3 research outputs found

    Unusual presentation of basilar artery stroke secondary to patent foramen ovale: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>We report a case of a patient presenting with neuropsychiatric manifestations secondary to paradoxical embolism</p> <p>Case presentation</p> <p>Unexplained rapid onset of confusion with amnesia and minimal neurological deficits can be a manifestation of various systemic causes of which stroke, either ischemic or hemorrhagic, is one. Thorough and systematic evaluation of these patients can be highly rewarding in terms of optimizing patient outcome. We report the case of a 45-year-old woman whose initial presentation was with acute onset of confusion, memory loss with personality change and headaches. A differential diagnosis of systemic illness and cerebral pathology was entertained. She was empirically treated for neurological infection. Brain imaging revealed bilateral thalamic and cerebellar infarction. Further evaluation with an aim to define the etiology, revealed the diagnosis of Patent Foramen Ovale with paradoxical embolism. The differential diagnosis of unexplained rapid onset of confusion, amnesia with minimal motor neurological deficits and relevant appropriate investigations are discussed in this case report.</p> <p>Conclusion</p> <p>This case highlights the importance of recognising the atypical manifestations of posterior fossa stroke. In young patients presenting with non-focal neuropsychiatric manifestations, paradoxical embolism, secondary to patent foramen ovale is a possible cause.</p

    An investigation into aripiprazole's partial D(2) agonist effects within the dorsolateral prefrontal cortex during working memory in healthy volunteers

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    Rationale: Working memory impairments in schizophrenia have been attributed to dysfunction of the dorsolateral prefrontal cortex (DLPFC) which in turn may be due to low DLPFC dopamine innervation. Conventional antipsychotic drugs block DLPFC D2 receptors, and this may lead to further dysfunction and working memory impairments. Aripiprazole is a D2 receptor partial agonist hypothesised to enhance PFC dopamine functioning, possibly improving working memory. Objectives: We probed the implications of the partial D2 receptor agonist actions of aripiprazole within the DLPFC during working memory. Investigations were carried out in healthy volunteers to eliminate confounds of illness or medication status. Aripiprazole’s prefrontal actions were compared with the D2/5-HT2A blocker risperidone to separate aripiprazole’s unique prefrontal D2 agonist actions from its serotinergic and striatal D2 actions that it shares with risperidone. Method: A double-blind, placebo-controlled, parallel design was implemented. Participants received a single dose of either 5 mg aripiprazole, 1 mg risperidone or placebo before performing the n-back task whilst undergoing fMRI scanning. Results: Compared with placebo, the aripiprazole group demonstrated enhanced DLPFC activation associated with a trend for improved discriminability (d’) and speeded reaction times. In contrast to aripiprazole’s neural effects, the risperidone group demonstrated a trend for reduced DLPFC recruitment. Unexpectedly, the risperidone group demonstrated similar effects to aripiprazole on d’ and additionally had reduced errors of commission compared with placebo. Conclusion: Aripiprazole has unique DLPFC actions attributed to its prefrontal D2 agonist action. Risperidone’s serotinergic action that results in prefrontal dopamine release may have protected against any impairing effects of its prefrontal D2 blockade
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