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Biomedical subjects

S E Starkstein

Publications and source records attributed to S E Starkstein.

123 records · Page 7Linked to original sources
PubMed1988

Mechanisms of mania after brain injury. 12 case reports and review of the literature.

Twelve patients who developed mania after a brain lesion are reported. Ages ranged from 20 to 83 years. Five patients had brain tumors (three frontal meningiomas, one temporal meningioma, and one temporal astrocytoma), four patients had stroke lesions (one frontal, one temporal, and two thalamocapsular), two patients had a traumatic frontal closed head injury, and one patient had a pituitary adenoma resection. Although seven patients had lesions restricted to the right hemisphere, four had bilateral or midline damage and one had a left hemisphere lesion. Damage to structures functionally connected to the obitofrontal cortex, mainly in the right hemisphere, seems to be associated with secondary mania. The possible roles of monoaminergic, genetic, and perinatal factors in the pathogenesis of secondary mania are discussed.

Adult↗
PubMed1988

Neuropsychological and neuroradiological correlates in Huntington's disease.

Measurements of cortical and subcortical atrophy were made on CT scans of 34 patients with Huntington's disease. Significant correlations were found between the bicaudate ratio (BCR) and an eye movement scale (r = 0.44, p less than 0.01), and activities of daily living scale (r = 0.57, p less than 0.001) and the Mini-Mental State Exam (r = 0.49, p less than 0.01). No correlations were found between BCR values and severity of chorea or voluntary motor impairment. A detailed neuropsychological evaluation of 18 Huntington's disease patients showed significant correlations between the BCR and Symbol Digit Modalities test (r = 0.65, p less than 0.01), and parts A (r = 0.72, p less than 0.001) and B (r = 0.80, p less than 0.0001) of the Trail Making Test. These data support work in primates that demonstrates the role of the caudate nucleus in cognitive and oculomotor functions, but not in motor control (which is governed by putamino-subthalamic systems). The specific cognitive skills correlated with caudate atrophy in Huntington's disease are those reported in primate work to be served by the frontal-caudate loop system: eye movements, conceptual tracking, set shifting and psychomotor speed.

Adolescent↗
PubMed1988

Disconnection syndrome in a right-handed patient with right hemispheric speech dominance.

The callosal disconnection syndrome is characterized by unilateral (left) tactile anomia, unilateral (left) agraphia and unilateral (left) ideomotor apraxia. We report on a right-handed patient, who developed a callosal disconnection syndrome due to the rupture of an anterior communicant aneurysm. As he had right hemisphere dominance for language and praxis, the signs described above were crossed. He also featured a left alien hand sign and motor aprosody. The authors believe this is the first case of callosal disconnection in a right-hander with crossed language and praxis functions.

Adult↗
PubMed1988

Comparison of spontaneously recovered versus nonrecovered patients with poststroke depression.

We followed 16 patients who developed depression immediately after a stroke for 6 months. By that time, six patients showed no depression (recovered group), while 10 patients were still depressed (nonrecovered group). There were no significant differences in demographic variables and social functioning between the groups, but the nonrecovered group showed less improvement in cognitive function and more physical impairments. Patients in the nonrecovered group had mainly cortical lesions, while those in the recovered group had mainly subcortical and posterior circulation strokes.

Adult↗
PubMed1988

Comparison of mania and depression after brain injury: causal factors.

Patients who developed secondary mania after brain injury (N = 17) had a significantly greater frequency of injury to right hemisphere areas connected with the limbic system than poststroke patients with major depression (N = 31), who had injury primarily in the left frontal cortex and basal ganglia. For patients without mood disturbance after brain injury (N = 28), the location of the lesion was not significant. Secondary mania patients also had a significantly greater frequency of family history of affective disorder than did the other two groups. These results suggest that an interaction between injury to certain areas of the right hemisphere and genetic factors or other neuropathological conditions produces secondary mania.

Aged↗
PubMed1988

PET imaging of cortical S2 serotonin receptors after stroke: lateralized changes and relationship to depression.

Patients with right-hemisphere strokes (N = 9) more than 1 year after injury had greater cortical binding of (3-N-[11C]methyl)spiperone than a similar group of patients with left-hemisphere strokes (N = 8) or normal control subjects (N = 17). The higher S2 serotonin receptor binding occurred in uninjured regions of the right parietal and temporal cortex. The ratio of binding in the ipsilateral to contralateral cortex showed a significant negative correlation with severity of depression scores in the left temporal cortex. These findings suggest that the biochemical response of the brain may be different depending on which hemisphere is injured and that some depressions may be a consequence of the failure to upregulate serotonin receptors after stroke.

Adult↗
PubMed1987

Mania after brain injury. A controlled study of causative factors.

Eleven patients who developed manic syndromes after brain injury (secondary mania) were studied. Six patients had depressive episodes before mania and five had a definite or possible family history of affective disorder. Eight had lesions involving limbic areas, and nine had right hemisphere involvement. In addition to focal brain injury, mean values for bifrontal and third ventricle/brain ratios of manic patients were significantly increased when compared with non-manic patients who had lesions matched for cause, location, volume, and time since injury. Results indicate that the confluence of either anterior subcortical atrophy and a focal lesion of a limbic or limbic-connected region of the right hemisphere, or genetic loading and a limbic-connected right hemisphere lesion may account for the rare occurrence and specific factors necessary to produce secondary mania.

Bipolar Disorder↗
PubMed1987

Comparison of cortical and subcortical lesions in the production of poststroke mood disorders.

Patients with single stroke lesions, verified by computerized tomography, involving either cortical tissue or restricted entirely to subcortical structures were examined for mood disorders. Those with left anterior lesions, either cortical or subcortical, had significantly greater frequency and severity of depression than patients with any other lesion location. A strong correlation between the severity of depression and proximity of the lesion to the frontal pole was observed for both left cortical and subcortical groups. Right hemisphere lesions did not show the same correlation with depression but were associated with a significantly higher incidence of undue cheerfulness. These findings demonstrate the importance of the location of subcortical lesions in poststroke mood disorders and suggest that anterior subcortical structures may play an important but lateralized role in the production or regulation of mood.

Aphasia↗
PubMedDate not supplied

Phenomenological comparisons of major depression following stroke, myocardial infarction or spinal cord lesions.

Patients with major depression admitted to hospital with acute stroke (n = 44), acute myocardial infarction (n = 25), or acute spinal cord injury (n = 12) were examined for differences in their phenomenological presentation of major depression. Depressed stroke patients were found to have significantly higher scores on the syndrome clusters for generalized anxiety and ideas of reference than depressed cardiac or spinal cord injury patients. In addition, significantly more stroke patients met diagnostic criteria for generalized anxiety disorder compared with the other two groups. Although spinal cord injury patients were younger, more likely to be treated with benzodiazepines, and less likely to be treated with beta-blockers, none of these factors distinguished stroke patients with anxious depression from stroke patients with depression only. These findings are consistent with the hypothesis that the etiology of depression following stroke may be different from that associated with myocardial infarction or spinal cord injury.

Adult↗
PubMedDate not supplied

Transient epileptic amnesia in dementia: a treatable unrecognized cause of episodic amnestic wandering.

The authors present two patients with dementia who displayed recurrent transient episodes of amnestic wandering and disorientation characterized by getting lost in familiar environments. At other times these patients did not wander or become disoriented. The inability to recall any information during these episodes, and the marked difference of the episodic amnesia exacerbations from the progressive amnesia characteristic of Alzheimer disease seen in these patients led to their evaluation. These clinical episodes and the bilateral interictal epileptiform electroencephalographic changes found in both patients led to the diagnosis of transient epileptic amnesia, a syndrome that can be diagnostically elusive. These transient amnestic wandering events subsided after treatment with antiepileptic drugs in both patients. The authors suggest that transient wandering of this type may be caused by ictal events or postictal confusional states. This report emphasizes the importance of recognizing transient epileptic amnesia as an easily treatable cause of episodic behavioral abnormalities responsive to antiepileptic therapy, especially in those patients who have a markedly inconsistent pattern of wandering, disorientation in familiar settings, and amnesia exacerbation manifested by no recall of the emotional stress of getting lost or of any information during these episodes. Recognition of this type of behavioral disruption and its proper treatment can lead to improved quality of life for these patients, maintain these patients in their homes and out of chronic care institutions longer, and facilitate the community's and caretaker's interactive roles with the patient.

Aged↗
PubMedDate not supplied

Theory of mind and pragmatic abilities in dementia.

OBJECTIVE: "Theory of Mind" (ToM) is the capacity to attribute mental states to oneself and to others and to interpret behavior in terms of mental states. Deficits in both ToM and pragmatic abilities have been described in patients with neurologic disorders, such as frontal lobe lesions and right hemisphere strokes, but have not been assessed in demented patients. METHODS: This study examined ToM and pragmatic abilities in a consecutive series of 34 patients with probable Alzheimer disease (AD) using a second-order false belief story, 11 short stories assessing understanding of social situations, and a test of pragmatic abilities assessing both indirect requests and-conversational implications. RESULTS: Sixty-five percent of AD patients with mild dementia could not pass a second-order false belief task, whereas no failures were found in a group of 10 age-comparable healthy controls. AD patients who did not pass the second-order false belief task had more severe deficits on tests of verbal anterograde memory, verbal comprehension, abstract thinking, and naming, as compared with AD patients who passed the task. AD patients also showed significantly more severe pragmatic deficits than age-comparable healthy controls, and there was a significant association between ToM and pragmatic deficits. On the other hand, there were no significant associations between ToM or pragmatic deficits, and behavioral problems frequently reported in AD such as depression, delusions, apathy, and irritability. CONCLUSIONS: This initial exploratory investigation demonstrated significant deficits in both ToM and pragmatic abilities in a consecutive series of AD patients with mild dementia.

Aged↗
PubMedDate not supplied

Brain atrophy in 18 patients with Down syndrome: a CT study.

Individuals with Down syndrome develop neuropathologic and in some cases clinical evidence of Alzheimer disease after age 40. We compared CT scans of 18 Down syndrome subjects, 26-70 years old (seven of whom satisfied criteria for dementia), with 175 screened normal volunteer control subjects for evidence of cortical and subcortical atrophy. CT scans were analyzed as a function of age and cognitive status. The suprasellar cistern ratio, presumed to measure mesial temporal-lobe atrophy (or hypoplasia), was correlated with severity of cognitive impairment, even when age effects were removed. The suprasellar cistern ratio predicted dementia status with an accuracy of greater than 75%. Brain measurements on CT scans showed a distinct pattern of increased abnormality with age in patients with Down syndrome; this differed clearly from that seen in controls.

Adult↗