Cerebral small vessel disease: cognition, mood, daily functioning, and imaging findings from a small pilot sample.

Cerebral small vessel disease, a leading cause of cognitive decline, is considered a relatively homogeneous disease process, and it can co-occur with Alzheimer's disease. Clinical reports of magnetic resonance imaging (MRI)/computed tomography and single photon emission computed tomography (SPECT) imaging and neuropsychology testing for a small pilot sample of 14 patients are presented to illustrate disease characteristics through findings from structural and functional imaging and cognitive assessment. Participants showed some decreases in executive functioning, attention, processing speed, and memory retrieval, consistent with previous literature. An older subgroup showed lower age-corrected scores at a single time point compared to younger participants. Performance on a computer-administered cognitive measure showed a slight overall decline over a period of 8-28 months. For a case study with mild neuropsychology findings, the MRI report was normal while the SPECT report identified perfusion abnormalities. Future research can test whether advances in imaging analysis allow for identification of cerebral small vessel disease before changes are detected in cognition.

Acute ischemic stroke and infections.

We present an overview of multiple infections in relation to acute ischemic stroke and the therapeutic options available. Conditions that are a direct cause of stroke (infectious endocarditis, meningoencephalitides, and human immunodeficiency virus infection), the pathophysiologic mechanism responsible for stroke, and treatment dilemmas are presented. Independently or in conjunction with conventional risk factors, chronic and acute infections can trigger an acute ischemic stroke through an accelerated process of atherosclerosis and immunohematologic alterations. Acute ischemic stroke has a negative impact on the antibacterial immune response, leading to stroke-induced immunodepression and infections, the most common poststroke medical complications. Poststroke infections are independent predictors of poor outcome. Antibiotic trials for poststroke infection prevention are reviewed. Although antibiotic prophylaxis is not the standard of care in acute stroke, current guidelines support prompt treatment of stroke-related infections.

Timing of symptomatic vasospasm in aneurysmal subarachnoid hemorrhage: the effect of treatment modality and clinical implications.

A better prediction of the time course of symptomatic vasospasm (SVSP) might have a significant impact on the management and prevention of delayed neurologic ischemic deficit (DIND). We studied the influence of the treatment for ruptured aneurysm on SVSP timing. We retrospectively analyzed data of consecutive patients with aneurysmal subarachnoid hemorrhage (aSAH) admitted in our center between 1999 and 2005, treated within 72 hours of the rupture by surgical clipping or endovascular coiling and in accordance with our neuroscience unit protocol. We analyzed the presence of SVSP and recorded the timing of occurrence after the aneurysmal repair intervention. Data on demographics, premorbid conditions, time elapsed from the subarachnoid hemorrhage onset and intervention, and clinical and radiologic characteristics at admission were collected. The first occurrence of postintervention SVSP was recorded and compared between the 2 treatment groups using a proportional hazards regression model, including significant covariates. Of the 67 patients analyzed, 21 (31%) underwent endovascular coiling and 46 (69%) underwent surgical clipping. The baseline variables were similar in the 2 groups. The median time from the procedure to clinical vasospasm was 4 days in the coiled patients and 7 days in the clipped patients. In a proportional hazards model regression analysis including age, sex, Fisher and Hunt-Hess grades, time between onset to procedure, and intervention type, only intervention type emerged as a significant predictor of time to SVSP after intervention (likelihood ratio chi2 = 16.8; P < .00). Treatment modality of ruptured intracranial aneurysm may influence the timing of SVSP occurrence.

Safety and effectiveness of endovascular therapy after 8 hours of acute ischemic stroke onset and wake-up strokes.

BACKGROUND AND PURPOSE: This is a retrospective review of patients who underwent endovascular recanalization > or = 8 hours after acute ischemic stroke symptom onset, including wake-up strokes, between June 2005 and June 2008. METHODS: Thirty patients with a premorbid modified Rankin score < or = 1 and NIHSS between 5 and 22 were included. All had admission CT, CTA, and CT perfusion scans to evaluate for salvageable brain tissue. Recanalization effectiveness was assessed by angiograms obtained within 30 hours after intervention. Patient, treatment characteristics, and immediate and 3-month outcomes were analyzed. RESULTS: Mean NIHSS at presentation was 13 (median=12). Mean interval between time last-seen well and angiogram was 12.75 hours (median=10). Twenty-six patients (86.7%) presented with complete-to-near-complete vessel occlusion (thrombolysis in myocardial infarction [TIMI] 0/1); 4 had partial vessel occlusion (TIMI 2). Interventions included intra-arterial pharmacological thrombolysis (n=10), mechanical thrombectomy(n=21; Merci, 16; intracranial stent, 9; extracranial stent, 3), angioplasty (n=14; intracranial, 11; extracranial, 3). Nine patients received GPIIb/IIIa inhibitors (eptifibatide); all received heparin. Partial-to-complete recanalization (TIMI 2/3) was achieved in 20 patients (66.7%). Procedure-related complications included vascular perforations (n=3) and femoral access site complication (n=1). One patient had an embolic anterior cerebral artery infarct during intervention; another had progression of brain stem infarct. Symptomatic intracerebral hemorrhage occurred in 3 patients (10%), with 2 being primarily subarachnoid in location. Total in-hospital mortality including procedural mortality, disease progression, or other comorbidities was 23.3% (n=7). Mean discharge NIHSS was 9.5, representing an overall NIHSS 3.5-point improvement. Overall, mean modified Rankin score at death or last follow-up (mean=10.6 months) was 4.2. At 3 months, total mortality was 33.3% (n=10), 20% had modified Rankin score < or = 2, and 33% had modified Rankin score < or = 3. Among survivors, mean modified Rankin score at 3-month follow-up was 3. CONCLUSION: Our data show that delayed endovascular revascularization of carefully selected patients is safe, effective, and improves clinical outcome.

Acute ischemic stroke and thrombolysis location: comparing telemedicine and stroke center treatment outcomes.

BACKGROUND: Telemedicine has been increasingly used as an option for acute ischemic stroke treatment at hospitals where neurological expertise is not available. The aim of this study was to compare the outcome of stroke patients treated with systemic thrombolysis at our academic hub regional stroke centers (hub) versus our spoke hospital telemedicine locations (spoke) METHODS: Data were retrospectively reviewed for consecutive patients admitted for stroke treatment with intravenous tissue plasminogen activator at our hub (128 patients) and at the spoke centers (27 patients) over a 2-year period. Mortality was selected as a primary outcome measure, and post-thrombolysis intracranial hemorrhage (PT-ICH) rate, hospital length of stay (LOS), and discharge modified Rankin Scale (mRS) score were selected as secondary outcome measures. Logistic regression models were used to determine the effect of thrombolysis treatment site on stroke outcomes. RESULTS: Demographic and clinical variables of patients treated at the hub versus spoke sites were similar, except for a lower initial platelet count and a shorter time from ictus onset to needle in the spoke group. With covariates, the treatment site (hub vs spoke) did not have a significant impact on mortality (10.9% vs 11.1%; P = 0.34), nor on PT-ICH (20.3% vs 33.3%; P < 0.35). Site did not reach significance in affecting discharge outcome: 52.3% versus 51.9% of patients had good outcomes (mRS 0-3) and 47.7% versus 48.1% patients had poor outcomes (mRS, 4-6; P = 0.16). Length of stay was also not significantly affected by site: 8.8 days versus 10.7 days (P < 0.23). CONCLUSION: The hub-and-spoke telemedicine model for acute ischemic stroke treatment seems to carry similar efficacy and safety outcomes at the regional academic hub and spoke centers.

MRI assessment followed by successful mechanical recanalization of a complete tandem (internal carotid/middle cerebral artery) occlusion and reversal of a 10-hour fixed deficit.

BACKGROUND: Mechanical clot extraction up to 8 hours after stroke onset is an alternative strategy for opening large vessels, especially for patients ineligible for intravenous thrombolysis. Safety beyond this therapeutic window is untested. METHODS: An 81-year-old woman presented 8 hours after she developed left-sided weakness and dysarthria with a National Institutes of Health Stroke Scale (NIHSS) score fluctuating between 6 and 13. Neuroimaging revealed a large perfusion deficit with no diffusion abnormalities. An emergent cerebral angiogram revealed a complete internal carotid artery terminus occlusion. RESULTS: Successful mechanical thrombectomy was performed without complication and resulted in almost complete reversal of the patient's deficit to an NIHSS score of 1, 10 hours after stroke onset. CONCLUSION: Patients with large hypoperfused areas and minimal diffusion abnormalities on the MRI may benefit from mechanical thrombectomy beyond an 8-hour window.

The value of CT angiography and transcranial doppler sonography in triaging suspected cerebral vasospasm in SAH prior to endovascular therapy.

BACKGROUND: Transcranial Doppler sonography (TCD) is a noninvasive method for detecting arterial cerebral vasospasm (CVS) in aneurysmal subarachnoid hemorrhage (SAH). Computed tomographic angiography (CTA) has been increasingly used for CVS diagnosis. The purpose of this study was to evaluate the degree of agreement between TCD and CTA in diagnosing clinical CVS following SAH, and to define the role of CTA in triaging patients prior to digital subtraction angiography (DSA) and endovascular intervention. METHODS: Fifty-five consecutive patients with aneurysmal SAH who underwent sequential TCD and CTA were analyzed. TCD CVS was defined as anterior circulation peak mean velocity (PMV) >160 cm/s, basilar artery (BA) PMV >90 cm/s, and Lindegaard ratio (LR) >6. CTA CVS was defined as >50% luminal narrowing in the affected vessel. Clinical CVS was defined as the onset of new focal neurological deficit attributed to delayed ischemic injury. RESULTS: Thirteen patients (24%) had clinical CVS and 42 patients (76%) were asymptomatic. All patients with clinical CVS had also radiological evidence of CVS (agreement 100%). In 35 patients without clinical CVS, both tests agreed for absence of CVS in 28 cases (agreement 83%). The remaining 7 asymptomatic patients had radiological CVS only, in disagreement with clinical absence of CVS (17%). CONCLUSIONS: Clinical evaluation and TCD can reliably diagnose CVS in symptomatic patients and PMV >180 cm/s, or can rule out CVS in asymptomatic patients with PMV <140 cm/s. In this category of patients, adding a CTA to clinical evaluation and TCD may not be warranted.

Systemic hemostasis with recombinant-activated factor VII followed by local thrombolysis with recombinant tissue plasminogen activator in intraventricular hemorrhage.

INTRODUCTION: A 51-year-old woman on warfarin thromboprophylaxis for transient ischemic attacks developed sudden onset nausea, vomiting, and decreased mental status, rapidly becoming comatose. Head computed tomography (CT) showed intracerebral hemorrhage, extending into all ventricular chambers, and acute obstructive hematocephalus requiring urgent ventricular drainage. CT angiogram showed no evidence of an aneurysm or vascular malformation. METHODS: The pretreatment international normalized ratio (INR) of 4.9 was rapidly corrected with recombinant activated factor VII and an external ventricular drain was placed. Despite accurate positioning, the ventriculostomy thrombosed and became nonfunctional. Recombinant tissue plasminogen activator was given intraventricularly and resulted in partial ventricular decompression within 24 hours, with dramatic improvement in the patient's level of consciousness. RESULTS: Repeated intraventricular fibrinolysis resulted in further reduction of the intraventricular hematoma within a few days and a good patient outcome. The patient did not require permanent ventricular shunt. CONCLUSION: To our knowledge, this is the first reported case of combined systemic enhancement of hemostasis and local fibrinolysis as a life-saving measure in intracranial hemorrhage.

What proportion of stroke is not explained by classic risk factors?

Ischemic stroke is a complex entity with multiple etiologies and variable clinical manifestations. The most frequent cause of stroke is atherosclerosis of cerebral vasculature followed by cardioembolism. Two thirds of strokes are explained by identifiable risk factors. Age, hypertension, and nonvalvular atrial fibrillation are by far the most frequent and well documented ones. Approximately 5% of strokes are caused by conditions other than atherosclerosis or heart disease, i.e., cervical arteries dissections, nonatherosclerotic vasculopathies, infectious or systemic vasculitis, and collagen vascular diseases. In spite of a thorough diagnostic evaluation, 30% of strokes remain cryptogenic, i.e., no specific cause is identified and the classic risk factors are not present. Identification of unknown environmental or genetic risk factors should be the subject of further research.

The history of the development of the cerebellar examination.

The cerebellar examination evolved from observations of experimental lesions made by neurophysiologists and clinical descriptions of patients with trauma to the cerebellum. At the beginning of the 19th century, neurophysiologists such as Luigi Rolando, Marie-Jean-Pierre Flourens, and John Call Dalton, Jr. ablated portions of the cerebellum of a variety of animals and observed staggering gait, clumsiness, and falling from side to side without loss of strength. They concluded that the cerebellum coordinated voluntary movements. In 1899, Joseph Francois Félix Babinski observed that patients with cerebellar lesions could not execute complex movements without breaking down into their elemental movements and described the defect as dysmetria. In 1902, Babinski coined the term dysdiodochokinesis to describe the inability to perform rapid execution of movements requiring alternate contractions of agonist and antagonist muscles. Gordon Holmes in 1904 described the phenomena of rebound, noting that if a limb ipsilateral to a cerebellar lesion is suddenly released from tension, the appendage will flail. In 1917, Gordon Holmes reported hypotonia and dysmetria in men wounded by gunshot wounds to their cerebellum. These observations were rapidly included in descriptions of the cerebellar examination in popular contemporaneous textbooks of neurology. Modern observations have demonstrated that the cerebellum influences such cognitive functions such as planning, verbal fluency, abstract reasoning, prosody, and use of correct grammar.