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Dive into the research topics where Stephanie Krüger is active.

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Featured researches published by Stephanie Krüger.


Neuroreport | 2001

Lower dopamine transporter binding potential in striatum during depression.

Jeffrey H. Meyer; Stephanie Krüger; Alan A. Wilson; Bruce K. Christensen; Verdell S. Goulding; Ayal Schaffer; Candace E. Minifie; Sylvain Houle; Doug Hussey; Sidney H. Kennedy

Previous studies suggest that there is a dopamine lowering process during major depressive episodes (MDE). To investigate this, we measured the dopamine transporter binding potential (DAT BP) in the striatum of depressed and healthy subjects using [11C]RTI-32 PET. The DAT, a predominantly presynaptic receptor, decreases in density after chronic dopamine depletion and the BP is proportional to receptor density. In all striatal regions, subjects with MDE had significantly lower DAT BP. Low striatal DAT BP in MDE is consistent with a downregulation of DAT in response to a dopamine lowering process. There was also a strong, highly significant, inverse correlation between striatal DAT BP and neuropsychological tests of dopamine-implicated symptoms in patients (i.e. patients with lower DAT BP performed better). Lower DAT BP itself reduces extracellular clearance of dopamine. Patients who did not decrease their striatal DAT BP failed to compensate for low dopamine and showed greater impairment on dopamine related tests.


Journal of Affective Disorders | 1995

Comorbidity of obsessive compulsive disorder in bipolar disorder

Stephanie Krüger; Robert G. Cooke; Gary Hasey; Thecla Jorna; Emmanuel Persad

The comorbidity of OCD and bipolar disorder has not been systematically examined. Therefore, we determined the frequency of patients meeting DSM-III criteria for OCD syndrome in a sample of 149 inpatients with DSM-III major affective disorder who had received a clinically reviewed structured diagnostic interview. The frequency of OCD syndrome was not significantly different between subjects with major depression (35.2%, n = 105) and bipolar disorder (35.1%, n = 37). This suggests that OCD is equally common in bipolar as in unipolar patients.


Cns Spectrums | 2000

Catatonia in affective disorder: new findings and a review of the literature.

Stephanie Krüger; Peter Bräunig

The historical development of the concept of catatonia in affective disorders and contemporary papers on this topic are reviewed. In addition, data from a current study on the frequency of catatonia in mixed mania are reported. Differences between catatonic and noncatatonic patients with mixed mania are presented and their relevance to clinical practice is discussed.


Journal of Psychopharmacology | 2003

Levetiracetam in the treatment of rapid cycling bipolar disorder.

Peter Bräunig; Stephanie Krüger

Levetiracetam (LEV) is a novel anticonvulsant that is currently investigated in bipolar disorder. It may be useful in the treatment of refractory and complicated cases, in which conventional mood stabilizers are not effective. We report two cases of rapid cycling bipolar disorder in which the add-on of LEV to a conventional treatment regimen improved symptoms of depression, as well as those of mania/mixed mania, and disrupted the severe rapid cycling pattern.


Comprehensive Psychiatry | 1996

An investigation of the self-report manic inventory as a diagnostic and severity scale for mania

Peter Bräunig; Gerald Shugar; Stephanie Krüger

The initial study on the Self-Report Manic Inventory (SRMI) reported that it reliably diagnosed mania. In the current study, we replicated the initial study on the SRMI. We also evaluated its ability to quantify manic symptomatology and to measure change during inpatient treatment. The findings show that manic patients are capable of reporting their symptoms, regardless of their insight into their condition. They also confirm that the SRMI is a reliable diagnostic instrument and that it performs consistently over time when used with a 1-week time format. The SRMI is also sensitive to clinical improvement in hospitalized patients undergoing treatment. The SRMI correlated well with the Young Mania-Rating Scale (YMRS), which served as an external validator of SRMI scores at the beginning and end of hospitalization. Factor analysis produced two groups of manic subjects who closely resemble the hedonistic euphoric type and the energized dysphoric type initially reported by Shugar et al.


Archive | 2010

Catatonia in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition [Editorial]

Andrew Francis; Max Fink; Francisco Appiani; Aksel Bertelsen; Tom G. Bolwig; Peter Bräunig; Stanley N. Caroff; Brendan T. Carroll; Andrea E. Cavanna; David Cohen; Olivier Cottencin; Manuel J. Cuesta; Jessica Daniels; Dirk M. Dhossche; Gregory L. Fricchione; Neera Ghaziuddin; David Healy; Donald F. Klein; Stephanie Krüger; Joseph Lee; Stephan C. Mann; Michael F. Mazurek; W. Vaughn McCall; William W. McDaniel; Georg Northoff; Victor Peralta; Georgios Petrides; Patricia I. Rosebush; Teresa A. Rummans; Edward Shorter

As international scholars of catatonia, we are concerned that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) proposes to delete the codes 295.2 (schizophrenia, catatonic type) and 293.89 (catatonia secondary to a medical condition) and to substitute a noncoded “catatonia specifier” as the principal identifier. We believe that these changes will badly serve clinical practice and research. We advocate a unique and broadly defined code for catatonia in DSM-V. Catatonia is common among hospitalized psychiatric patients, including adults, adolescents, and occasionally children. In the 10 principal prospective studies from sites around the world, catatonia syndrome was identified in a mean (SEM) percentage of 9.8% (1.4%) of adult admissions (Table 1). These patients have multiple signs of catatonia (commonly >5); 68% (6%) are mute, and 62% (3%) are negativistic or withdrawn. Some are unable to eat, requiring parenteral nutrition and/or medication. TABLE 1 Prospective Studies of the Incidence of Catatonia Once catatonia is recognized, first-line treatment with benzodiazepines usually brings prompt relief, although high doses may be needed. If catatonia persists, electroconvulsive therapy is often rapidly beneficial. Every prospective study confirms that catatonia syndrome exists, occasionally becomes malignant, and requires prompt treatment. Under the proposed new guidelines for DSM-V, patients with catatonia syndrome will lack an informative diagnosis. Mutism, negativism, and withdrawal prevent assessment for mood, cognitive, and psychotic symptoms and impede proper delineation of episodes of prior illness. Without findings for a specific diagnosis, it is rational to use a provisional diagnosis of the catatonia syndrome to allow tests and treatments to proceed. Lacking recognition and treatment, catatonia may persist or worsen with adverse or life-threatening results. On the other hand, when patients with catatonia are identified and treated, they become verbal and interactive, allowing interviews and more definitive diagnoses, regardless of the primary pathological findings. When patients cannot provide information, clinicians may conflate or misdiagnose catatonia with schizophrenia (as in the DSM-IV schema), impute a psychotic process, foster the unproven use of neuroleptics, and risk adverse effects, such as conversion to malignant catatonia or the neuroleptic malignant syndrome. Similarly, assignment of catatonia to “psychosis not otherwise specified” (298.9, DSM-IV and DSM-V) would be erroneous because these patients often either lack hallucinations and delusions or cannot be assessed for them. The proposed elimination of DSM-IV “catatonia due to a general medical condition” (293.89) renders the coding for catatonia arising from general medical conditions problematic. At clinical presentation, the medical/toxic factors are rarely known, as time is often needed to identify these etiologies. We also note that noncoded specifiers are not useful for research on nosology, treatment, and outcome. To address all these issues, we urge inclusion in DSM-V of a specific diagnostic code for catatonia. One simple option is to retain the 293.89 code but revise its formulation to broadly encompass the catatonia syndrome without imputing a link to either primary psychiatric or general medical conditions. A unique and broadly defined code would foster recognition of the catatonia syndrome and permit research on nosology, treatment, and outcome. These goals are not met with the DSM-V plan for noncoded modifiers.


American Journal of Psychiatry | 2001

Changes in Regional Brain Glucose Metabolism Measured With Positron Emission Tomography After Paroxetine Treatment of Major Depression

Sidney H. Kennedy; Kenneth R. Evans; Stephanie Krüger; Helen S. Mayberg; Jeffrey H. Meyer; Sonia McCann; Andrew I. Arifuzzman; Sylvain Houle; Franco J. Vaccarino


Journal of Neuropsychiatry and Clinical Neurosciences | 2000

Prevalence of obsessive-compulsive disorder in schizophrenia and significance of motor symptoms.

Stephanie Krüger; Peter Bräunig; Jürgen Höffler; Gerald Shugar; Ingrid Börner; Julia Langkrär


Journal of Neuropsychiatry and Clinical Neurosciences | 2001

Intravenous Valproic Acid in the Treatment of Severe Catatonia

Stephanie Krüger; Peter Bräunig


Psychiatrische Praxis | 2005

Katatonie: Eine Übersicht

Peter Bräunig; Stephanie Krüger

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Jeffrey H. Meyer

Centre for Addiction and Mental Health

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Robert G. Cooke

Centre for Addiction and Mental Health

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Alan A. Wilson

Centre for Addiction and Mental Health

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Ayal Schaffer

Sunnybrook Health Sciences Centre

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Doug Hussey

Centre for Addiction and Mental Health

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