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Aneesh B Singhal

Publications and source records attributed to Aneesh B Singhal.

At least 19 recordsLinked to original sources
PubMed2007

Narrative review: reversible cerebral vasoconstriction syndromes.

Reversible cerebral vasoconstriction syndromes (RCVS) comprise a group of diverse conditions, all characterized by reversible multifocal narrowing of the cerebral arteries heralded by sudden (thunderclap), severe headaches with or without associated neurologic deficits. Reversible cerebral vasoconstriction syndromes are clinically important because they affect young persons and can be complicated by ischemic or hemorrhagic strokes. The differential diagnosis of RCVS includes conditions associated with thunderclap headache and conditions that cause irreversible or progressive cerebral artery narrowing, such as intracranial atherosclerosis and cerebral vasculitis. Misdiagnosis as primary cerebral vasculitis and aneurysmal subarachnoid hemorrhage is common because of overlapping clinical and angiographic features. However, unlike these more ominous conditions, RCVS is usually self-limited: Resolution of headaches and vasoconstriction occurs over a period of days to weeks. In this review, we describe our current understanding of RCVS; summarize its key clinical, laboratory, and imaging features; and discuss strategies for diagnostic evaluation and treatment.

Cerebral Arterial Diseases↗
PubMed2006

The real estate factor: quantifying the impact of infarct location on stroke severity.

BACKGROUND AND PURPOSE: The severity of the neurological deficit after ischemic stroke is moderately correlated with infarct volume. In the current study, we sought to quantify the impact of location on neurological deficit severity and to delineate this impact from that of volume. METHODS: We developed atlases consisting of location-weighted values indicating the relative importance in terms of neurological deficit severity for every voxel of the brain. These atlases were applied to 80 first-ever ischemic stroke patients to produce estimates of clinical deficit severity. Each patient had an MRI and National Institutes of Health Stroke Scale (NIHSS) examination just before or soon after hospital discharge. The correlation between the location-based deficit predictions and measured neurological deficit (NIHSS) scores were compared with the correlation obtained using volume alone to predict the neurological deficit. RESULTS: Volume-based estimates of neurological deficit severity were only moderately correlated with measured NIHSS scores (r=0.62). The combination of volume and location resulted in a significantly better correlation with clinical deficit severity (r=0.79, P=0.032). CONCLUSIONS: The atlas methodology is a feasible way of integrating infarct size and location to predict stroke severity. It can estimate stroke severity better than volume alone.

Aged↗
PubMed2006

Effects of common medications on cerebral vasospasm after subarachnoid haemorrhage.

Cerebral vasospasm is a common and serious complication of aneurysmal subarachnoid haemorrhage (SAH). At present, no consistently effective preventative and therapeutic measures are available, perhaps because of incomplete understanding of the pathogenesis of vasospasm. Experimental studies provide evidence that the incidence and severity of vasospasm after SAH can be modulated by drugs that affect neurotransmitter levels, intracellular signalling mechanisms, vascular smooth muscle function, inflammation and cellular proliferation, and the concentration of 'spasmogenic' factors. Preliminary clinical studies indicate that some illicit drugs and common prescription medications can have similar effects in humans. Recognition of these pharmacological effects is important because medications that can worsen or alleviate vasospasm are frequently administered to SAH patients to treat coincident medical problems.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

A pilot study of normobaric oxygen therapy in acute ischemic stroke.

BACKGROUND AND PURPOSE: Therapies that transiently prevent ischemic neuronal death can potentially extend therapeutic time windows for stroke thrombolysis. We conducted a pilot study to investigate the effects of high-flow oxygen in acute ischemic stroke. METHODS: We randomized patients with acute stroke (<12 hours) and perfusion-diffusion "mismatch" on magnetic resonance imaging (MRI) to high-flow oxygen therapy via facemask for 8 hours (n=9) or room air (controls, n=7). Stroke scale scores and MRI scans were obtained at baseline, 4 hours, 24 hours, 1 week, and 3 months. Clinical deficits and MR abnormalities were compared between groups. RESULTS: Stroke scale scores were similar at baseline, tended to improve at 4 hours (during therapy) and 1 week, and significantly improved at 24 hours in hyperoxia-treated patients. There was no significant difference at 3 months. Mean (+/-SD) relative diffusion MRI lesion volumes were significantly reduced in hyperoxia-treated patients at 4 hours (87.8+/-22% versus 149.1+/-41%; P=0.004) but not subsequent time points. The percentage of MRI voxels improving from baseline "ischemic" to 4-hour "non-ischemic" values tended to be higher in hyperoxia-treated patients. Cerebral blood volume and blood flow within ischemic regions improved with hyperoxia. These "during-therapy" benefits occurred without arterial recanalization. By 24 hours, MRI showed reperfusion and asymptomatic petechial hemorrhages in 50% of hyperoxia-treated patients versus 17% of controls (P=0.6). CONCLUSIONS: High-flow oxygen therapy is associated with a transient improvement of clinical deficits and MRI abnormalities in select patients with acute ischemic stroke. Further studies are warranted to investigate the safety and efficacy of hyperoxia as a stroke therapy.

Adult↗
PubMed2005

Normobaric hyperoxia extends the reperfusion window in focal cerebral ischemia.

A major limitation in thrombolysis for acute ischemic stroke is the restricted time window for safe and effective therapy. Any method that can extend the reperfusion time window would be important. In this study, we show that normobaric hyperoxia extends the time window for effective reperfusion from 1 to 3 hours in rats subjected to focal cerebral ischemia. Normobaric hyperoxia did not increase cellular markers of superoxide generation or brain levels of matrix metalloproteinase-9. Normobaric hyperoxia may be a clinically feasible adjunct method for significantly increasing the time window for effective thrombolytic therapy in acute ischemic stroke.

Animals↗
PubMed2005

Advances in stroke neuroprotection: hyperoxia and beyond.

Refinements in patient selection, improved methods of drug delivery, use of more clinically relevant animal stroke models, and the use of combination therapies that target the entire neurovascular unit make stroke neuroprotection an achievable goal. This article provides an overview of the major mechanisms of neuronal injury and the status of neuroprotective drug trials and reviews emerging strategies for treatment of acute ischemic stroke. Advances in the fields of stem cell transplantation, stroke recovery, molecular neuroimaging, genomics, and proteomics will provide new therapeutic avenues in the near future. These and other developments over the past decade raise expectations that successful stroke neuroprotection is imminent.

Brain↗
PubMed2005

Relationship between hyperglycemia and symptomatic vasospasm after subarachnoid hemorrhage.

OBJECTIVE: To determine the relationship between blood glucose levels (mg/dL) and occurrence of symptomatic vasospasm (VSP) and clinical outcomes after aneurysmal subarachnoid hemorrhage. DESIGN: Retrospective observational study of 352 patients with subarachnoid hemorrhage admitted within 48 hrs of ictus between January 1995 and June 2002. SETTING: Neurointensive care unit. PATIENTS: Adult patients admitted after subarachnoid hemorrhage. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Variables included age; Hunt-Hess classification score; Fisher group; insulin use; infectious disease status; history of diabetes mellitus; and blood glucose values. Poor clinical outcome was defined by a modified Rankin score > or =3, and hyperglycemia was defined by a blood glucose level >140 mg/dL. Mean daily blood glucose values were assessed from admission to development of VSP or day 14. Mean admission blood glucose value, mean inpatient blood glucose value, insulin use, infectious disease status, Hunt-Hess classification score, Fisher group, and history of diabetes mellitus were entered in a Cox proportional hazards model. VSP occurred in 103 (29.2%) of 352 patients. Mean admission blood glucose values (176.6 +/- 40.3 mg/dL vs. 162.3 +/- 47.8 mg/dL; p = .01) and mean inpatient blood glucose values (166.2 +/- 24.7 mg/dL vs. 155.8 +/- 29.7 mg/dL; p = .001) were significantly higher in patients with VSP. Mean inpatient blood glucose value (relative risk, 1.01; 95% confidence interval, 1.0-1.03; p = .04), Hunt-Hess classification score > or =3 (relative risk, 2.23; 95% confidence interval, 1.21-3.99; p = .02), and Fisher group score of 3 (relative risk, 1.28; 95% confidence interval, 1.15-3.1; p = .05) increased the risk for VSP. Hyperglycemia was associated with longer length of stay in the neurointensive care unit (14.5 +/- 7.1 days vs. 11.6 +/- 5.4 days; p < .001) and poor outcome at discharge (modified Rankin score > or =3: 58.9% vs. 18.8%; p < .001). CONCLUSIONS: Mean inpatient blood glucose value is associated with the development of VSP and may represent a target for therapy to prevent VSP and improve clinical outcomes.

Blood Glucose↗
PubMed2005

Reversible posterior leukoencephalopathy, cerebral vasoconstriction, and strokes after intravenous immune globulin therapy in guillain-barre syndrome.

The authors report a patient with Guillain-Barré syndrome who developed acute hypertension, reversible posterior leukoencephalopathy syndrome, ischemic and hemorrhagic strokes, and reversible cerebral arterial vasoconstriction shortly after initiating intravenous immune globulin therapy. Possible interrelationships and mechanisms of these complications are discussed.

Aged↗
PubMed2005

Postpartum angiopathy and other cerebral vasoconstriction syndromes.

The phenomenon of reversible cerebral arterial segmental vasoconstriction has been associated with several conditions including pregnancy and puerperium ("postpartum angiopathy"), thunderclap headache, and use of vasoconstrictive medications. Patients with cerebral vasoconstriction typically present with sudden, severe, and recurrent ("thunderclap") headaches and can develop strokes. Cerebral vasoconstriction syndromes are under- recognized, are poorly characterized, and are frequently misdiagnosed as primary cerebral vasculitis. This article presents an illustrative case report and reviews the historical aspects, clinical and imaging characteristics, etiology, differential diagnosis, management, and prognosis of cerebral vasoconstriction syndromes.

Adult↗
PubMed2004

Postpartum angiopathy with reversible posterior leukoencephalopathy.

BACKGROUND: Postpartum angiopathy (PPA) is a cerebral vasoconstriction syndrome of uncertain cause that affects large and medium-sized cerebral arteries. Postpartum angiopathy is frequently complicated by ischemic stroke. The reversible posterior leukoencephalopathy syndrome (RPLS) is a distinct clinical-radiological entity characterized by transient vasogenic edema on brain imaging. The pathophysiological features of RPLS are related to small-vessel dysfunction and breakdown of the blood-brain barrier. OBJECTIVES: To report the coexistence of PPA and RPLS in 4 patients and to discuss possible interrelationships between these 2 entities. DESIGN: Four case reports and a review of the literature. RESULTS: Four women developed a clinical-radiological syndrome overlapping PPA and eclampsia shortly after an uncomplicated pregnancy. All had acute severe ("thunderclap") headaches and hypertension. Three developed seizures. All patients had reversible angiographic narrowing of large and medium-sized cerebral arteries. Serial magnetic resonance imaging showed transient nonischemic brain lesions, resembling the lesions described in patients with RPLS. The results of extensive tests for cerebral vasculitis were negative. CONCLUSION: These cases, and the literature, suggest an interrelationship between RPLS and cerebral vasoconstriction syndromes such as PPA.

Adult↗
PubMed2004

Spontaneous hyperacute postischemic hemorrhage leading to death.

Hyperacute, spontaneous, and severe parenchymal postischemic hemorrhage is considered rare but might be frequently misdiagnosed as primary intracerebral hemorrhage. The authors report 2 patients with catastrophic postischemic hemorrhage unrelated to anticoagulation, thrombolytics, or coagulopathy. Patient 1 was a 73-year-old woman with left posterior frontal lobe infarction, followed at 5.5 hours by massive postischemic hemorrhage leading to death. Patient 2 was a 52-year-old man with recent brain irradiation who developed left middle cerebral artery occlusion and basal ganglia infarction. Initial gradient-echo magnetic resonance imaging (MRI) showed petechial hemorrhage within areas of infarction and widespread old microbleeds. He developed massive postischemic hemorrhage at 12 hours, leading to death. The authors conclude that early brain imaging is essential to distinguish postischemic from primary brain hemorrhage. In patients with ischemic stroke, MRI findings such as hyperacute petechial hemorrhage or chronic cerebral microbleeds might predict subsequent parenchymal hemorrhage and thus have implications for tissue plasminogen activator use.

Acute Disease↗
PubMed2004

Effect of clipping, craniotomy, or intravascular coiling on cerebral vasospasm and patient outcome after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Although several recent studies have suggested that the incidence of vasospasm after aneurysmal subarachnoid hemorrhage is lower in patients undergoing aneurysmal coiling as compared with clipping, other studies have had conflicting results. We reviewed our experience over 8 years and assessed whether clipping, craniotomy, or coiling affects patient outcomes or the risk for vasospasm. METHODS: We included 515 patients with aneurysmal subarachnoid hemorrhage, identified prospectively from November 2000 to February 2003 (243 patients) and retrospectively from November 1995 to October 2000 (272 patients), by using International Classification of Diseases, 9th Revision, codes for subarachnoid hemorrhage. We classified patients as follows: clipping (413 patients), coiling (79 patients), and craniotomy (436 patients, including all 413 patients who underwent clipping plus 23 who underwent coiling as well as craniotomy for various reasons). We studied four outcome measures: total vasospasm, symptomatic vasospasm, poor outcome (modified Rankin score 3-6), and in-hospital mortality. To assess the risk of total vasospasm and symptomatic vasospasm, we performed multivariate regression analyses adjusting for age, Fisher grade, Hunt and Hess grade, aneurysm location (anterior versus posterior circulation), and aneurysm treatment modality. To assess the risk for poor outcome and in-hospital mortality, we adjusted for all the above variables as well as for total and symptomatic vasospasm. RESULTS: In the clipping group there was 63% total vasospasm and 28% symptomatic vasospasm; in the coiling group there was 54% total vasospasm and 33% symptomatic vasospasm; and in the craniotomy group there was 64% total vasospasm and 28% symptomatic vasospasm. In the multivariate analysis, age <50 years (P = 0.0099) and Fisher Grade 3 (P < 0.00001) predicted total vasospasm, and Fisher Grade 3 (P < 0.000001) and Hunt and Hess Grade IV or V (P = 0.018) predicted symptomatic vasospasm. Predictors of poor outcome were age >or=50 years (P < 0.0001), Fisher Grade 3 (P = 0.0072), Hunt and Hess Grade IV or V (P < 0.00001), symptomatic vasospasm (P < 0.0001), and coiling (P = 0.0314 versus clipping and P = 0.045 versus craniotomy). Predictors of in-hospital mortality were age >or= 50 years (P = 0.0030), Hunt and Hess Grade IV or V (P = 0.0001), symptomatic vasospasm (P < 0.00001), and coiling (P = 0.008 versus clipping and P = 0.0013 versus craniotomy). There was no significant difference in total vasospasm or symptomatic vasospasm when patients who underwent clipping or craniotomy were compared with patients who underwent coiling. In patients with Hunt and Hess Grade I to III ("good grade"), clipping and craniotomy were associated with better outcome and less in-hospital mortality, but there was no difference in total vasospasm or symptomatic vasospasm versus coiling. In patients with Hunt and Hess Grade IV or V ("poor grade"), there was no difference in any outcome measure among the treatment groups. CONCLUSION: In a single-center, retrospective, nonrandomized study, performance of clipping and/or craniotomy had significantly better outcome and lower mortality at discharge than coiling in good-grade patients but had no effect on total vasospasm or symptomatic vasospasm in good- or poor-grade patients.

Craniotomy↗
PubMed2004

Cerebral vasoconstriction syndromes.

Stroke from reversible cerebral arterial vasoconstriction has been described in a variety of conditions, including migraine, pregnancy, puerperium (postpartum angiopathy), use of vasoconstrictive drugs, Call-Fleming syndrome, and benign angiopathy of the central nervous system. Although vasoconstriction is an important cause of ischemic and hemorrhagic stroke in young individuals, vasoconstriction syndromes have not been well characterized and remain under-recognized. Misdiagnosis is common because the clinical and radiological features can overlap with conditions such as primary cerebral vasculitis. With the advent of newer, noninvasive angiography techniques and the escalating use of vasoactive drugs, it is likely that clinicians will encounter more patients with vasoconstriction-induced stroke. This article reviews the history, clinical and radiological characteristics, differential diagnosis, and management of cerebral vasoconstriction syndromes.

Cerebral Arteries↗
PubMed2003

Correlation between brain reorganization, ischemic damage, and neurologic status after transient focal cerebral ischemia in rats: a functional magnetic resonance imaging study.

The pattern and role of brain plasticity in stroke recovery has been incompletely characterized. Both ipsilesional and contralesional changes have been described, but it remains unclear how these relate to functional recovery. Our goal was to correlate brain activation patterns with tissue damage, hemodynamics, and neurologic status after temporary stroke, using functional magnetic resonance imaging (fMRI). Transverse relaxation time (T2)-weighted, diffusion-weighted, and perfusion MRI were performed at days 1 (n = 7), 3 (n = 7), and 14 (n = 7) after 2 hr unilateral middle cerebral artery occlusion in rats. Functional activation and cerebrovascular reactivity maps were generated from contrast-enhanced fMRI during forelimb stimulation and hypercapnia, respectively. Before MRI, rats were examined neurologically. We detected loss of activation responses in the ipsilesional sensorimotor cortex, which was related to T2 lesion size (r = -0.858 on day 3, r = -0.979 on day 14; p < 0.05). Significant activation responses in the contralesional hemisphere were detected at days 1 and 3. The degree of shift in balance of activation between the ipsilesional and contralesional hemispheres, characterized by the laterality index, was linked to the T2 and apparent diffusion coefficient in the ipsilesional contralesional forelimb region of the primary somatosensory cortex and primary motor cortex at day 1 (r = -0.807 and 0.782, respectively; p < 0.05) and day 14 (r = -0.898 and -0.970, respectively; p < 0.05). There was no correlation between activation parameters and perfusion status or cerebrovascular reactivity. Finally, we found that the laterality index and neurologic status changed in parallel over time after stroke, so that when all time points were grouped together, neurologic status was inversely correlated with the laterality index (r = -0.571; p = 0.016). This study suggests that the degree of shift of activation balance toward the contralesional hemisphere early after stroke increases with the extent of tissue injury and that functional recovery is associated mainly with preservation or restoration of activation in the ipsilesional hemisphere.

Animals↗
PubMed2003

Subarachnoid hemorrhage without evident cause on initial angiography studies: diagnostic yield of subsequent angiography and other neuroimaging tests.

OBJECT: The aim of this study was to assess the diagnostic yield of imaging tests performed in patients in whom the cause of subarachnoid hemorrhage (SAH) had not been demonstrated on initial angiography. METHODS: By reviewing medical records of 806 patients with SAH who had been admitted during a 6.5-year period, the authors identified 86 in whom initial transfemoral catheter angiography failed to reveal the cause of SAH. Clinical and radiological data were analyzed to determine the diagnostic yield of subsequent catheter angiography, computerized tomography (CT) angiography, magnetic resonance (MR) angiography, and MR imaging of the brain and spine for various subtypes of SAH (bleeding not visualized on CT studies [CT-negative SAH], perimesencephalic SAH, and nonperimesencephalic SAH). Of 41 patients with nonperimesencephalic SAH, 36, 32, and 21 underwent repeated catheter angiography, CT angiography, and MR angiography, respectively; brain MR imaging was performed in 23 patients (18 with Gd and 15 with susceptibility contrast sequences), and spine MR imaging in 17. Of 36 patients with perimesencephalic SAH, 31, 23, and 17 underwent repeated catheter angiography, CT angiography, and MR angiography, respectively; brain MR imaging was performed in 18 patients (17 with Gd and 11 with susceptibility contrast sequences), and spine MR imaging in 14. Of nine patients with SAH not visualized on CT scanning, three, one, and six underwent repeated catheter angiography, CT angiography, and MR angiography, respectively; brain MR imaging was performed in eight patients (five with Gd and three with susceptibility contrast sequences), and spine MR imaging in seven. The cause of SAH could be determined in only four patients, all with nonperimesencephalic SAH. The only test that yielded a diagnosis was catheter angiography (three aneurysms on the second and one on the third angiography, all surgically secured). Diffusion-weighted MR imaging demonstrated small, deep infarcts in five patients. CONCLUSIONS: Repeated catheter angiography remains the most sensitive test to determine the cause of SAH that is not demonstrated on initial angiography, particularly in the subtype of nonperimesencephalic SAH. Newer, noninvasive imaging techniques provide little diagnostic yield.

Adult↗
PubMed2003

Diffusion-weighted magnetic resonance imaging abnormalities in Bartonella encephalopathy.

The authors describe 2 patients with new-onset, refractory status epilepticus and serological evidence for Bartonella infection. Brain magnetic resonance imaging (MRI) in patient 1 showed transient diffusion abnormalities in the posterior (pulvinar) thalami. In patient 2, brain MRI showed several enhancing cortical lesions, of which one lesion was bright on diffusion-weighted imaging (DWI). In patients with unexplained, refractory seizures, the presence of DWI abnormalities warrants a search for unusual infectious or inflammatory disorders, like Bartonella encephalitis.

Adult↗
PubMed2002

Diffusion MRI in three types of anoxic encephalopathy.

We report the clinical and diffusion-weighted MRI (DWI) features of three patients with different types of anoxic brain injury: attempted hanging (hypoxic hypoxia), carbon monoxide poisoning (histotoxic hypoxia), and hanging with cardiac arrest (hypoxic-ischemic encephalopathy, HIE). The first two patients, but not the third, recovered substantial neurological function. The distribution of DWI abnormalities was different and correlated well with the distinct neuropathological features of these entities. The prognosis after anoxic encephalopathy depends on the underlying mechanism and its severity, which may be reflected by DWI abnormalities.

Adolescent↗