Authors :
Presenting Author: Krishna Parekh, DO – UT Southwestern Medical Center
Luz Reiley, MD – Neurology – Stony Brook University Hospital; Sayedatun Nessa, MD – Neurology – Stony Brook University Hospital
Rationale:
Lyme disease, caused by Borrelia burgdorferi, is the most prevalent bacterial tick-borne illness, while herpes simplex encephalitis (HSE) is the most common acute viral encephalitis in the United States. Both diseases have diverse and non-specific clinical manifestations including fever, altered mentation, cranial nerve palsies, and skin rash. HSE commonly presents as seizures with various EEG abnormalities in temporal lobes and MRI T2-FLAIR hyperintensities. Seizures and MRI brain findings are rare in lyme neuroborreliosis (LNB). Both diseases have lymphocytic pleocytosis but cerebrospinal fluid (CSF) studies can be diagnostically delayed or have negative confirmatory tests which leads to repeat lumbar puncture (LP). Ertapenem is a carbapenem used to treat multidrug resistant pathogens which may cause seizures at a frequency of 0.2-0.5%; risk factors include renal insufficiency, older age, current infection, interaction with neurotoxic drugs, and brain injury. We present a case of an elderly patient with no prior seizures and recent ertapenem use who presented with seizures with EEG and MRI findings suspicious for HSE but had LNB.Methods:
An elderly woman with a history of hypertension, type-2 diabetes, anemia, right parotidectomy, and radiation to head and neck 29 years ago, complicated by recent surgical treatment of osteoradionecrosis of jaw and mandibular abscess, with recent six doses of ertapenem presented with acute confusion followed by a witnessed generalized seizure. On exam, she was disoriented with a right facial droop. Patient was empirically started on broad spectrum antibiotics and acyclovir for meningitis after LP. EEG revealed frequent runs of fast beta spikes seen over the right temporal region at times evolving into brief focal electrographic seizures with intermittent lower voltage focal slowing over the right hemisphere (A). Brain MRI with contrast revealed T1 post-contrast enhancement and T2-FLAIR hyperintensity in the right temporal lobe concerning for HSE versus seizure epiphenomenon in the right temporal lobe (B). Initial CSF was cloudy with 72 WBC/µL with 90% neutrophil predominance with 29K RBCs (corrected WBC 48), protein 93.3 mg/dL, glucose 91 mg/dL (CSF/serum glucose 91/145, 0.6 normal ratio). Serum serology was positive for lyme disease. Lyme Western Blot IgG was positive with 6/10 bands. CSF paired index was positive (1.19); this was highly consistent with LNB. HSV I/II PCR was negative. Repeat CSF analysis with lymphocytic predominance and negative HSV I/II PCR.
Results:
Levetiracetam 1.5g BID was administered with no EEG improvement. Seizures were aborted by fosphenytoin load and was started on a maintenance dose of 100 mg TID. LNB was treated with ceftriaxone 2g daily for 21 days. Patient had cognitive improvement after ceftriaxone and phenytoin treatment. Conclusions:
LNB may mimic HSE on EEG and MRI and present a diagnostic challenge as symptoms can be diverse and non-specific. Ertapenem may lower seizure threshold thus clinicians should have early suspicion and evaluate for risk factors in patients with acute symptomatic seizures. Funding: N/A