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Episodic aphasia following a motor vehicle collision
  1. Albert Aboseif1,
  2. Emily F Maly1,
  3. Faez H Syed1,
  4. Vineet Punia2,
  5. Amy Kunchok3,
  6. Justin R Abbatemarco3
  1. 1Department of Neurology, Cleveland Clinic, Cleveland, Ohio, USA
  2. 2Epilepsy Center, Department of Neurology, Cleveland Clinic, Cleveland, Ohio, USA
  3. 3Mellen Center for Multiple Sclerosis Treatment and Research, Cleveland Clinic, Cleveland, Ohio, USA
  1. Correspondence to Dr Justin R Abbatemarco, Mellen Center for Multiple Sclerosis Treatment and Research, Cleveland Clinic, Cleveland, Ohio, USA; ABBATEJ2{at}ccf.org

https://doi.org/10.1136/pn-2024-004181

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    Case presentation

    A 29-year-old man presented to the emergency department after a motor vehicle collision, with aphasia, perseveration and no memory of the events leading up to the crash. His serum lactate was elevated, plasma glucose was normal, and urine toxicology was negative. CT scans of the head and neck were normal. He was thought to have had a first-time seizure and was discharged with a neurology follow-up.

    One week later, he had an episode of aphasia and headache, progressing to a focal-to-bilateral tonic-clonic seizure, which resolved with lorazepam. There were no clear risk factors for epilepsy, and there was no personal or family history of seizures. On examination, he had fluctuating aphasia, right-sided neglect, right-hand apraxia, finger agnosia, acalculia and right-left confusion. An MR scan of the brain without contrast 6 days after symptom onset was normal (figure 1A). He was started on levetiracetam before discharge home.

    Figure 1

    (A) MR scan of the brain 6 days after the index visit, showing normal appearances. (B) MR scan of the brain 23 days after the index event, showing T2/FLAIR hyperintensity in the left parieto-occipital lobes and T1-weighted gadolinium enhancement in the leptomeninges and cortical/subcortical regions. (C) MR scan of the brain 40 days after the index event, before treatment, showing subtle improvement in leptomeningeal disease but persistent T2/FLAIR changes and an increase in patchy cortical enhancement. (D) MR scan of the brain 5 weeks after treatment showing significant improvement in the FLAIR hyperintensities and both leptomeningeal and parenchymal enhancement. FLAIR, fluid-attenuated inversion recovery.

    Questions for consideration

    How would you localise his transient neurological deficits?

    Examination identified a tetrad of agraphia, acalculia, right-left disorientation and finger agnosia.1 This syndrome, often referred to as Gerstmann syndrome, usually localises to the dominant parietal lobe. The transient and recurrent nature of his symptoms suggested focal seizures as the underlying cause.1

    Three …

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    Footnotes

    • AA and EFM are joint first authors.

    • X @albertaboseif

    • AA and EFM contributed equally.

    • Contributors JRA, AA and EFM: drafting, revision of the manuscript for content, including medical writing for content, major role in acquisition of data, study concept for design, analysis or interpretation of data. AK, VP and FHS: interpreted the data and revised the manuscript for intellectual content.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests JRA served on scientific advisory boards for of EMD Serono, Genentech, Horizon Therapeutics & TG Therapeutics; has received research support from Horizon Therapeutics. AK discloses personal compensation for consulting for Genentech, Horizon therapeutics, Alexion and EMD Serono. The remaining authors have no relevant disclosures.

    • Provenance and peer review Not commissioned. Externally peer reviewed by Emma Tallantyre, Cardiff, UK.