Biomedical subjects

S E Starkstein

Publications and source records attributed to S E Starkstein.

At least 109 records · Page 6Linked to original sources

PubMed1989

Developmental and hormonal factors in the sexually dimorphic, asymmetrical response to focal cortical lesions.

The developmental and hormonal determinants of the lateralized response to focal cortical suction lesions were examined in a series of experiments. In an initial study, Sprague-Dawley male rats 25, 30, 55 or 90 days of age, received right unilateral focal frontocortical suction lesions. Only 90-day-old rats developed hyperactivity, suggesting a specific role for maturational factors in the production of this response. Prepubertally castrated adult male rats receiving right frontocortical suction lesions at 90 days also failed to develop hyperactivity, suggesting that sexual maturational factors and/or the presence of testosterone are necessary for the expression of this response. Testosterone implants, producing physiological relevant levels of circulating testosterone reinstated the hyperactivity response to adult cortical lesions in prepubertally castrated male rats. Similar lesions in the left hemisphere, however, did not produce hyperactivity in castrated male rats with testosterone replacement. Finally, in ovariectomized adult female rats, testosterone did not allow the expression of a hyperactivity response to right frontocortical suction lesions. Together, these results demonstrate both an organizational and permissive role for sex steroids in the sexually dimorphic asymmetrical response to cortical injury.

Aging↗

PubMed1989

Brain atrophy in Huntington's disease. A CT-scan study.

CT-scan measurements of cortical and subcortical atrophy were carried out in 34 patients with Huntington's disease (HD). While a significant correlation was observed between parameters of subcortical atrophy (bicaudate ratio, bifrontal ratio and third ventricular ratio) and duration of the disease, there was no significant correlation between these parameters and age. On the other hand, measurements of cortical atrophy (frontal fissure ratio and cortical sulci ratio) correlated significantly with age but not with duration of the disease. When a group of 24 HD patients were compared on CT-scan measurements with a group of 24 age-matched normal controls, significant differences were obtained for all the variables examined, but the bicaudate ratio showed the highest sensitivity and specificity. Even mildly affected patients, with duration of motor symptoms less than 3 years had higher bicaudate ratios than age-matched controls.

Adult↗

PubMed1989

Depression and cognitive impairment in Parkinson's disease.

Neuropsychological deficits including cognitive impairment as well as depression are among the most frequent and important mental disorders found in patients with Parkinson's disease (PD). It has never been determined, however, whether there is a specific relationship between cognitive impairment and depression. A consecutive series of patients with PD was therefore examined for the presence of depression and neuropsychological deficits. Severity of depression was found to be the single most important factor associated with the severity of cognitive impairment. When PD patients with major depression were compared with an age and stage-matched group of nondepressed patients with PD using a neuropsychological battery, major depressed patients performed significantly worse than the nondepressed patients on all aspects of neuropsychological function tested. These impairments were most pronounced on frontal lobe tasks.

Cognition↗

PubMed1989

Evoked potentials, reaction time and cognitive performance in on and off phases of Parkinson's disease.

Seven patients with Parkinson's disease and severe motor fluctuations were studied with event-related potentials, reaction and movement times and neuropsychological tests while in "off" and "on" phases. While there was a significant decrement in the P300 latency of the event-related potentials and in the duration of movement time in the "on" phase, no significant differences between on and off phases were observed in reaction time and neuropsychological tasks.

Aged↗

PubMed1989

Lateralization of dementia of depression in stroke patients.

In a group of stroke patients with left-hemisphere lesions, those with major depression performed significantly below nondepressed patients on four of nine cognitive domains examined with a neuropsychological test battery. Among patients with right-hemisphere stroke, those with major depression did not perform below nondepressed patients on any of the nine cognitive domains. The differential effect of depression on cognitive performance between left- and right-hemisphere lesion groups could not be accounted for by demographic variables, neurological symptoms, lesion location, or lesion size. Poststroke major depression appeared to produce a decline in cognitive performance or dementia of depression that depended on the laterality of the lesion.

Brain↗

PubMed1989

Cognitive impairments in different stages of Parkinson's disease.

A consecutive series of 94 patients with Parkinson's disease (PD) were evaluated for the presence of depression and neuropsychological deficits. Patients were divided into groups based on the severity of their PD symptoms and then further subdivided into depressed and nondepressed groups. Both stage of PD and existence of depression had significant effects on neuropsychological performance. The nondepressed group with severe symptoms showed deficits in cognitive tasks involving motor speed, and the depressed patients with severe symptoms demonstrated impairments in frontal-lobe-related tasks.

Aged↗

PubMed1989

Dementia of depression among patients with neurological disorders and functional depression.

Cognitive performance on the Mini-Mental State Examination (MMSE) was assessed in depressed patients (diagnosis of major depression) with cerebrovascular lesions, with Parkinson's disease, or with functional depression (no known brain lesions). Controls for patients with brain lesions or Parkinson's disease were nondepressed patients with the same conditions. Controls for functionally depressed patients were age-matched normal individuals. Depressed patients had significantly lower total MMSE scores than their nondepressed counterparts, but depression did not have an effect on cognitive performance across the three disease groups. The only significant difference between depressed and nondepressed patients shared by all three groups was poorer performance by depressed patients on the delayed-recall task. The findings suggest that major depression may lead to a specific pattern of cognitive deficits independent of coexisting brain pathology.

Brain Damage, Chronic↗

PubMed1989

Emotional behavior after a Wada test in a patient with secondary mania.

Soon after treatment of a right basotemporal vascular malformation using an embolization procedure, a 25-year-old patient developed an acute episode of mania. Two months later the patient was still manic, and a second embolization was scheduled. Before it was conducted, a Wada test was carried out to determine speech dominance. No changes in manic symptoms were observed after amytal injections into the left middle cerebral, right frontopolar, or right middle cerebral arteries. This finding suggests that secondary mania may not be the result of "release" of the left hemisphere following a right hemisphere lesion but instead may be related to specific disturbances within the right hemisphere.

Adult↗

PubMed1989

Affective disorders and cerebral vascular disease.

Empirical studies have recently demonstrated that major and minor depressive disorders occur in 30-50% of stroke patients, and last more than one year without treatment, although they do respond to tricyclic antidepressants. These mood disorders are not strongly associated with severity of impairment, demographic characteristics, social supports or prior personal history, but major depression is often strongly associated with left frontal or left basal ganglia lesions and pre-existing subcortical atrophy. While the aetiology of these mood disorders remains unknown, serotonergic or noradrenergic dysfunction may play a role. Mania is a rare complication of stroke: the clinical presentation and response to treatment are usually the same as mania without brain injury. Post-stroke mania is strongly associated with both a right hemisphere lesion in a limbic-connected area and a second predisposing factor, such as genetic loading for affective disorder, pre-existing subcortical atrophy or seizure disorder. This disorder may be mediated through frontal lobe dysfunction. The lesion method represents a potentially fruitful technique for investigating the mechanisms of affective disorder.

Bipolar Disorder↗

PubMed1989

Mood changes after right-hemisphere lesions.

Ninety-three patients with acute stroke lesions restricted to the right hemisphere were examined for the presence of mood changes. While 46 patients showed no mood changes, 19 were unduly cheerful, 17 had developed major depression, and 11 had developed minor depression. Although there were no significant between-groups differences in other demographic variables, neurological deficits, activities of daily living, cognitive impairment, or quality of social support, patients with major depression had a significantly higher frequency of familial history of psychiatric disorder and lesions of the parietal cortex than patients with either no mood change or major depression following left-hemisphere lesions. On the other hand, undue cheerfulness was significantly associated with lesions of the right frontal operculum. These findings suggest that major depression following right-hemisphere lesions may have a different aetiology and mechanism than major depression following left frontal or basal ganglia lesions.

Activities of Daily Living↗

PubMed1989

Depression in patients with early versus late onset of Parkinson's disease.

We examined correlates of depression in patients whose onset of Parkinson's disease (PD) began before age 55 (early-onset group) compared with patients whose onset was after age 55 (late-onset group). The early-onset group showed a significantly higher frequency of depression than the late-onset group. When both groups were matched for duration of the disease, the early-onset group still showed a significantly higher frequency of depression, whereas tremor, akinesia, and rigidity were significantly more severe in the late-onset group. A stepwise regression analysis showed that in the early-onset group, depression scores were significantly correlated with scores of cognitive impairment and duration of the disease, while in the late-onset group, depression scores were significantly correlated with impairments in activities of daily living. These data suggest that depression in patients with early-onset PD may have a different etiology than in patients with late-onset PD.

Aged↗

PubMed1989

Psychic akinesia following bilateral pallidal lesions.

After suffering a carbon monoxide intoxication, a thirty-nine-year-old patient presented a marked behavioral change, with a severe anterograde and retrograde amnesia, extreme placidity, bulimia, and hypersexuality. This picture lasted for twenty days. Placidity and anterograde amnesia persisted, while marked psychic akinesia and abnormal involuntary movements soon appeared. A CT scan disclosed bilateral low density lesions involving the pallidum. The patient showed marked improvement after treatment with bromocriptine.

Adult↗

PubMed1989

Mood disorders following stroke: new findings and future directions.

Previous investigations by our group and others have demonstrated that poststroke depressions are not fully explained by the severity of associated impairment. We have consistently found, however, a strong association between development of major depression and left anterior brain injury. Recent studies have demonstrated that either left anterior cortical or subcortical lesions may lead to the development of major depression and that preexisting subcortical atrophy may play an important permissive role in the development of major depression. Patients with a mild degree of ventricular enlargement perhaps related to perinatal damage may be more likely to develop poststroke major depression following a lesion of the left frontal cortex or left basal ganglia than a patient without preexisting atrophy. Poststroke mania, on the other hand, is strongly associated with right hemisphere lesions as well as a preexisting subcortical atrophy and sometimes a family history of affective disorder. Thus, mania following brain injury may require the convergence of two factors: a right hemisphere brain injury and either a preexisting subcortical atrophy or a genetic vulnerability. PET scan findings have suggested that the biochemical response of the two hemispheres to stroke may be different. Right hemisphere stroke produces an increase in serotonin receptor binding, which is not found following comparable left hemisphere strokes. Within the left hemisphere, the lower the serotonin binding, the more severe the depression. This suggests that the right but not the left hemisphere may have an ability to increase serotonin binding in noninjured regions, producing a biochemical "compensation" for damage. This differential biochemical response to injury between the right and left hemisphere may partially explain why left hemisphere injury leads to depression and right hemisphere injury (in special circumstances) lead to mania. There remain, however, numerous unanswered questions and many important areas for future research. Although this area of neuropsychiatry is just beginning to develop, it is hoped that insights gained from studying mood disorders in brain-injured patients may also help to illuminate mechanisms involved in affective disorder in patients without brain injury.

Aged↗

PubMed1988

Behavioral abnormalities induced by frontal cortical and nucleus accumbens lesions.

In previous studies, we have demonstrated that in male rats, unilateral right hemisphere lesions of either the frontolateral cortex or the nucleus accumbens (NAS) result in significant postoperative locomotor hyperactivity. In the present study we carried out two experiments to assess whether the production of hyperactivity in response to these two lesions is mediated through a common mechanism. In the first experiment, male Sprague-Dawley rats received either unilateral frontocortical suction and/or unilateral electrolytic lesions of the NAS. Only rats with lesions of the right hemisphere (suction and/or electrolytic) developed locomotor hyperactivity. Similar lesions in the left hemisphere did not result in behavioral changes. While both right cortical and NAS lesions alone produced hyperactivity, there was no additive effect of both lesions. In the second experiment, the effect of cortical lesions on NAS dopaminergic activity was assessed. Male Sprague-Dawley rats received either a right, left or sham frontocortical suction lesion, and were sacrificed 1, 2, and 4 weeks after surgery. Right hemisphere suction lesions produced a significant bilateral increase in NAS and caudate nucleus dopamine turnover (as measured by DOPAC/DA ratio) 4 weeks post-lesion, while similar left hemisphere lesions did not. These findings suggest that lesions in the dorsolateral frontal cortex and NAS may affect locomotor activity through a common mechanism mediated through the NAS.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1988

Differential mood changes following basal ganglia vs thalamic lesions.

Patients with computed tomographic scan-verified unilateral lesions in the basal ganglia or thalamus were examined for the presence of poststroke mood disorders. Patients with left-sided basal ganglia lesions (mainly in the head of the caudate nucleus) showed a significantly higher frequency and severity of depression, as compared with patients with right-sided basal ganglia or thalamic (left- or right-sided) lesions. Results suggest that damage to biogenic amine pathways and/or frontocaudate projections may play an important role in the modulation of mood.

Aphasia↗

PubMed1988

Comparison of patients with and without poststroke major depression matched for size and location of lesion.

Patients who developed major depression within two years following stroke (n = 13) were compared with patients who did not become depressed in the same period (n = 13) but who did have a similar size and location of lesion as in the depressed group. Although the depressed patients were not significantly different from the nondepressed patients in background characteristics, history of depressive disorder, neurological impairment, or social functioning, the depressed group had greater cognitive impairment as measured by Mini-Mental State score. In addition, the depressed group had significantly larger lateral and third ventricular to brain ratios than nondepressed patients on computed tomographic scan analysis. The results suggest that poststroke depression itself may produce an intellectual impairment; subcortical atrophy, which likely preceded the stroke lesion, may produce a vulnerability for depression following stroke.

Aged↗

PubMed1988

Bilateral opercular syndrome and crossed aphemia due to a right insular lesion: a clinicopathological study.

A right-handed male patient suddenly noted lower bilateral facial and lingual palsy, and inability to masticate and swallow, but with preserved automatic functions. He was mute, communicating only through writing, but verbal comprehension was normal (aphemia). On anatomopathological examination, an ischemic infarction of the entire right insula, with mild extension to the fronto-temporoparietal operculum was observed. The left hemisphere was normal. The clinical findings suggest a bilateral opercular syndrome due to a right hemisphere lesion and a crossed aphemia.

Cerebral Cortex↗

PubMed1988

Depressive disorders following posterior circulation as compared with middle cerebral artery infarcts.

Patients with cerebrovascular lesions in the posterior circulation territory (PC) were compared with patients having middle cerebral artery territory (MCA) strokes for the presence of mood disorders. Both groups showed a similar profile of clinical symptoms of depression during the acute evaluation in hospital. Patients with posterior circulation lesions involving the brainstem and/or cerebellum demonstrated a significantly lower frequency of depression than patients with MCA lesions or patients with posterior circulation lesions involving the left cerebral hemisphere. Moreover, depression following brainstem and/or cellebellar infarcts was of significantly shorter duration than depression following MCA lesions. These differences in the frequency and duration of depression following brainstem/cerebellar as compared with MCA lesions were not explained by differences in lesion volume, physical impairment, cognitive deficits or quality of social support. They suggest that PC and MCA induced depression may have different aetiologies.

Cerebral Arteries↗