Location
Suwanee, GA
Start Date
11-5-2023 1:00 PM
End Date
11-5-2023 4:00 PM
Description
Background:
Taenia solium is a cestode endemic to regions of Latin America, Asia, sub-Saharan Africa and Oceania, and serves as the most common cause of acquired epilepsy in the world. T. solium eggs are transmitted fecal-orally when a human or pig host ingests contaminated food or water. Larvae hatch from the intestines and invade into muscle, tissue, or organs, forming cysts called cysticerci. Cysticerci involving the central nervous system is termed neurocysticercosis (NCC). Patients with NCC typically remain asymptomatic for 3-5 years in the viable stage until the host’s immune response is activated in the degenerating stage. Immune-mediated degradation of cysticerci and subsequent inflammation and edema in the nonviable stage may manifest as new onset seizures, headache, and other neurological deficits caused by increasing intracranial pressure. The diagnosis of NCC in non-endemic areas is based on clinical symptoms, history of travel to an endemic region, and presence of classic ring-enhancing lesions on neuroimaging.
Case Description:
A healthy 27-year-old male presents with new onset seizures. The first episode was witnessed by his wife who stated he was washing dishes before he fell to the ground convulsing. The seizure spontaneously resolved upon arrival of the ambulance. The patient denies symptoms of fever, fatigue, unexplained weight change, headaches, focal neurologic deficit, visual changes, cough, rash, recent illness, or head trauma. Further history is noncontributory except for note of travel to China four years ago to visit his in-laws.
Vital signs are within normal range. In the Emergency Department, he suffers another witnessed seizure and is treated with lorazepam. He is disoriented and combative in his postictal state necessitating sedation with intubation. A CBC, CMP, troponin, HIV, toxicology, and tuberculosis screen are largely normal. Lumbar puncture reveals elevated leukocytes with normal glucose and protein levels. Parasitology report and blood cultures remain negative throughout the visit. Computerized tomography (CT) scan and contrasted magnetic resonance imaging (MRI) of the brain show a 3-4 millimeter calcified, ring-enhancing lesion in the right frontal lobe with surrounding edema. He is diagnosed with NCC based on symptoms, travel history, and neuroimaging findings.
Conclusion/Discussion:
This is an uncomplicated nine-year longitudinal case study of a patient with NCC presenting with new onset seizures four years after traveling to China. Symptomatic management at the time of diagnosis included dexamethasone for brain edema and levetiracetam for prevention of further seizures. Antiparasitics, which can be used in viable or degenerating stages, were not utilized in our patient due to the evidence of a nonviable calcified cysticercus on imaging. The patient ultimately opted for surgical removal of the lesion to definitively treat his seizures. A six-month postoperative MRI confirmed resolution of abnormal findings, at which point the patient was weaned off levetiracetam. Nine years later, the patient remains seizure-free and without complications.
Embargo Period
6-14-2023
Included in
A nine-year longitudinal case study of a 27-year-old male with neurocysticercosis presenting with new onset seizures
Suwanee, GA
Background:
Taenia solium is a cestode endemic to regions of Latin America, Asia, sub-Saharan Africa and Oceania, and serves as the most common cause of acquired epilepsy in the world. T. solium eggs are transmitted fecal-orally when a human or pig host ingests contaminated food or water. Larvae hatch from the intestines and invade into muscle, tissue, or organs, forming cysts called cysticerci. Cysticerci involving the central nervous system is termed neurocysticercosis (NCC). Patients with NCC typically remain asymptomatic for 3-5 years in the viable stage until the host’s immune response is activated in the degenerating stage. Immune-mediated degradation of cysticerci and subsequent inflammation and edema in the nonviable stage may manifest as new onset seizures, headache, and other neurological deficits caused by increasing intracranial pressure. The diagnosis of NCC in non-endemic areas is based on clinical symptoms, history of travel to an endemic region, and presence of classic ring-enhancing lesions on neuroimaging.
Case Description:
A healthy 27-year-old male presents with new onset seizures. The first episode was witnessed by his wife who stated he was washing dishes before he fell to the ground convulsing. The seizure spontaneously resolved upon arrival of the ambulance. The patient denies symptoms of fever, fatigue, unexplained weight change, headaches, focal neurologic deficit, visual changes, cough, rash, recent illness, or head trauma. Further history is noncontributory except for note of travel to China four years ago to visit his in-laws.
Vital signs are within normal range. In the Emergency Department, he suffers another witnessed seizure and is treated with lorazepam. He is disoriented and combative in his postictal state necessitating sedation with intubation. A CBC, CMP, troponin, HIV, toxicology, and tuberculosis screen are largely normal. Lumbar puncture reveals elevated leukocytes with normal glucose and protein levels. Parasitology report and blood cultures remain negative throughout the visit. Computerized tomography (CT) scan and contrasted magnetic resonance imaging (MRI) of the brain show a 3-4 millimeter calcified, ring-enhancing lesion in the right frontal lobe with surrounding edema. He is diagnosed with NCC based on symptoms, travel history, and neuroimaging findings.
Conclusion/Discussion:
This is an uncomplicated nine-year longitudinal case study of a patient with NCC presenting with new onset seizures four years after traveling to China. Symptomatic management at the time of diagnosis included dexamethasone for brain edema and levetiracetam for prevention of further seizures. Antiparasitics, which can be used in viable or degenerating stages, were not utilized in our patient due to the evidence of a nonviable calcified cysticercus on imaging. The patient ultimately opted for surgical removal of the lesion to definitively treat his seizures. A six-month postoperative MRI confirmed resolution of abnormal findings, at which point the patient was weaned off levetiracetam. Nine years later, the patient remains seizure-free and without complications.