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Dive into the research topics where Vani Rao is active.

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Featured researches published by Vani Rao.


Biological Psychiatry | 2007

Neuropsychological Functioning in Bipolar Disorder and Schizophrenia

David J. Schretlen; Nicola G. Cascella; Stephen M. Meyer; Lisle Kingery; S. Marc Testa; Cynthia A. Munro; Ann E. Pulver; Paul Rivkin; Vani Rao; Catherine M. Diaz-Asper; Faith Dickerson; Robert H. Yolken; Godfrey D. Pearlson

BACKGROUND Some patients with bipolar disorder (BD) demonstrate neuropsychological deficits even when stable. However, it remains unclear whether these differ qualitatively from those seen in schizophrenia (SZ). METHODS We compared the nature and severity of cognitive deficits shown by 106 patients with SZ and 66 patients with BD to 316 healthy adults (NC). All participants completed a cognitive battery with 19 individual measures. After adjusting their test performance for age, sex, race, education, and estimated premorbid IQ, we derived regression-based T-scores for each measure and the six cognitive domains. RESULTS Both patient groups performed significantly worse than NCs on most (BD) or all (SZ) cognitive tests and domains. The resulting effect sizes ranged from .37 to 1.32 (mean=.97) across tests for SZ patients and from .23 to .87 (mean=.59) for BD patients. The Pearson correlation of these effect sizes was .71 (p<.001). CONCLUSIONS Patients with bipolar disorder suffer from cognitive deficits that are milder but qualitatively similar to those of patients with schizophrenia. These findings support the notion that schizophrenia and bipolar disorder show greater phenotypic similarity in terms of the nature than severity of their neuropsychological deficits.


Psychosomatics | 2009

Neuropsychiatric Problems After Traumatic Brain Injury: Unraveling the Silent Epidemic

Sandeep Vaishnavi; Vani Rao; Jesse R. Fann

BACKGROUND Traumatic brain injury (TBI) is a significant public health concern. According to the Centers for Disease Control and Prevention, about 1.4 million people in the United States sustain a TBI annually. OBJECTIVE This review places particular emphasis on the current knowledge of effective treatment of TBI symptoms, and proposes directions for future research. RESULTS Neuropsychiatric problems are more prevalent and longer-lasting in TBI patients than in the general population. About 40% of TBI victims suffer from two or more psychiatric disorders, and a similar percentage experience at least one unmet need for cognitive, emotional, or job assistance 1 year after injury. The entire spectrum of TBI severity, from mild to severe, is associated with an increase in psychiatric conditions. CONCLUSION Despite the high incidence of severe consequences of TBI, there are scarce empirical data to guide psychiatric treatment. Some approaches that have been helpful include cognitive and behavioral therapy and pharmacologic treatment. The authors list specific research recommendations that could further identify useful therapeutic interventions.


International Journal of Geriatric Psychiatry | 2000

The benefits and risks of ECT for patients with primary dementia who also suffer from depression

Vani Rao; Constantine G. Lyketsos

Major depression afflicts 20–25% of patients with dementia. Of these, about a third do not improve with antidepressant therapy and may be suitable candidates for electronconvulsive treatment (ECT). However, the use of ECT is dementia patients is concerning due to possible adverse effects on memory and cognition. Outcome studies of ECT in patients with primary dementia and depression are very rare.


Journal of Neuropsychiatry and Clinical Neurosciences | 2009

Aggression after traumatic brain injury: prevalence and correlates

Vani Rao; Paul A. Rosenberg; Melaine Bertrand; Saeed Salehinia; Jennifer Spiro; Sandeep Vaishnavi; Pramit Rastogi; Kathy Noll; David J. Schretlen; Jason Brandt; Edward E. Cornwell; Michael Makley; Quincy Samus Miles

Aggression after traumatic brain injury (TBI) is common but not well defined. Sixty-seven participants with first-time TBI were evaluated for aggression within 3 months of injury. The prevalence of aggression was found to be 28.4%, predominantly verbal aggression. Post-TBI aggression was associated with new-onset major depression (p=0.02), poorer social functioning (p=0.04), and increased dependency in activities of daily living (p=0.03), but not with a history of substance abuse or adult/childhood behavioral problems. Implications of the study include early screening for aggression, evaluation for depression, and consideration of psychosocial support in aggressive patients.


Epilepsy Research | 2002

Psychiatric complications in patients with epilepsy: a review

Laura Marsh; Vani Rao

At least 50-60% of patients with epilepsy develop psychiatric disturbances, particularly mood, anxiety, and psychotic disorders. This article, aimed at the non-psychiatric clinician, reviews the differential diagnosis and treatment of psychiatric disturbances in epilepsy and focuses on the evaluation of psychiatric phenomena relative to the ictal state or the periictal and interictal periods. Pharmacological and non-pharmacological therapies are reviewed. A final section discusses potential interactions between antiepileptic and psychiatric medications.


Brain Injury | 2008

Prevalence and types of sleep disturbances acutely after traumatic brain injury

Vani Rao; Jennifer Spiro; Sandeep Vaishnavi; Pramit Rastogi; Michelle M. Mielke; Kathy Noll; Edward E. Cornwell; David J. Schretlen; Michael Makley

Primary objective: To assess the prevalence of and risk factors for sleep disturbances in the acute post-traumatic brain injury (TBI) period. Research design: Longitudinal, observational study. Methods and procedures: Fifty-four first time closed-head injury patients were recruited and evaluated within 3 months after injury. Pre-injury and post-injury sleep disturbances were compared on the Medical Outcome Scale for Sleep. The subjects were also assessed on anxiety, depression, medical comorbidity and severity of TBI. Main outcomes and results: Subjects were worse on most sleep measures after TBI compared to before TBI. Anxiety disorder secondary to TBI was the most consistent significant risk factor to be associated with worsening sleep status. Conclusions: Anxiety is associated with sleep disturbances after TBI. Further studies need to be done to evaluate if this is a causal relationship.


Neuropsychology (journal) | 2007

Serum uric acid and cognitive function in community-dwelling older adults

David J. Schretlen; Anjeli B. Inscore; H.A. Jinnah; Vani Rao; Barry Gordon; Godfrey D. Pearlson

Among possible markers of age-related cognitive decline, uric acid (UA) is controversial because it has antioxidant properties but is increased in diseases that often lead to cognitive impairment. In this study of 96 elderly adults, participants with mildly elevated (but normal) serum UA were 2.7 to 5.9 times more likely to score in the lowest quartile of the sample on measures of processing speed, verbal memory, and working memory. Even after controlling for age, sex, race, education, diabetes, hypertension, smoking, and alcohol abuse, the multivariate-adjusted odds of poor verbal memory and working memory remained significant (ps < .05). Despite its antioxidant properties, these findings suggest that even mild elevations of UA might increase the risk of cognitive decline among older adults.


Psychiatric Clinics of North America | 2002

PSYCHIATRIC ASPECTS OF TRAUMATIC BRAIN INJURY

Vani Rao; Constantine G. Lyketsos

TBI is a complex heterogenous disease that can produce a variety of psychiatric disturbances, ranging from subtle deficits in cognition, mood, and behavior to severe disturbances that cause impairment in social, occupational, and interpersonal functioning. With improvement and sophistication in acute trauma care, a number of individuals are able to survive the trauma but are left with several psychiatric sequelae. It is important for psychiatrists to be aware of this entity because an increasing number of psychiatrists will be involved in the care of these patients. Treatment should be interdisciplinary and multifaceted, with the psychiatrist working in collaboration with the patient, caregiver, family, other physicians, and therapists. The goal of treatment should be to stabilize symptoms; maximize potential; minimize disability; and increase productivity socially, occupationally, and interpersonally.


Schizophrenia Research | 2010

Gray-matter abnormalities in deficit schizophrenia.

Nicola G. Cascella; Vani Rao; Godfrey D. Pearlson; Akira Sawa; David J. Schretlen

Deficit schizophrenia (D-SZ) has been proposed as a putative disease subtype defined by prominent, primary negative symptoms that endure as trait-like features during periods of clinical stability. In this study, we acquired magnetic resonance images of the whole brain using a 1.5 T scanner in 19 outpatients with D-SZ, 31 with non-deficit schizophrenia (ND-SZ), and 90 healthy adults. Voxel-based morphometry was used to investigate differences in regional gray-matter volume (GMV) between outpatients with D-SZ and ND-SZ, and between the combined patient subgroups and healthy adults. Compared to healthy adults outpatients with schizophrenia showed GMV reductions, especially in left frontal and temporal cortices and in the left insula. The D-SZ subgroup showed reduced GMV in the insula bilaterally and in the left superior frontal, middle temporal and occipital gyri. Regions in which GMV reductions best distinguished D-SZ from ND-SZ patients included the superior frontal gyrus (Brodmann area 8) and superior temporal gyrus (Brodmann areas 22, 38) bilaterally, the left supplementary motor area (Brodmann area 6), left anterior cingulate, left cuneus and right putamen. These results suggest that patients with deficit schizophrenia have brain abnormalities that differ from those of patients with non-deficit schizophrenia. Further, the neuroanatomic differences between these two putative subtypes of schizophrenia involve brain regions that appear to be associated with the negative symptoms that define the deficit syndrome of schizophrenia.


Neurology | 2004

Dementia in hippocampal sclerosis resembles frontotemporal dementia more than Alzheimer disease

David M. Blass; Kimmo J. Hatanpaa; Jason Brandt; Vani Rao; Martin Steinberg; Juan C. Troncoso; Peter V. Rabins

Objective: To characterize the clinical course of pathologically diagnosed hippocampal sclerosis dementia (HSD). Background: Dementia associated with HSD is incompletely characterized. Previous studies suggest similarities to both Alzheimer disease (AD) and frontotemporal dementia (FTD). Methods: Case-control analysis of the clinical course of patients with HSD, FTD, and AD from a neuropathology autopsy series conducted by a university hospital. Case histories were reviewed. Cumulative prevalence of behavioral, cognitive, psychiatric, and language symptoms were compared between groups, as was time of symptom onset. Clinical diagnostic criteria for FTD and AD were applied to case histories. Sensitivity and specificity of clinical FTD diagnostic criteria (Report of the Work Group on FTD and Pick’s disease) were computed. Results: Cumulative prevalence of symptoms in HSD was most similar to that of FTD and differed from AD. Behavioral abnormalities such as decreased grooming and inappropriate behavior were more prevalent in HSD and FTD than AD. Hyperorality, inappropriate behavior, and decreased interest had earlier onset in HSD and FTD. Cognitive symptoms of disorientation, dyscalculia, apraxia, and agnosia were more prevalent in AD, as were psychiatric symptoms of hallucinations, delusions, and aggression. Most HSD patients met diagnostic criteria for FTD. Criteria sensitivity was 64.0% and specificity was 73.7%. Conclusions: FTD is a clinical syndrome associated with heterogeneous neuropathology. The clinical course of HSD is more similar to that of FTD than AD. These findings, together with the neuropathologic data presented in the accompanying article, support expanding the scope of FTD (Pick complex) to include HSD.

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Constantine G. Lyketsos

Johns Hopkins University School of Medicine

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David J. Schretlen

Johns Hopkins University School of Medicine

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Jennifer Spiro

Johns Hopkins University

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Durga Roy

Johns Hopkins University School of Medicine

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Matthew E. Peters

Johns Hopkins University School of Medicine

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Una D. McCann

Johns Hopkins University School of Medicine

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Jason Brandt

Johns Hopkins University School of Medicine

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