Authors :
Presenting Author: Matthew Preszler, MD – University of Toledo
Fahham Asghar, MD – University of Toledo
Mohamad Alsakka, MD – University of Toledo
Ajaz Sheikh, MD – University of Toledo
Rationale:
The advent of anti-amyloid therapy for Alzheimer’s dementia has created a new frontier in neurology. Amyloid-related imaging abnormalities (ARIA) are one possible complication and can be associated with adverse outcomes. However, the available literature regarding this is minimal. Here we report a patient with ARIA who eventually developed intraparenchymal hemorrhage and seizures in the affected brain region.Methods: Case report
Results:
A 73-year-old female was diagnosed with mild Alzheimer’s type dementia and started on lecanemab infusions after an appropriate qualifying evaluation. Routine MRI brain after the fourth lecanemab infusion showed evidence of ARIA with vasogenic edema most pronounced in the left temporo-occipital region and microhemorrhage in the left thalamus. This was not present on baseline MRI brain and anti-amyloid therapy was stopped. Approximately one week after her last infusion, the patient developed aphasia and a subsequent generalized clinical seizure for which she was treated at an outside hospital. Work-up at that time showed intraparenchymal hemorrhage (IPH) into the edematous area of the left temporo-occipital region. She was discharged on LEV 500 mg BID.
Two weeks later, she presented again with aphasia and was found to have a high degree of epileptogenicity originating from the left temporal and parietal regions on EEG. Abnormal EEG findings included left temporal PLEDs, electrographic seizures, and ictal-interictal continuum. The patient’s electrographic seizures rarely had clear clinical correlation as she remained persistently aphasic and became encephalopathic. Notably, three gelastic seizures were identified localizing to the left temporal region. Repeat MRI brain revealed the previously known left hemispheric edema and IPH. However, diffusion restriction in the left pulvinar area and occipital cortex was newly identified and highly suggestive of postictal change. For this reason, the ictal-interictal continuum was believed to represent status epilepticus and treated aggressively with ASMs. Ultimately, she received a FOS load (20 mg/ kg) and titrated to maintenance doses of LEV 2 g BID and LCM 150 mg BID. Additionally, pulse dose glucocorticoids (IV methylprednisolone 1 g daily for 5 days) were given for treatment of cerebral edema.
Her EEG gradually improved with decreased frequency of the PLEDs and cessation of electrographic seizures. Clinically, the patient’s mentation and aphasia improved significantly although she continued to have evidence of transcortical sensory aphasia at the time of discharge. She was discharged on LEV and LCM as well as oral prednisone with a starting dose of 1 mg/ kg and gradual taper over 12 weeks.
Conclusions:
We report a patient who developed IPH and status epilepticus including three gelastic seizures as a complication of treatment with anti-amyloid therapy. She responded well to ASM and glucocorticoid treatment. This case demonstrates a potential management approach to complications of anti-amyloid therapy as well as the first reported gelastic seizures in this patient population.Funding: None