2026 ECNP Congress

PS01-1128

At the crossroads of neurology and psychiatry: an Alzheimer-related corticobasal syndrome with seizure

Gülsüm Irem Kılınç — H. evran, F. guney, M. ak · necmettin erbakan medicine faculty, pschiatry, KONYA, Türkiye

2026 ECNP Congress

INTRODUCTION

Corticobasal syndrome (CBS) is characterized by asymmetric parkinsonism, rigidity, myoclonus, and apraxia, and may be associated with corticobasal degeneration and Alzheimer’s disease (AD). CBS-AD overlap with prominent neuropsychiatric symptoms and seizures is uncommon, poses diagnostic challenges, and requires close neurology-psychiatry collaboration.[1], [2]

OBJECTIVE

To present a rapidly progressive CBS case possibly linked to AD, with prominent seizures and neuropsychiatric symptoms, highlighting the importance of integrated neurology-psychiatry collaboration for diagnosis and management.

CASE PRESENTATION

A 54-year-old woman with premorbid anxious traits reported forgetfulness, decreased speech, difficulty following lines while reading, perseveration, executive dysfunction, decline in fine motor skills, difficulty organizing daily activities, and misplaced objects in her late forties. On initial neurological assessment, the Mini-Mental State Examination (MMSE) score was 24–25. Neurological examination was largely unremarkable, but the clock-drawing test showed a poorly formed circle, incorrect numerical placement, and inability to draw the hands. Magnetic resonance imaging revealed significant atrophy in the left frontotemporal region. Electroencephalogram (EEG) showed mild encephalopathic changes. Dementia treatment with donepezil and memantine was initiated; sertraline was added for anxiety.

About one year later, following a significant psychosocial stressor, the patient’s condition markedly deteriorated. The patient’s independence in daily activities declined progressively. Myoclonic jerks during sleep were reported. During the neurological examination, the MMSE score was 12. Asymmetric praxis deficits included limited left-arm use, unreliable clock drawings, visuospatial hemineglect, impaired finger-to-nose testing, and difficulty imitating learned movements. These findings are consistent with CBS. A repeat EEG revealed moderate diffuse cerebral dysfunction.

FDG-PET demonstrated bilateral parieto-frontal-temporal hypometabolism with a temporoparietal predominance, suggesting underlying AD pathology. [3]

In parallel, prominent neuropsychiatric symptoms emerged. The patient showed increased anxiety, spatial disorientation in familiar settings, couldn’t recognize her home, and talked to her reflection in mirrors. Furthermore, several episodes occurred, lasting minutes, resembling tonic-clonic seizures with loss of consciousness, tonic posture, eye deviation, and postictal confusion. [5]

One episode caused a vertebral fracture. Seizures were successfully managed with levetiracetam. For differential diagnosis, a comprehensive genetic panel examined 40 neurodegenerative genes (including ACE, ADAM10, APOE, APP, MAPT, PSEN1, PSEN2, SNCA, GBA1, GRN); no pathogenic variants were found.

DISCUSSION

Although asymmetric apraxia and cortical signs supported CBS, FDG-PET findings suggested underlying AD pathology, illustrating overlapping clinical manifestations across neurodegenerative disorders such as AD and corticobasal degeneration. Seizures are rare in CBS but may be related to AD pathology. The patient’s seizure history, causing vertebral fractures, highlights its diagnostic importance and impact on mortality and morbidity. Another salient point is the parallel between neuropsychiatric symptoms and neurodegeneration, emphasizing the close link between neurology and psychiatry in atypical neurodegenerative diseases and the need for holistic assessment.

CONCLUSION

CBS may progress rapidly with underlying AD pathology, showing neuropsychiatric symptoms and seizures. In atypical cases, other neurodegenerative diseases should be considered. This atypical AD-related CBS case with seizures and neuropsychiatric symptoms emphasizes the need for comprehensive neurological and psychiatric evaluation for accurate diagnosis and treatment. [4]

References

  1. Hassan, A., Whitwell, J. L., & Josephs, K. A. (2011). The corticobasal syndrome–Alzheimer’s disease conundrum. Expert Review of Neurotherapeutics, 11(11), 1569–1578. https://doi.org/10.1586/ern.11.153
  2. Sakae N, Josephs KA, Litvan I, Murray ME, Duara R, Uitti RJ, Wszolek ZK, van Gerpen J, Graff-Radford NR, Dickson DW. Clinicopathologic subtype of Alzheimer’s disease presenting as corticobasal syndrome. Alzheimers Dement. 2019 Sep;15(9):1218-1228. doi: 10.1016/j.jalz.2019.04.011. Epub 2019 Aug 6. PMID: 31399334; PMCID: PMC9262170.
  3. Cerami C, et al. “FDG-PET patterns associated with underlying pathology in corticobasal syndrome.” Neurology. 2019. PMCID: PMC6442013 PMID: 30700592
  4. Porsteinsson AP, et al. Neuropsychiatric symptoms in Alzheimer’s disease: Past, present and future. Ageing Res Rev. 2026.PMC12782149
  5. Doğan B, et al. Corticobasal Syndrome as Alzheimer’s Disease Subtype: A Case Report. Turk J Neurol. 2023 DOI: 10.4274/tnd.2022.09481