Clinical-Neurological Features and Cognitive Deficit in Chronic Alcoholic Encephalopathies

Post-Stroke Psychosis and Neuropsychiatric Disturbances in an Older Adult: A Diagnostic Challenge and Case Report

Post-stroke neuropsychiatric disturbances may manifest as affective, cognitive, behavioral, or psychotic symptoms and may represent a diagnostic challenge, particularly when structural epilepsy coexists with brain lesions involving different vascular territories. We present the case of a 67-year-old man with a history of arterial hypertension, type 2 diabetes mellitus, and obstructive sleep apnea syndrome, who had experienced ischemic strokes in the territories of the right posterior cerebral artery and the left middle cerebral artery approximately one month before admission, with residual nonfluent aphasia and right upper-limb paresis. Fifteen days before admission, he experienced a late-onset focal seizure and was started on lacosamide. He subsequently developed progressive anxiety, depressed mood, psychomotor agitation, cognitive decline, behavioral changes, persecutory delusions, ideas of reference, and visual and auditory hallucinations. During the evaluation, he was conscious, without evident fluctuations in the level of consciousness or clinical findings consistent with delirium. Metabolic and infectious studies did not identify an alternative cause. Brain computed tomography showed right occipital and left frontoparietal encephalomalacia, as well as cerebral small-vessel disease, without evidence of intracranial hemorrhage or a new acute ischemic event. Video-EEG monitoring did not record epileptiform activity or electrographic seizures during the monitoring period. Brain magnetic resonance imaging was requested to rule out additional structural lesions; however, the study could neither be completed nor retrieved because the patient was transferred to another institution. During the observed hospital stay, he remained neurologically stable, without new focal deficits or recurrent seizures. He received symptomatic treatment with olanzapine, lacosamide was continued, and he underwent joint evaluation by the Neurology and Psychiatry services. The exact doses, subsequent pharmacological adjustments, and longitudinal course of the psychiatric symptoms could not be established because institutional follow-up was lost after the transfer. This case highlights the complexity of distinguishing post-stroke psychiatric manifestations from a new cerebrovascular event, delirium, nonconvulsive epileptic activity, postictal states, and primary psychiatric disorders. Integration of the clinical timeline, mental status examination, neuroimaging, and electrophysiological studies is essential to guide diagnosis and establish individualized treatment.

Posterior cortical atrophy with initial psychiatric presentation: a case report

Posterior cortical atrophy (PCA) is a rare neurodegenerative syndrome most commonly associated with atypical Alzheimer’s disease. It is characterized by progressive visuospatial and visuoperceptual deficits with relative sparing of memory and language in early stages. Diagnosis is frequently delayed or missed due to clinical heterogeneity, subtle early symptoms, and limited sensitivity of routine cognitive screening tools. Psychiatric symptoms may further obscure the underlying neurological disorder. This case highlights the diagnostic challenges posed by PCA presenting in the context of prominent psychiatric symptoms, combined with a rapid clinical decline. A 68-year-old white Danish male presented with suicidal ideation and was initially admitted to a psychiatric ward. He had a remote history of a suicide attempt and a family history of suicide but no known neurodegenerative disease. Within a short period, severe cognitive and functional impairment became evident, dominated by visuospatial deficits, apraxia, simultanagnosia, optic ataxia, and features of Gerstmann and Balint syndromes, with relative preservation of memory and language. Neuroimaging revealed marked posterior cortical atrophy and parieto-occipitotemporal hypometabolism with sparing of the posterior cingulate cortex. Cerebrospinal fluid analysis showed mildly reduced amyloid-β1–42 and markedly elevated neurofilament light chain levels. Electroencephalography demonstrated focal posterior slowing without epileptiform activity. Extensive evaluation excluded autoimmune, epileptic, metabolic, and prion-related causes. Based on the clinical syndrome, characteristic neuroimaging findings, and supportive CSF biomarkers, a diagnosis of posterior cortical atrophy likely related to underlying Alzheimer’s disease pathology was made. Disease-specific treatment was discussed but not initiated due to patient preference. This case illustrates how posterior cortical atrophy may be overlooked, particularly when psychiatric symptoms dominate the initial presentation. It underscores the importance of considering neurodegenerative disorders in older patients with atypical psychiatric presentations or unexplained functional decline. Early recognition of PCA is crucial for accurate diagnosis, appropriate counseling, and tailored supportive care.

Cerebellar Cognitive Affective Syndrome in Spinocerebellar Ataxia Type 6

Background: Spinocerebellar ataxia type 6 (SCA6) has traditionally been classified as a "pure" cerebellar syndrome; however, converging evidence points to non-motor involvement. Characterization of its cognitive-affective profile remains limited, constraining the understanding of its full clinical spectrum. Objectives: To investigate non-motor manifestations in SCA6 and contribute to a more comprehensive characterization of its cognitive-affective profile through standardized neuropsychological assessment. Methods: A monocentric, cross-sectional case-control study included nine patients with genetically confirmed SCA6 and eight healthy controls matched for age and years of education. Participants were assessed using the Cerebellar Cognitive Affective/Schmahmann Syndrome Scale (CCAS-S), the Scale for the Assessment and Rating of Ataxia (SARA), and a comprehensive neuropsychological battery. Anxiety and depressive symptoms were also assessed. Results: Compared with controls, SCA6 patients showed poorer performance on time-dependent measures sensitive to inhibitory control and selective attention and on tasks involving visuoconstructive and visuomotor integration, as well as poorer verbal episodic memory, with a trend toward poorer confrontation naming; motor slowing and reduced processing speed cannot be ruled out. Anxiety was significantly elevated. Cerebellar motor dysfunction predicted a higher number of failed CCAS-S domains, even after controlling for disease duration. Conclusions: These exploratory findings suggest cognitive and affective alterations in SCA6 beyond the motor domain, warranting investigation within the Cerebellar Cognitive Affective Syndrome framework. Given the small sample, absence of correction for multiple comparisons, and potential motor and processing-speed confounds, results are preliminary. They highlight the relevance of targeted neuropsychological assessment and may inform more individualized care strategies.

Early Detection OF Cognitive Disorders in Patients with Chronic Cerebral Ischemia

Parkinson’s Disease Dementia: Etiology, Mechanisms, Diagnosis, Management and Future Directions

Parkinson’s disease dementia (PDD) is a common, disabling, and prognostically important neurocognitive syndrome arising in the context of established Parkinson’s disease (PD). It represents one of the major late-stage manifestations of synucleinopathy and reflects the convergence of cortical Lewy body pathology, cholinergic degeneration, dopaminergic network dysfunction, Alzheimer-type co-pathology, neuroinflammation, vascular injury, and age-related vulnerability. Clinically, PDD is characterized by progressive impairment in attention, executive function, visuospatial processing, memory retrieval, and behavioural regulation, typically accompanied by neuropsychiatric symptoms such as visual hallucinations, apathy, depression, anxiety, delusions, REM sleep behaviour disorder, and fluctuating cognition. The diagnostic distinction between PDD and dementia with Lewy bodies remains anchored in the oneyear rule, although biological and clinicopathological evidence increasingly supports their conceptualization as overlapping Lewy body dementias. Diagnosis remains primarily clinical, supported by neuropsychological testing, structural and functional imaging, exclusion of reversible contributors, and emerging biomarkers including α-synuclein seed amplification assays, amyloid and tau biomarkers, and neurodegeneration markers. Rivastigmine remains the bestsupported symptomatic pharmacologic therapy, while management requires systematic rationalization of dopaminergic and anticholinergic medication, treatment of neuropsychiatric complications, sleep optimization, rehabilitation, caregiver support, and advanced-care planning. Disease-modifying therapies remain investigational, but future directions include biological staging, precision phenotyping, synuclein-targeted immunotherapy, lysosomal enhancement, neuroinflammation modulation, digital biomarkers, and integrated trials across the Lewy body disease spectrum. Keywords: Parkinson’s disease dementia; Lewy body dementia; α-synuclein; cognitive impairment; rivastigmine; dementia with Lewy

Spectrum of central nervous system damage associated with alcohol misuse

Alcohol misuse remains one of the most important modifiable risk factors for death and disability. In neurology, it is linked to central nervous system damage, ranging from acute encephalopathies and withdrawal complications, strokes and trauma, to chronic cognitive syndromes and structural damage affecting the cerebellum and corpus callosum. The clinical presentation is often non‑specific, and concomitant metabolic disturbances, liver disease, infections, and trauma may delay proper diagnosis. This article provides a concise, practical review of the most clinically relevant clinicopathological phenotypes associated with long‑term alcohol misuse and nutritional deficiencies. Issues discussed include key mechanisms (direct neurotoxicity of ethanol and its metabolites, oxidative stress, neuroinflammation, impaired energy metabolism, and thiamine and magnesium deficiency) as well as the clinical picture and diagnostic approach to Wernicke encephalopathy and Korsakoff syndrome, Marchiafava–Bignami disease, alcohol‑related cerebellar degeneration, and cortical laminar necrosis including Morel’s laminar sclerosis. Typical features on magnetic resonance imaging and principles of differential diagnosis with stroke, central nervous system infection, and metabolic encephalopathy are summarised. Long‑term consequences of prenatal alcohol exposure, referred to as foetal alcohol spectrum disorders, are also discussed. In acute presentations, immediate intravenous thiamine administration before glucose, together with the simultaneous correction of metabolic abnormalities, is emphasised as a time‑critical intervention. For chronic syndromes, sustained abstinence, rehabilitation, and psychological support remain the cornerstone of care.