The neurobehavioural spectrum of acute stroke: when vascular lesions mimic psychiatric syndromes

Introduction: Acute stroke is typically recognized by abrupt onset of focal neurological deficits. However, some patients present with symptoms suggestive of other conditions – the so-called “stroke chameleons.” A subset of these patients presents with behavioural, affective or cognitive symptoms that resemble primary psychiatric disorders, such as agitation, disinhibition, psychosis or affective lability. These presentations are particularly challenging in the emergency setting, where the absence of obvious lateralizing signs can lead to misdiagnosis as delirium, substance intoxication or acute psychiatric illness. In particular, right hemisphere lesions have been associated with impaired insight, hemispatial neglect, emotional dysregulation and altered social cognition – all of which may dominate the clinical picture and conceal its vascular origin.

Aims: To review the most common psychiatric manifestations of acute stroke, with focus on behavioural presentations that mimic psychiatric syndromes, the neuroanatomical correlates of these symptoms and the diagnostic factors that contribute to their delayed recognition in the emergency setting.

Methods: A narrative review of the literature was conducted using publications indexed in the PubMed database, focusing on relevant reviews and case reports published over the last decade, from 2016 to 2026. The search focused on articles addressing acute stroke with predominant behavioural, affective, cognitive or psychotic symptoms, as well as studies examining lesion localisation and network-based models of brain-behaviour relationships.

Results: Behavioural presentations of acute stroke most often include agitation, disorganized behaviour, emotional lability, apathy, poor insight, and, less commonly, delusions or hallucinations. Data from systematic reviews indicate a predominance of right hemisphere lesions, particularly in the right frontal, temporal, and parietal regions, as well as the right caudate nucleus. These locations are consistent with disruption of distributed networks involved in salience attribution, attention, self-monitoring and emotional regulation. In right hemisphere stroke, anosognosia and neglect may further reduce awareness of neurological impairment. Beyond focal lesion models, current accounts emphasize large-scale network dysfunction, notably involving frontoparietal and salience systems, as a mechanism linking vascular injury to behavioural change.

Diagnostic difficulty is compounded by overlap with delirium, iatrogenic effects, metabolic disturbances and pre-existing psychiatric diagnoses. In acute care, cognitive biases among practitioners such as anchoring on a psychiatric explanation, premature closure and under-recognition of subtle neurological signs may delay neuroimaging and adequate (and timely) treatment. Emerging evidence highlights the importance of subtle neurological signs (e.g., gaze deviation, inattention, asymmetry) and vascular risk profiles in raising suspicion for underlying neurovascular events.

Conclusions: Acute stroke can present as a psychiatric syndrome in which behavioural and cognitive disturbances predominate over focal deficits. Recognition of these presentations requires a network-based understanding of brain–behaviour relationships, with particular attention to right hemisphere and fronto-subcortical dysfunction. Increased awareness of the psychiatric spectrum of stroke presentation can facilitate earlier identification, prompt neuroimaging and provide a more accurate differentiation from primary psychiatric disorders in the acute clinical setting.

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