An autopsy-proven case of Corticobasal degeneration heralded by Pontine infarction

Dallah Yoo, Sung Hye Park, Sungwook Yu, Tae Beom Ahn

Research output: Contribution to journalArticlepeer-review


Background: Neurodegenerative disorders are characterized by insidious progression with poorly-delineated long latent period. Antecedent clinical insult could rarely unmask latent neurodegenerative disorders. Here, we report an autopsy-proven case of corticobasal degeneration which was preceded by a lacunar infarction. Case presentation: A 58-year-old man presented with acute ataxia associated with a lacunar infarction in the right paramedian pons. His ataxia persisted with additional progressive gait difficulty and left arm clumsiness. Six months later, a follow-up neurological examination showed asymmetrical bradykinesia, apraxia, dystonic posturing, postural instability, and mild ataxia of the left limbs. Cognitive examination revealed frontal executive dysfunction and visuospatial difficulties. Dopamine transporter imaging scan demonstrated bilateral reduced uptakes in mid-to-posterior putamen, more prominent on the right side. Levodopa-unresponsive parkinsonism, asymmetric limb dystonia, and ideomotor apraxia became more conspicuous, while limb ataxia gradually vanished. The patient became unable to walk without assistance after 1 year, and died 4 years after the symptom onset. Autopsy findings showed frontoparietal cortical atrophy, ballooned neurons, and phosphorylated tau-positive astrocytic plaques and neuropil threads with gliosis and neuronal loss, confirming the corticobasal degeneration. Conclusions: The case illustrates that precedent clinical events such as stroke might tip a patient with subclinical CBS into overt clinical manifestations.

Original languageEnglish
Article number148
JournalBMC Neurology
Issue number1
StatePublished - Dec 2021


  • Autopsy
  • Case report
  • Corticobasal degeneration
  • Stroke


Dive into the research topics of 'An autopsy-proven case of Corticobasal degeneration heralded by Pontine infarction'. Together they form a unique fingerprint.

Cite this