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Featured researches published by T. R. Price.


The Lancet | 1984

NORTRIPTYLINE TREATMENT OF POST-STROKE DEPRESSION: A DOUBLE-BLIND STUDY

JohnR Lipsey; GodfreyD. Pearlson; RobertG Robinson; Krishna Rao; T. R. Price

The efficacy of nortriptyline in the treatment of post-stroke depression was assessed by a double-blind study in thirty-four patients. Half of the patients had major depression. There was a significantly greater improvement in depression in patients treated with nortriptyline than in a similar group of placebo-treated patients. Depression was measured by the Hamilton depression scale, Zung depression scale, present state examination, and an overall depression scale. Successfully treated patients had serum nortriptyline levels in the therapeutic range. Post-stroke depressions are common, severe, and longstanding, and the demonstrated efficacy of nortriptyline provides an important addition to the treatments available for stroke patients.


Stroke | 1993

Apathy following cerebrovascular lesions.

Sergio E. Starkstein; J P Fedoroff; T. R. Price; R Leiguarda; Robert G. Robinson

Background and Purpose Although apathy has been reported to constitute a frequent sequela of stroke lesions, there have been no prospective studies on the frequency and correlates of apathy after stroke lesions. In the present study, we examined the frequency and correlates of apathy in a consecutive series of 80 patients with cerebrovascular lesions. Methods We included patients within the first 10 days after a stroke lesion. Patients were examined with a comprehensive neuropsychiatry battery that included the Apathy Scale. Results Eighteen patients (22.5%) showed apathy, nine of whom were also depressed. On the other hand, 18 patients (22.5%) showed depression in the absence of apathy. Although depression and apathy may exist independent of one another, major depression (but not minor depression) was associated with an increased frequency of apathy. Apathy was also significantly associated with older age, cognitive impairments, and deficits in activities of daily living. Finally, apathy was significantly associated with lesions in the posterior limb of the internal capsule. Conclusions These findings demonstrate that apathy is a frequent finding among patients with acute stroke lesions and may coexist with important emotional and cognitive poststroke disturbances. (Stroke. 1993;24:1625-1630.)


Stroke | 1992

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

Sergio E. Starkstein; J P Fedoroff; T. R. Price; R Leiguarda; Robert G. Robinson

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. (Stroke 1992;23:1446‐1453)


Neurology | 1994

Neuropsychological and neuroradiologic correlates of emotional prosody comprehension

Sergio E. Starkstein; J. P. Federoff; T. R. Price; Ramón Leiguarda; Robinson Rg

We examined a series of 59 patients with acute stroke lesions for the presence of comprehension emotional aprosody. Based on a standardized assessment of comprehension of emotional intonation, 29 patients (49%) showed emotional aprosody (17% “mild” aprosody [n = 10] and 32% “severe” aprosody [n = 19]). Patients with comprehension emotional aprosody showed a higher frequency of extinction on double-simultaneous stimulation, anosognosia, and deficits in facial emotion comprehension. Patients with comprehension emotional aprosody also showed a higher frequency of right-hemisphere lesions involving the basal ganglia and the temporoparietal cortex and more severe frontal and diencephalic atrophy. Comprehension emotional aprosody was not necessarily associated with poststroke depression (PSD) since patients with and without PSD showed similar impairments in emotional prosody comprehension.


American Journal of Psychiatry | 1988

Comparison of mania and depression after brain injury: causal factors

Robinson Rg; Judith D. Boston; Sergio E. Starkstein; T. R. Price


British Journal of Psychiatry | 1986

Depression influences intellectual impairment in stroke patients.

Robinson Rg; K. Bolla-Wilson; E. Kaplan; John R. Lipsey; T. R. Price


American Journal of Psychiatry | 1991

Are depressive symptoms nonspecific in patients with acute stroke

Fedoroff Jp; Sergio E. Starkstein; Rajesh M. Parikh; T. R. Price; Robinson Rg


British Journal of Psychiatry | 1983

Mood change following bilateral hemisphere brain injury.

John R. Lipsey; Robinson Rg; Godfrey D. Pearlson; Krishna Rao; T. R. Price


American Journal of Psychiatry | 1985

The dexamethasone suppression test and mood following stroke

Lipsey; Robinson Rg; Godfrey D. Pearlson; Krishna Rao; T. R. Price


Stroke | 1988

Post-stroke depression and lesion location.

Robert G. Robinson; Sergio E. Starkstein; T. R. Price

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Robinson Rg

Johns Hopkins University

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Krishna Rao

Johns Hopkins University School of Medicine

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J P Fedoroff

Johns Hopkins University School of Medicine

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John R. Lipsey

Johns Hopkins University School of Medicine

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R Leiguarda

Johns Hopkins University School of Medicine

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GodfreyD. Pearlson

Johns Hopkins University School of Medicine

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