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Unique Identifier

98405366

Authors

Fairman KA. Drevets WC. Kreisman JJ. Teitelbaum F.

Institution

Health Management Services Department of Express Scripts/ValueRx, Inc.,
Maryland Heights, MO, USA.

Title

Course of antidepressant treatment drug type, and prescriber's specialty.

Source

Psychiatric Services. 49(9):1180-6, 1998 Sep.

MeSH Subject Headings

Adult
Aged
*Antidepressive Agents, Tricyclic / tu [Therapeutic Use]
*Depression / dt [Drug Therapy]
Female
Health Maintenance Organizations / sn [Statistics & Numerical Data]
Human
Male
Medication Errors / sn [Statistics & Numerical Data]
Middle Age
*Patient Compliance / sn [Statistics & Numerical Data]
Psychiatry / sn [Statistics & Numerical Data]
Retrospective Studies
Self Medication / sn [Statistics & Numerical Data]
*Serotonin Uptake Inhibitors / tu [Therapeutic Use]
*Specialties, Medical / sn [Statistics & Numerical Data]
Statistics
Support, Non-U.S. Gov't
United States

Abstract

OBJECTIVE: The study examined whether the relationship between the course of antidepressant treatment and the type of prescriber-psychiatrist or nonpsychiatrist-varied by whether a tricyclic antidepressant or a selective serotonin reuptake inhibitor (SSRI) was prescribed. METHODS: Pharmacy claims from a nationwide database were analyzed retrospectively. A total of 3,101 adults who did not have a prescription for antidepressants for nine months and who were then given a prescription for a tricyclic or an SSRI antidepressant were followed for 13 to 16 months after the initial prescription. Outcome measures were rates of treatment termination before one month and subtherapeutic dosing, defined as having received no prescribed daily dosages at or above commonly cited thresholds. RESULTS: Among tricyclic-treated patients, psychiatrists' patients were significantly more likely than nonpsychiatrists' patients to continue in treatment for more than one month (72 percent versus 62 percent). Among patients taking tricyclics for at least three months, those with at least one prescription from a psychiatrist had a significantly higher rate of therapeutic dosing than those with all prescriptions from a nonpsychiatrist (70 percent versus 25 percent). For SSRI-treated patients, rates of termination and therapeutic dosing did not differ significantly by prescriber type. In multivariate equations that controlled for selected differences, effects of drug type and prescriber type were independent when persistence in treatment was analyzed, and interactive when subtherapeutic dosing was analyzed. CONCLUSIONS: Policy making about antidepressant pharmacotherapy should include assessments of the relationships between drug selection and patient outcome across a variety of clinical settings.

Registry Numbers

0 (Antidepressive Agents, Tricyclic). 0 (Serotonin Uptake Inhibitors).

Unique Identifier

99007307

Authors

Ongur D. Drevets WC. Price JL.

Institution

Department of Anatomy and Neurobiology, Washington University School of
Medicine, St. Louis, MO 63110, USA.

Title

Glial reduction in the subgenual prefrontal cortex in mood disorders.

Source

Proceedings of the National Academy of Sciences of the United States of
America. 95(22):13290-5, 1998 Oct 27.

MeSH Subject Headings

Adult
*Bipolar Disorder / pa [Pathology]
*Brain / pa [Pathology]
*Depressive Disorder / pa [Pathology]
Female
Human
Male
Middle Age
*Neuroglia / pa [Pathology]
*Prefrontal Cortex / pa [Pathology]
Reference Values
Schizophrenia / pa [Pathology]
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S

Abstract

Mood disorders are among the most common neuropsychiatric illnesses, yet little is known about their neurobiology. Recent neuroimaging studies have found that the volume of the subgenual part of Brodmann's area 24 (sg24) is reduced in familial forms of major depressive disorder (MDD) and bipolar disorder (BD). In this histological study, we used unbiased stereological techniques to examine the cellular composition of area sg24 in two different sets of brains. There was no change in the number or size of neurons in area sg24 in mood disorders. In contrast, the numbers of glia were reduced markedly in both MDD and BD. The reduction in glial number was most prominent in subgroups of subjects with familial MDD (24%, P = 0.01) or BD (41%, P = 0.01). The glial reduction in subjects without a clear family history was lower in magnitude and not statistically significant. Consistent with neuroimaging findings, cortical volume was reduced in area sg24 in subjects with familial mood disorders. Schizophrenic brains studied as psychiatric controls had normal neuronal and glial numbers and cortical volume. Glial and neuronal numbers also were counted in area 3b of the somatosensory cortex in the same group of brains and were normal in all psychiatric groups. Glia affect several processes, including regulation of extracellular potassium, glucose storage and metabolism, and glutamate uptake, all of which are crucial for normal neuronal activity. We thus have identified a biological marker associated with familial mood disorders that may provide important clues regarding the pathogenesis of these common psychiatric conditions.

Unique Identifier

98336768

Authors

Drevets WC. Ongur D. Price JL.

Institution

Department of Psychiatry, University of Pittsburgh School of Medicine, PA
15238, USA.

Title

Neuroimaging abnormalities in the subgenual prefrontal cortex: implications
for the pathophysiology of familial mood disorders. [Review] [57 refs]

Source

Molecular Psychiatry. 3(3):220-6, 190-1, 1998 May.

MeSH Subject Headings

Bipolar Disorder / ge [Genetics]
*Bipolar Disorder / pa [Pathology]
*Bipolar Disorder / ri [Radionuclide Imaging]
Depression / ge [Genetics]
*Depression / pa [Pathology]
*Depression / ri [Radionuclide Imaging]
Family Health
Gyrus Cinguli / pa [Pathology]
Human
Magnetic Resonance Imaging
*Prefrontal Cortex / pa [Pathology]
Prefrontal Cortex / ri [Radionuclide Imaging]
Tomography, Emission-Computed

Abstract

The prefrontal cortex (PFC) ventral to the genu of the corpus callosum has been implicated in the modulation of visceral responses to stressful and emotionally provocative stimuli, based upon analysis of lesion effects involving this area in humans and experimental animals. In a recent magnetic resonance imaging (MRI) study of familial mood disorders, we demonstrated that the mean grey matter volume of this cortex is abnormally reduced in subjects with major depressive disorder (MDD) and bipolar disorder, irrespective of their treatment status or current mood state. Moreover, in preliminary histopathological assessments of subgenual PFC tissue taken post mortem from subjects with MDD and bipolar disorder we obtained results suggesting that this decrement in grey matter volume is associated with a reduction in glia without an equivalent loss of neurons. The potential functional significance of these neuroimaging and microscopic abnormalities is discussed with respect to evidence that subgenual PFC dysfunction may disturb stress-related autonomic and neuroendocrine responses and reward-related mesolimbic dopamine function. These data may thus hold important implications for the development of neural models of mood disorders that can account for the abnormal hedonic, motivational, neuroendocrine, and autonomic manifestations evident in these idiopathic conditions. [References: 57]

Unique Identifier

98336757

Authors

Drevets WC. Ongur D. Price JL.

Institution

University of Pittsburgh School of Medicine, PA 15238, USA.

Title

Reduced glucose metabolism in the subgenual prefrontal cortex in unipolar
depression.

Source

Molecular Psychiatry. 3(3):190-1, 1998 May.

MeSH Subject Headings

*Depressive Disorder / me [Metabolism]
*Depressive Disorder / ri [Radionuclide Imaging]
*Glucose / me [Metabolism]
Human
*Prefrontal Cortex / me [Metabolism]
Tomography, Emission-Computed

Registry Numbers

50-99-7 (Glucose).

Unique Identifier

98170006

Authors

Drevets WC.

Institution

Department of Psychiatry, University of Pittsburgh Medical Center,
Pennsylvania 15213, USA.

Title

Functional neuroimaging studies of depression: the anatomy of melancholia.
[Review] [76 refs]

Source

Annual Review of Medicine. 49:341-61, 1998.

MeSH Subject Headings

Affect / ph [Physiology]
Brain / me [Metabolism]
*Brain / pa [Pathology]
Brain / pp [Physiopathology]
Cerebral Cortex / me [Metabolism]
Cerebral Cortex / pa [Pathology]
Cerebral Cortex / pp [Physiopathology]
Cerebrovascular Circulation / ph [Physiology]
Depressive Disorder / me [Metabolism]
*Depressive Disorder / pa [Pathology]
Depressive Disorder / pp [Physiopathology]
Depressive Disorder / th [Therapy]
*Diagnostic Imaging
Emotions / ph [Physiology]
Glucose / me [Metabolism]
Human
Image Processing, Computer-Assisted
Magnetic Resonance Imaging
Mood Disorders / me [Metabolism]
Mood Disorders / pa [Pathology]
Mood Disorders / pp [Physiopathology]
Mood Disorders / th [Therapy]
Neurons / ph [Physiology]
Neurophysiology
Patient Selection
Tomography, Emission-Computed
Tomography, Emission-Computed, Single-Photon

Abstract

Functional brain imaging techniques, which permit noninvasive measures of neurophysiology and neuroreceptor binding, are powerful and sensitive tools for research aimed at elucidating the pathophysiology of major depression. The application of these technologies in depression research has produced several studies of resting cerebral blood flow (BF) and glucose metabolism in subjects imaged during various phases of illness and treatment. This review examines these data and the principles relevant to their interpretation and discusses the insights they provide into the anatomical correlates of depression. Within the anatomical networks implicated in emotional processing by other types of evidence, these BF and metabolic data demonstrate that major depression is associated with reversible, mood state-dependent, neurophysiological abnormalities in some structures and irreversible, trait-like abnormalities in other structures. In some of the regions in which trait-like abnormalities appear, abnormal metabolic activity appears at least partly related to the anatomical abnormalities identified in magnetic resonance imaging (MRI) studies of depression. [References: 76]

Registry Numbers

50-99-7 (Glucose).

Unique Identifier

97271894

Authors

Drevets WC. Price JL. Simpson JR Jr. Todd RD. Reich T. Vannier M. Raichle ME.

Institution

Department of Psychiatry, Mallinckrodt Institute of Radiology, Washington
University School of Medicine, St Louis, Missouri 63110, USA.

Title

Subgenual prefrontal cortex abnormalities in mood disorders [see comments].

Comments

Comment in: Nature 1997 Apr 24;386(6627):769-70

Source

Nature. 386(6627):824-7, 1997 Apr 24.

MeSH Subject Headings

Adult
Affect
*Bipolar Disorder / pa [Pathology]
Case-Control Studies
*Depressive Disorder / pa [Pathology]
Female
Glucose / me [Metabolism]
Human
Magnetic Resonance Imaging
Male
Prefrontal Cortex / bs [Blood Supply]
Prefrontal Cortex / me [Metabolism]
*Prefrontal Cortex / pa [Pathology]
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S
Tomography, Emission-Computed

Abstract

Pathological disturbances of mood may follow a 'bipolar' course, in which normal moods alternate with both depression and mania, or a 'unipolar' course, in which only depression occurs. Both bipolar and unipolar disorders can be heritable illnesses associated with neurochemical, neuroendocrine and autonomic abnormalities. The neurobiological basis for these abnormalities has not been established. Using positron emission tomographic (PET) images of cerebral blood flow and rate of glucose metabolism to measure brain activity, we have now localized an area of abnormally decreased activity in the prefrontal cortex ventral to the genu of the corpus callosum in both familial bipolar depressives and familial unipolar depressives. This decrement in activity was at least partly explained by a corresponding reduction in cortical volume, as magnetic resonance imaging (MRI) demonstrated reductions in the mean grey matter volume in the same area of 39 and 48% in the bipolar and unipolar samples, respectively. This region has previously been implicated in the mediation of emotional and autonomic responses to socially significant or provocative stimuli, and in the modulation of the neurotransmitter systems targeted by antidepressant drugs.

Registry Numbers

50-99-7 (Glucose).

Unique Identifier

96376668

Authors

Price JL. Carmichael ST. Drevets WC.

Institution

Department of Anatomy, Washington University School of Medicine, St. Louis,
MO 63110, USA.

Title

Networks related to the orbital and medial prefrontal cortex; a substrate for
emotional behavior?. [Review] [30 refs]

Source

Progress in Brain Research. 107:523-36, 1996.

MeSH Subject Headings

Animal
*Brain Mapping
Corpus Striatum / ph [Physiology]
*Emotions / ph [Physiology]
Limbic System / ph [Physiology]
*Nerve Net / ph [Physiology]
Neurons, Afferent / ph [Physiology]
*Prefrontal Cortex / ph [Physiology]
Thalamus / ph [Physiology]

Unique Identifier

95115799

Authors

Drevets WC. Burton H. Videen TO. Snyder AZ. Simpson JR Jr. Raichle ME.

Institution

Division of Radiation Sciences, Mallinckrodt Institute of Radiology,
Washington University School of Medicine, St Louis, Missouri 63110.

Title

Blood flow changes in human somatosensory cortex during anticipated
stimulation [see comments].

Comments

Comment in: Nature 1995 Jan 19;373(6511):198-9

Source

Nature. 373(6511):249-52, 1995 Jan 19.

MeSH Subject Headings

Adult
*Attention / ph [Physiology]
Cerebrovascular Circulation
Electric Stimulation
Face / ir [Innervation]
Face / ph [Physiology]
Female
Fingers / ir [Innervation]
Fingers / ph [Physiology]
Human
Male
*Somatosensory Cortex / bs [Blood Supply]
*Somatosensory Cortex / ph [Physiology]
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S
Toes / ir [Innervation]
Toes / ph [Physiology]
Tomography, Emission-Computed

Abstract

Positron emission tomography (PET) measurements of brain blood flow were used to monitor changes in the human primary and secondary somatosensory cortices during the period when somatosensory stimuli were expected. In anticipation of either focal or innocuous touching, or localized, painful shocks, blood flow decreased in parts of the primary somatosensory cortex map located outside the representation of the skin area that was the target of the expected stimulus. Specifically, attending to an impending stimulus to the fingers produced a significant decrease in blood flow in the somatosensory zones for the face, whereas attending to stimulation of the toe produced decreases in the zones for the fingers and face. Decreases were more prominent in the side ipsilateral to the location of the expected stimulus. No significant changes in blood flow occurred in the region of the cortex representing the skin locus of the awaited stimulation. These results are concurrent with a model of spatial attention in which potential signal enhancement may rely on generalized suppression of background activity.

Unique Identifier

95050360

Authors

Drevets WC.

Institution

Department of Psychiatry, Washington University School of Medicine, St.
Louis, Mo 63110-1093.

Title

Geriatric depression: brain imaging correlates and pharmacologic
considerations. [Review] [105 refs]

Source

Journal of Clinical Psychiatry. 55 Suppl A:71-81; discussion 82, 98-100,
1994 Sep.

MeSH Subject Headings

Age Factors
Aged
Antidepressive Agents / ae [Adverse Effects]
*Antidepressive Agents / tu [Therapeutic Use]
*Brain / pa [Pathology]
Brain / pp [Physiopathology]
Brain / ra [Radiography]
Bupropion / tu [Therapeutic Use]
Cerebral Arteriosclerosis / di [Diagnosis]
Cerebral Arteriosclerosis / pp [Physiopathology]
Cerebrovascular Circulation
Cyclohexanols / tu [Therapeutic Use]
Depressive Disorder / di [Diagnosis]
*Depressive Disorder / dt [Drug Therapy]
Depressive Disorder / pp [Physiopathology]
Human
Magnetic Resonance Imaging
Models, Neurological
Monoamine Oxidase Inhibitors / tu [Therapeutic Use]
Serotonin Uptake Inhibitors / tu [Therapeutic Use]
Tomography, X-Ray Computed

Abstract

The clinical approach to geriatric major depression involves a variety of special etiopathophysiologic, pharmacokinetic, and pharmacodynamic considerations. In regard to pathophysiology, modern brain imaging and postmortem assessments are elucidating neuropathologic changes in elderly depressives that challenge the notion that geriatric depression is simply a functional brain disorder. These data suggest (but do not yet establish) that many patients who experience depression onset at a late age may acquire affective disease on an arteriosclerotic basis. In contrast, elderly depressives who experience depression onset at an early age are more likely to have acquired depression due to genetic factors but may nevertheless develop degenerative neuropathologic changes over time. The presence of these neuropathologic changes appears to increase elderly patients' risk for developing the adverse central nervous system (CNS) effects of antidepressant treatments. They thereby add another level of complexity to the management of an age group in which pharmacokinetic and pharmacodynamic changes already contribute to the likelihood of adverse drug reactions. Fortunately, the last decade of antidepressant drug development has produced several new agents (including the serotonin selective reuptake inhibitors and more recently, venlafaxine and nefazodone) with substantially reduced CNS and cardiovascular toxicity that facilitate effective treatment of geriatric depression. [References: 105]

Registry Numbers

0 (Antidepressive Agents). 0 (Cyclohexanols). 0 (Monoamine Oxidase
Inhibitors). 0 (Serotonin Uptake Inhibitors). 34841-39-9 (Bupropion).
93413-69-5 (venlafaxine).

Unique Identifier

93359554

Authors

Moss LE. Neppe VM. Drevets WC.

Institution

Washington University School of Medicine, Department of Psychiatry, St.
Louis, MO 63110.

Title

Buspirone in the treatment of tardive dyskinesia.

Source

Journal of Clinical Psychopharmacology. 13(3):204-9, 1993 Jun.

MeSH Subject Headings

Adult
Aged
*Antipsychotic Agents / ae [Adverse Effects]
Antipsychotic Agents / tu [Therapeutic Use]
*Buspirone / ad [Administration & Dosage]
Buspirone / ae [Adverse Effects]
Dose-Response Relationship, Drug
Dyskinesia, Drug-Induced / di [Diagnosis]
*Dyskinesia, Drug-Induced / dt [Drug Therapy]
Female
Human
Male
Middle Age
Neurologic Examination / de [Drug Effects]
Psychiatric Status Rating Scales
*Psychotic Disorders / dt [Drug Therapy]
Psychotic Disorders / px [Psychology]

Abstract

Eight patients with mild to severe tardive dyskinesia (TD) were treated for 12 weeks with buspirone in dosages of up to 180 mg/day in an open-label study. Changes in TD severity were assessed by the Abnormal Involuntary Movement Scale. The rater was blind to buspirone dosage. Buspirone was well tolerated by most subjects. A within-subjects comparison of pretreatment and post-treatment Abnormal Involuntary Movement Scale scores revealed a mean improvement of 4.4 (p < 0.01). Improvement was also observed in neuroleptic-induced extrapyramidal side effects such as parkinsonism and akathisia. Scores on the Hamilton Rating Scale for Anxiety and the Brief Psychiatric Rating Scale did not change during the 12-week study. The results of this open-label pilot study suggest that relatively high doses of buspirone may be efficacious in the treatment of TD.

Registry Numbers

0 (Antipsychotic Agents). 36505-84-7 (Buspirone).

Unique Identifier

93126522

Authors

Drevets WC. Raichle ME.

Institution

Department of Psychiatry, Washington University School of Medicine, St.
Louis, MO 63110.

Title

Neuroanatomical circuits in depression: implications for treatment
mechanisms. [Review] [129 refs]

Source

Psychopharmacology Bulletin. 28(3):261-74, 1992.

MeSH Subject Headings

Depressive Disorder / dt [Drug Therapy]
*Depressive Disorder / pa [Pathology]
Depressive Disorder / th [Therapy]
Human

Abstract

We previously investigated the functional neuroanatomy of familial pure depressive disease (FPDD) using positron emission tomography (PET) measurements of regional blood flow and obtained evidence that flow is increased in the left prefrontal cortex, amygdala, and medial thalamus and is decreased in the medial caudate. These data along with other evidence suggested that circuits involving the prefrontal cortex, amygdala, and related parts of the striatum, pallidum, and medial thalamus are involved in the pathophysiology of FPDD. One of these circuits, the limbic-thalamo-cortical circuit, which includes the amygdala, the medio-dorsal thalamus, and parts of the ventral and medial prefrontal cortex, may be engaged in abnormal reverberatory activity that maintains the cognitive and emotional set of depression. Using this hypothesis as a neural model to investigate antidepressant treatment mechanisms, we review evidence that the changes in dopaminergic, serotonergic, and noradrenergic function induced by somatic antidepressant therapies may yield modulatory effects on limbic-thalamo-cortical activity. We also discuss preliminary findings of treatment-associated changes in this circuit in studies comparing PET images acquired before and during antidepressant treatment. [References: 129]

Unique Identifier

92407637

Authors

Drevets WC. Videen TO. Price JL. Preskorn SH. Carmichael ST. Raichle ME.

Institution

Department of Psychiatry, Washington University School of Medicine, St.
Louis, Missouri 63110.

Title

A functional anatomical study of unipolar depression.

Source

Journal of Neuroscience. 12(9):3628-41, 1992 Sep.

MeSH Subject Headings

Adult
Amygdaloid Body / bs [Blood Supply]
Amygdaloid Body / ri [Radionuclide Imaging]
Brain / ri [Radionuclide Imaging]
Cerebrovascular Circulation
*Depressive Disorder / pp [Physiopathology]
Depressive Disorder / ri [Radionuclide Imaging]
Female
Frontal Lobe / bs [Blood Supply]
Frontal Lobe / ri [Radionuclide Imaging]
Human
Male
Middle Age
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S
Tomography, Emission-Computed

Abstract

The functional neuroanatomy of unipolar major depression was investigated using positron emission tomography to measure differences in regional cerebral blood flow (BF). A relatively homogeneous subject group was obtained using criteria for familial pure depressive disease (FPDD), which are based upon family history as well as upon symptoms and course. Because of the absence of certain knowledge about the pathophysiology of mood disorders and their underlying functional neuroanatomy, we used data obtained from the subtraction of composite images from one-half of depressed and control subjects to identify candidate regions of interest. The major cortical region defined in this manner was statistically tested on a second set of subjects. Using this strategy, we found increased BF in an area that extended from the left ventrolateral prefrontal cortex onto the medial prefrontal cortical surface. Based upon the connectivity between these portions of the prefrontal cortex and the amygdala and evidence that the amygdala is involved in emotional modulation, activity was measured in the left amygdala and found to be significantly increased in the depressed group. A separate group of subjects with FPDD who were currently asymptomatic were also imaged to determine whether these findings represented abnormalities associated with the depressed state, or with a trait difference that might underlie the tendency to become depressed. Only the depressed group had increased activity in the left prefrontal cortex, suggesting that this abnormality represents a state marker of FPDD. Both the depressed and the remitted groups demonstrated increased activity in the left amygdala, though this difference achieved significance only in the depressed group. This suggests that the abnormality involving the left amygdala may represent a trait marker of FPDD, though further assessment in a larger sample size is necessary to establish this. These data along with other evidence suggest that a circuit involving the prefrontal cortex, amygdala, and related parts of the striatum, pallidum, and medial thalamus is involved in the functional neuroanatomy of depression.

Unique Identifier

92302837

Authors

Drevets WC. Videen TQ. MacLeod AK. Haller JW. Raichle ME.

Title

PET images of blood flow changes during anxiety: correction [letter].

Source

Science. 256(5064):1696, 1992 Jun 19.

MeSH Subject Headings

*Anxiety / pp [Physiopathology]
*Cerebrovascular Circulation
Human
Muscles / bs [Blood Supply]
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S
Tomography, Emission-Computed

Unique Identifier

89105629

Authors

Drevets WC. Rubin EH.

Institution

Department of Psychiatry, Washington University School of Medicine, St.
Louis, MO 63110.

Title

Psychotic symptoms and the longitudinal course of senile dementia of the
Alzheimer type.

Source

Biological Psychiatry. 25(1):39-48, 1989 Jan.

MeSH Subject Headings

Aged
Alzheimer Disease / di [Diagnosis]
*Alzheimer Disease / px [Psychology]
*Capgras Syndrome / px [Psychology]
*Delusions / px [Psychology]
Female
*Hallucinations / px [Psychology]
Human
Longitudinal Studies
Male
Manuals
Neuropsychological Tests
Psychometrics
*Psychotic Disorders / px [Psychology]
Support, U.S. Gov't, P.H.S

Abstract

Delusions, misidentifications and hallucinations occur frequently throughout the course of senile dementia of the Alzheimer type (SDAT). Rates of psychosis among subjects with moderate to severe SDAT range from 42% to 84% in our study group; at least half of persons with SDAT with no prior psychiatric history will display psychosis at some point during the course of dementia. Furthermore, psychotic symptoms are associated with accelerated cognitive deterioration, but not with increased mortality.

Unique Identifier

89302520

Authors

Rubin EH. Drevets WC. Burke WJ.

Institution

Department of Psychiatry, Washington University School of Medicine, St Louis,
MO 63110.

Title

The nature of psychotic symptoms in senile dementia of the Alzheimer type.

Source

Journal of Geriatric Psychiatry & Neurology. 1(1):16-20, 1988 Jan.

MeSH Subject Headings

Aged
Aged, 80 and over
*Alzheimer Disease / px [Psychology]
Body Image
Confusion / px [Psychology]
Cross-Sectional Studies
*Delirium, Dementia, Amnestic, Cognitive Disorders / px [Psychology]
Delusions / px [Psychology]
Hallucinations / px [Psychology]
Human
Longitudinal Studies
Paranoid Disorders / px [Psychology]
Psychiatric Status Rating Scales
Support, U.S. Gov't, P.H.S

Abstract

The Alzheimer Disease Research Center at Washington University's medical school has gathered a large sample of subjects with senile dementia of the Alzheimer type (SDAT) who are free of other potentially complicating medical, neurologic and psychiatric disorders. Using this homogeneous population, we have characterized psychotic symptoms associated with SDAT. Three groups of symptoms occur commonly: paranoid delusions, misidentification syndromes, and hallucinations. The nature and frequency of these syndromes are discussed.

Unique Identifier

88108410

Authors

Drevets WC. Rubin EH.

Institution

Department of Psychiatry, Washington University School of Medicine, St Louis,
Missouri 63110.

Title

Erotomania and senile dementia of Alzheimer type.

Source

British Journal of Psychiatry. 151:400-2, 1987 Sep.

MeSH Subject Headings

Aged
Alzheimer Disease / co [Complications]
*Alzheimer Disease / px [Psychology]
*Bipolar Disorder / et [Etiology]
Case Report
*Delusions / et [Etiology]
Female
Human
Sex Behavior

Abstract

A case of erotomania in a 75-year-old female with senile dementia of Alzheimer type (SDAT) is described. This case demonstrates the presence of an elaborately systematised delusion in SDAT, and the influence of the progression of SDAT on this delusion.