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Biomedical subjects

S E Starkstein

Publications and source records attributed to S E Starkstein.

At least 73 records · Page 4Linked to original sources
PubMed1993

SPECT findings in patients with primary mania.

Five patients with a manic episode and 7 age-comparable control subjects were studied with single-photon emission computed tomography and [99mTc]d,l-hexamethylpropyleneamine oxime. Manic patients showed significantly lower blood flow in the basal portion of the right temporal lobe compared with normal control subjects. Moreover, manic patients showed a left-right asymmetry (a significantly lower perfusion in the right versus left temporal basal cortex), as well as a dorsal-ventral asymmetry (a significantly lower perfusion in the right temporal basal versus dorsal cortex). These findings suggest that the right basotemporal cortex may play an important role in the production of primary mania.

Adult↗
PubMed1993

A preliminary study of cortical S2 serotonin receptors and cognitive performance following stroke.

Cortical serotonin receptor binding was measured with positron-emission tomography (PET) in uninjured regions of cortex in 26 stroke patients. Cognitive function was assessed with the Mini-Mental State Exam (MMSE) and a neuropsychological test battery. Left frontal cortex serotonin binding was correlated positively with MMSE total score (r = 0.50, P = 0.01) and with the MMSE concentration, writing, and copying tasks (r = 0.42, 0.56, 0.53, respectively; P < 0.05). Tests of orientation and repetition of difficult phrases were significantly correlated with serotonin binding (r = 0.53 and 0.52, respectively; P < 0.05). These findings suggest that cognitive performance after stroke may be influenced by alterations in the serotonergic system.

Adult↗
PubMed1993

ECT in a patient with a frontal craniotomy and residual meningioma.

Electroconvulsive therapy (ECT) was used to treat a patient with a large left frontal craniotomy and remaining frontal meningioma. Treatment was successful and uneventful. ECT should be considered in the treatment of drug-resistant depressed patients with craniotomies and remaining tumor.

Brain Neoplasms↗
PubMed1992

Neuropsychological correlates of brain atrophy in Huntington's disease: a magnetic resonance imaging study.

Magnetic resonance imaging and a comprehensive cognitive evaluation were carried out in a series of 29 patients with mild to moderate Huntington's disease (HD). A factor analysis of the neuropsychological test scores provided three factors: a memory/speed-of-processing factor, a "frontal" factor, and a response inhibition factor. The memory/speed factor correlated significantly with measures of caudate atrophy, frontal atrophy, and atrophy of the left (but not the right) sylvian cistern. There were no significant correlations between the "frontal" or response inhibition factors and measures of cortical or subcortical brain atrophy. Our findings confirm that subcortical atrophy is significantly correlated with specific cognitive deficits in HD, and demonstrate that cortical atrophy also has important association with the cognitive deficits of patients with HD.

Adult↗
PubMed1992

A prospective longitudinal study of depression, cognitive decline, and physical impairments in patients with Parkinson's disease.

A consecutive series of 105 patients with Parkinson's disease were examined for the presence of affective disorders, cognitive deficits, and impairments in activities of daily living (ADLs); 92 received the same evaluation 12 months after the initial examination. On the basis of the initial psychiatric findings, patients were divided into major, minor, and non-depressed groups. Patients with major depression showed a significantly greater cognitive decline, deterioration in ADLs, and further advance through the Hoehn and Yahr stages than patients with either minor depression or no depression.

Activities of Daily Living↗
PubMed1992

Anosognosia in patients with cerebrovascular lesions. A study of causative factors.

BACKGROUND AND PURPOSE: Psychological and biological hypotheses have been proposed to explain anosognosia. We correlated the presence of anosognosia with the presence and severity of psychiatric disturbances, neglect, intellectual impairments, and computed tomographic evidence of lesion size, location, and measurements of brain atrophy. METHODS: A series of 80 patients with acute stroke were assessed using a battery of psychiatric and neuropsychological tests and computed tomography. RESULTS: There were five main findings. First, 27 (28%) of the 96 patients originally screened showed anosognosia. Second, patients with anosognosia had significantly higher frequencies of hemispatial neglect and related phenomena, as well as deficits in recognizing facial emotions and in receptive prosody. Third, depression was equally frequent among patients with and without anosognosia. Fourth, patients with anosognosia had a significantly higher frequency of right hemisphere lesions, primarily involving the temporoparietal junction, thalamus, and basal ganglia. Fifth, patients with anosognosia showed significantly more subcortical brain atrophy, primarily involving the frontal white matter and diencephalic areas. CONCLUSIONS: The present study demonstrates that anosognosia does not "protect" stroke patients from depressive feelings; rather, it represents arousal-attentional disorders after lesions in specific areas of the right hemisphere in nonaphasic patients with preexisting subcortical atrophy.

Aged↗
PubMed1992

Depression in patients with acute traumatic brain injury.

OBJECTIVE: This study was undertaken to examine patients with closed head injuries for the presence of depressive disorders. METHOD: A consecutive series of 66 patients with closed head injuries but no significant spinal cord or other organ system injury were examined by means of a semistructured psychiatric interview. The Hamilton Rating Scale for Depression as well as scales measuring impairment in activities of daily living, intellectual functioning, and social functioning were administered. The patients' CT scans were also examined. RESULTS: Seventeen patients had major depression and two had minor depression. The presence of left dorsolateral frontal lesions and/or left basal ganglia lesions and, to a lesser extent, parietal-occipital and right hemisphere lesions was associated with an increased probability of developing major depression. Compared to the nondepressed group, the group with major depression had a higher frequency of previous psychiatric disorder and showed evidence of poorer social functioning. CONCLUSIONS: Major depression occurs in about one-quarter of patients after traumatic brain injury. This is the same frequency as in other major disorders such as stroke. Major depression appears to be provoked by one or more factors that include poor premorbid social functioning and previous psychiatric disorder or injury to certain critical brain locations.

Activities of Daily Living↗
PubMed1992

Reliability, validity, and clinical correlates of apathy in Parkinson's disease.

The authors examined a consecutive series of 50 patients for the presence of apathy, depression, anxiety, and neuropsychological deficits using a neuropsychological battery that included a recently designed apathy scale. This scale was found to be reliable and valid in the diagnosis of apathy in patients with PD. Of patients in the study, 12% showed apathy as their primary psychiatric problem, and 30% were both apathetic and depressed. Patients with apathy (with or without depression), showed significantly more deficits in both tasks of verbal memory and time-dependent tasks. Results suggest that apathy is a frequent finding in PD, is significantly associated with specific cognitive impairments, and may have a different mechanism than depression.

Aged↗
PubMed1992

Reduction of CSF monoamine metabolites in poststroke depression: a preliminary report.

Monoamine metabolites were measured in the cerebrospinal fluid (CSF) of depressed and nondepressed patients with acute stroke lesions and in nondepressed patients without stroke lesions. Depressed stroke patients had a significantly lower concentration of CSF 5-hydroxyindoleacetic acid (5-HIAA; a serotonin metabolite) than the other two groups. These findings suggest that poststroke depression may be mediated by serotonergic mechanisms.

Adult↗
PubMed1992

Paralimbic frontal lobe hypometabolism in depression associated with Huntington's disease.

We measured regional cerebral glucose metabolism using 2-[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography in depressed and nondepressed patients with early Huntington's disease (HD), compared with appropriately matched controls. Caudate, putamen, and cingulate metabolism was significantly lower in patients with HD than in control subjects, independent of mood state. Orbital frontal-inferior prefrontal cortex hypometabolism, however, differentiated depressed patients from both nondepressed patients and normal controls. These findings implicate selective dysfunction of the paralimbic regions of the frontal lobes in the mood disorder of HD. The metabolic pattern is similar to that in depression associated with Parkinson's disease, suggesting that the integrity of pathways linking paralimbic frontal cortex and the basal ganglia may be integral to the normal regulation of mood.

Affect↗
PubMed1991

Manic-depressive and pure manic states after brain lesions.

Although mania is a rare complication of brain lesions, recent reports have emphasized the importance of lesion location and genetic predisposition in these patients. In the present study we compared patients who developed a bipolar affective disorder (i.e., mania and depression) after a brain lesion with patients who only developed mania. Although no significant between-group differences were found on demographic variables, the manic-depressed group showed significantly more impairments on the Mini Mental State Exam than the mania only group. All the bipolar patients had subcortical lesions (mainly right head of the caudate and right thalamus), while patients with unipolar mania had significantly higher frequency of cortical involvement (mainly right orbitofrontal and basotemporal cortices). It is suggested that subcortical and cortical right hemisphere lesions may produce different neurochemical and/or remote metabolic brain changes that may underlie the production of either a bipolar disease or a unipolar mania.

Bipolar Disorder↗
PubMed1991

Transcortical aphasia. Importance of the nonspeech dominant hemisphere in language repetition.

While a relative preservation of repetition in acute transcortical aphasia (TA) has usually been associated with the functional integrity of the speech dominant (left) perisylvian area, recent amytal data (Bando et al., 1986) have suggested a fundamental role of the nondominant (right) hemisphere in language repetition. The neuroradiological correlates of repetition were studied in a consecutive series of 21 patients with acute TA. A similar frequency of either perisylvian or extraperisylvian pathology was found. In 2 patients with perisylvian pathology, the injection of amytal in the hemisphere contralateral to the lesion abolished repetition. Positron emission tomography (PET) in another patient revealed marked hypometabolism over the entire left cortical mantle ipsilateral to a basal ganglia lesion, suggesting that preserved repetition was carried out by right hemisphere structures. This was confirmed in a second patient with left extraperisylvian pathology, in whom a second lesion in the right hemisphere resulted in impaired repetition. These findings suggest that the spared contralateral hemisphere may subserve residual repetition in some transcortical aphasic patients with a lesion within or outside the speech-dominant perisylvian area.

Aged↗
PubMed1991

Dementia of depression in Parkinson's disease and stroke.

Depression is a frequent finding in patients with neurological disorders. These depressions, however, have similar phenomenology, duration, biological markers, and response to treatment as depressions in patients with no known brain injuries (i.e., functional depression). In the present article, we review evidence that suggests the dementia of depression exists among severely depressed patients with cerebrovascular lesions or Parkinson's disease (PD). We conclude that: a) in patients with either stroke lesions or PD, depression is significantly associated with cognitive deficits; b) this association is only true for patients with major depression (i.e., it is not present in patients with minor depression); and c) patients with poststroke depression and patients with PD and depression have a severity and profile of cognitive deficits similar to those found in patients with primary major depression.

Cerebrovascular Disorders↗
PubMed1991

Alzheimer's disease in a patient with posterior cortical atrophy.

Posterior cortical atrophy (PCA) is characterised by slowly progressive dementia with cognitive and perceptual deficits suggestive of bilateral parieto-occipital disease. A case is reported of a patient with PCA and neuropathological findings consistent with Alzheimer's disease.

Alzheimer Disease↗
PubMed1991

Sleep disorders, pain, and depression in Parkinson's disease.

A consecutive series of patients with Parkinson's disease (PD) were examined for the presence of sleep disturbances, pain, and depression. We found that patients with PD and major depression had significantly more sleep disturbances and severe pain than non-depressed patients with PD. Moreover, depression scores accounted for most of the variance in a stepwise regression analysis of the effect of numerous clinical variables on either sleep disorders or pain severity. These findings suggest that depression is the most important factor associated with the common problems of sleep disorder and pain among patients with PD.

Aged↗
PubMed1991

Are depressive symptoms nonspecific in patients with acute stroke?

OBJECTIVE: Some investigators have suggested that major depression might be overdiagnosed in stroke patients because of changes in appetite, sleep, or sexual interest caused by their medical illness; others have suggested that depression may be underdiagnosed in stroke patients who deny symptoms of depression because of anosognosia, neglect, or aprosody. The authors' goal was to determine how frequently depressive symptoms occur in acute stroke patients with and without depressed mood to estimate how often diagnostic errors of inclusion or exclusion may be made. METHOD: They examined the rate of autonomic and psychological symptoms of depression in 205 patients who were consecutively hospitalized for acute stroke. Eighty-five (41%) of these patients had depressed mood, and 120 (59%) had no mood disturbance. Forty-six (54%) of the 85 patients with depressed mood (22% of all patients) were assigned the DSM-III diagnosis of major depression. RESULTS: The 120 patients without mood disturbance had a mean of one autonomic symptom, but the 85 patients with depressed mood had a mean of almost four. Tightening the diagnostic criteria to account for one more nonspecific autonomic symptom decreased the number of patients with major depression by only three; adding two more criteria decreased the number by only five. Thus, the rate of DSM-III major depression was 1% higher than the rate with one extra nonspecific autonomic symptom and 2% higher than the rate with two extra criteria. Conversely, loosening diagnostic criteria to account for denial of depressive illness increased the rate of major depression by only 5%. CONCLUSIONS: Both autonomic and psychological depressive symptoms are strongly associated with depressed mood in acute stroke patients.

Acute Disease↗
PubMed1991

Risk factors for developing atypical (schizophreniform) psychosis following stroke.

Five patients who developed an atypical schizophreniform psychosis following right hemisphere stroke are described and compared to five patients matched for lesion size and location who did not develop any psychopathology after stroke. The patients who developed the schizophreniform illness had a larger frontal horn ratio and larger third ventricle ratio on CT head scans than did the comparison group. This finding suggests that preexisting subcortical atrophy and a right hemisphere lesion location are risk factors for developing schizophreniform disorder following stroke.

Aged↗