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Seizure with Brain Lesions

 

Am Fam Physician. 2019 Nov 15;100(10):639-641.

A 42-year-old man presented after a seizure that lasted approximately four or five minutes. The patient said he had a “weird feeling” before the seizure and a headache afterward. He had not traveled recently and did not have fever, chills, nausea, vomiting, confusion, neck stiffness, head trauma, urinary or bowel incontinence, or other medical problems. He was not taking any medications. The patient immigrated 20 years earlier from Central America. He had a seizure 17 years prior, for which he took an unknown medication.

His vital signs were normal. Results of a complete neurologic examination were normal with no focal deficits. Laboratory tests were significant for a lactate level of 36.9 mg per dL (4.1 mmol per L) and mild hyperbilirubinemia. Findings on a complete blood count, basic metabolic panel, and urinalysis were unremarkable. Computed tomography (CT) of the head revealed multiple lesions. A lumbar puncture showed a white blood cell count of 2 per μL (2 × 106 per L), red blood cell count of 198 per μL (198 × 106 per L), protein level between 4 and 8 mg per dL (0.04 and 0.08 g per L), and glucose level between 5 and 8 mg per dL (0.3 and 0.4 mmol per L). Findings on magnetic resonance imaging (MRI) of the brain were abnormal (Figure 1).

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FIGURE 1


FIGURE 1

Question

Based on the patient's history and radiologic findings, which one of the following is the most likely diagnosis?

A. Brain metastases.

B. Coccidioidomycosis.

C. Cysticercosis.

D. Toxoplasmosis.

E. Tuberculosis.

Discussion

The answer is C: cysticercosis. Cysticercosis is a syndrome caused by infection with Taenia solium larvae, a pork tapeworm that is endemic in Central and South America, Asia, India, and sub-Saharan Africa. Transmission most commonly occurs with consumption of undercooked pork; however, there may be fecal-oral transmission via human carriers in nonendemic areas. Ingested eggs subsequently grow into larvae, leading to cystic lesions.1 These lesions develop in the brain parenchyma and can cause nonspecific neurologic symptoms, including seizures and headaches. Onset of symptoms usually occurs three to five years after exposure, although infection may be asymptomatic or subclinical for decades.2 Intraparenchymal cysticercosis presents as a single ring-enhancing cystic lesion on CT or MRI.

The diagnosis can be confirmed if imaging studies show a contrast-enhancing scolex (the head portion of

Address correspondence to Merima Bucaj, DO, at merima.bucaj@abrazohealth.com. Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations.

References

show all references

1. Kraft R. Cysticercosis: an emerging parasitic disease. Am Fam Physician. 2007;76(1):91–96. Accessed August 15, 2019. https://www.aafp.org/afp/2007/0701/p91.html...

2. White AC Jr, Coyle CM, Rajshekhar V, et al. Diagnosis and treatment of neurocysticercosis. 2017 clinical practice guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH). Clin Infect Dis. 2018;66(8):1159–1163.

3. Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol. 2014;13(12):1202–1215.

4. Saubolle MA, McKellar PP, Sussland D. Epidemiologic, clinical and diagnostic aspects of coccidioidomycosis. J Clin Microbiol. 2007;45(1):26–30.

5. Porter SB, Sande MA. Toxoplasmosis of the central nervous system in the acquired immunodeficiency syndrome. N Engl J Med. 1992;327(23):1643–1648.

6. Bernaerts A, Vanhoenacker FM, Parizel PM, et al. Tuberculosis of the central nervous system: overview of neuroradiological findings. Eur Radiol. 2003;13(8):1876–1890.

This series is coordinated by John E. Delzell Jr., MD, MSPH, associate medical editor.

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