hemisphere. Twelve patients received intravenous rtPA without significant improvement; 9 patients were not candidates for intravenous rtPA. All patients received intra-arterial rtPA. The IIb/IIIa inhibitors were administered intravenously in 3 patients, intra-arterially in 16, and both intravenously and intra-arterially in 2. Balloon angioplasty was performed in 18 patients. Complete or partial recanalization was achieved in 17 of the 21 patients. After thrombolysis, 15 improved clinically. Three patients (14%) sustained an asymptomatic intracerebral hemorrhage after thrombolytic therapy. No patient was clinically worse after intervention. At last follow-up (mean, 8.5 mo), 13 patients were functionally independent (modified Rankin score, 0-3) and 8 were disabled or dead. CONCLUSION: IIb/IIIa inhibitors are an alternative for achieving recanalization. The risk of hemorrhage may be low. As part of an escalating protocol that includes pharmacological and mechanical thrombolysis, IIb/IIIa inhibitors may improve clinical outcomes.

Arterial thrombosis induced by IVIg and its treatment with tPA.

IV immunoglobulin therapy can lead to vascular events through increased serum viscosity and possibly other mechanisms. The authors describe the successful use of tissue plasminogen activator in three of four patients who developed cerebral and peripheral arterial thrombosis after treatment with IV immunoglobulin.