Urgent Message: Headaches are common, but when patients present with concurrent psychiatric symptoms, seizures, and signs of increased intracranial pressure, clinical teams might consider asking about recent travel to assess for possible neurocysticercosis.
Naail Tariq, Cavan Scheetz, Michael Weinstock, MD
Citation: Tariq N, Scheetz C, Weinstock M. Headache and Paranoid Delusions: A Case Report of Missed Neurocysticercosis. J Urgent Care Med. 2023;17(X);31-34.
Abstract
Introduction
Headache is a common urgent care complaint. While most headaches have a benign etiology, it is important for clinicians to consider secondary causes of headache, especially in cases with worrisome associated symptoms.
Clinical Presentation
A 32-year-old Hispanic man presented with headache and paranoid delusions that someone was following him.
Physical and Laboratory Findings
The patient’s objective assessment included a normal neurological and general physical exam finding. Initial labs showed only mild leukocytosis.
Case Resolution
The patient was discharged to follow-up with mental health services, however, he returned to the emergency department via ambulance after experiencing multiple seizures. Additional evaluation with lumbar puncture and head CT revealed findings suggestive of neurocysticercosis. He was subsequently treated with vancomycin and albendazole and his symptoms resolved.
Conclusion
This case highlights the importance of considering travel history and geographic specific illnesses and intracranial causes for patients presenting with acute psychiatric symptoms concurrent with somatic symptoms, such as headache, as well as careful review of social history to assess risk of infections or malignancy.
Introduction
It is estimated that 50% of the adult population in the world is affected by headaches at some point in life.1 Headaches account for about 12 million visits in the United States per year.2 Non-traumatic headaches are responsible for 0.5 to 4.5% of the visits to the emergency department (ED).3 When assessing a patient for a headache, it is important to differentiate primary headaches, such as tension headaches and migraines, from secondary headaches, such as those from infection or malignancy.4 When considering the use of neuroimaging and/or lumbar puncture, it is critical to include an evaluation for red-flag symptoms that may indicate a secondary etiology such as fever, neurologic deficits, papilledema, rash, neck stiffness, sudden onset, severity of pain, and impaired consciousness.2, 4
While many clinicians assess for focal neurologic changes and systemic signs, apparently psychiatric symptoms may also be manifestations of organic neurologic disease. Such apparently psychiatric symptoms are often varied and nonspecific.5 It is important for clinicians to have a high index of suspicion for the possibility of neurologic illnesses when assessing the patient with new onset of apparently psychiatric symptoms, especially if there is no history of prior behavioral health disorders.6
Clinical Presentation
A 32-year-old Hispanic man with no past medical history presented to the urgent care center complaining of a headache and paranoid thoughts. He stated that earlier in the week, he developed a throbbing headache in the back of his neck which radiated into his occiput.
The day after the headache began, he developed persistent thoughts that someone was following him, and trying to hurt him. He denied any auditory or visual hallucinations but stated that he “felt their presence.” He reported he felt compelled to repeatedly look over his shoulder to check if he was being followed. He denied fever, ear pain, sore throat, vision or hearing changes, cough, chest pain, abdominal pain, vomiting, and gastrointestinal or urinary symptoms. He denied having paranoid delusions before and prior psychiatric illness. He admitted to smoking tobacco and occasional cocaine use.
Physical and Laboratory Exam Findings
The patient’s general appearance was normal. He was smiling and laughing and appropriately engaged during the interaction. There were no apparent neurological deficits and his cardiopulmonary and abdominal were also unremarkable. He was afebrile and had normal vital signs. A urine drug screen was entirely negative, and a complete blood count was significant only for mild leukocytosis.
Management
The patient was discharged with a presumptive diagnosis of paranoia and anxiety and was told to follow up with a primary care provider. His headache was treated with a prescription of 600 mg ibuprofen tablets as needed, and he was given education about mental health. Return precautions were provided for worsening symptoms including increasing headaches, changes in vision or hearing, and increased hallucinations or paranoia.
Differential diagnosis
A differential diagnosis for presentations with headache and paranoia includes brain masses (particularly involving the frontal or temporal lobes), meningitis, encephalitis, cerebrovascular accident (CVA), stimulant abuse/intoxication, alcohol or other withdrawal syndrome, and psychiatric illnesses including acute psychotic disorder, schizophrenia, bipolar disorder, and depression. This patient denied red-flag symptoms associated with headache, and there were no concerning vitals or physical exam findings.
Case Continuation and Timeline
The patient presented to the emergency department by ambulance 6 hours after discharge from UC after having multiple seizures. The family who witnessed the event told the emergency physician that the patient became confused and was unable to walk steadily. He subsequently had a generalized tonic-clonic seizure. On repeat physical exam, the patient was somnolent and minimally responsive. Petechiae were noted on the upper chest, neck, and head.
Diagnostic Assessment and Case Conclusion
The patient was isolated due to concern for meningitis. A lumbar puncture was performed, which showed moderate leukocytes without organisms and was otherwise unremarkable. A non-contrast computed tomography (CT) scan showed findings consistent with neurocysticercosis. There was an active lesion in the right frontal lobe as well as multiple chronic lesions elsewhere in the brain.
Specialist consult during the hospitalization opined the active lesion in the frontal lobe was the likely cause of the patient’s behavioral changes, seizure, and headache. Since the patient had no potential for recent exposure to T. Solium and chronic lesions were noted on the CT, the patient’s presentation suggested an acute reactivation of chronic neurocysticercosis. The patient was admitted to the hospital and started on albendazole and admitted until he was clinically stable for outpatient follow-up.
Discussion
Cysticercosis is a preventable parasitic infection caused by the larval stage (enclosed sacs containing the parasite) of the pork tapeworm, Taenia solium.7 Cysticercosis is the most common parasitic disease worldwide, with an estimated prevalence of greater than 50 million infected individuals. It is endemic to Mexico, South, and Central America, as well as parts of Africa and Asia.8 Cysticercosis is acquired through ingestion of undercooked pork from pigs infected with T. solium.9 Symptoms can be diverse and depend on the sites of infection as the parasite may be disseminated in various tissues.
Neurocysticercosis (NCC) occurs when T. solium afflicts the central nervous system.10 It is a leading cause of acquired epilepsy worldwide and has become increasingly prevalent in developed countries due to increased travel and immigration of individuals in endemic regions.9 NCC is typically diagnosed on neuroimaging (either CT or MRI) and confirmed via serology. Neuroimaging is useful in localizing and determining the stage of the cysts, which affects treatment and prognosis.11
If left untreated, NCC’s mortality typically due to complications from cerebral edema, hydrocephalus, and seizures.11 NCC’s mortality is dependent on the location of the cysts.12 Intraparenchymal cysts are more likely to present with seizures, and are associated with a better prognosis.12 Extra-parenchymal cysts are more likely to cause hydrocephalus, mass effect, intracranial hypertension, stroke, vasculitis and cranial nerve involvement, and therefore have a higher risk of lethal complications.13
Initial management of NCC is typically inpatient and includes antiepileptics, corticosteroids to reduce inflammation, and the antiparasitic agent, albendazole.12,14 In the United States, the rise of NCC cases can be attributed to an influx of immigrants from endemic regions. While data for the prevalence of NCC in the U.S. is limited, estimates of cases range from 0.2 to 0.6 cases per 100,000 people in the general population, and 1.5 to 1.8 cases per 100,000 Hispanics, for a total estimate of 1,320 – 5,050 new cases of NCC diagnosed in the United States annually.13 The Centers for Disease Control and Prevention (CDC) considers NCC one of five neglected parasitic infections and has designated it as a priority due for increased monitoring, prevention, and appropriate treatment.8 It is estimated that up to 2% of ED visits for seizures in the US are related to NCC. However, the entirety of the burden of NCC in the United States is still largely unknown as it is only reportable in Arizona, California, New Mexico, Oregon, and Texas, and under-reporting is believed to be common even in those regions.9
NCC Diagnosis and Management
NCC should be suspected in patients presenting with seizures and signs of increased intracranial pressure (ICP), the two most common clinical signs. MRI or non-contrast CT scan will generally reveal typical abnormalities when NCC is present. In the absence of risk factors such as increased cranial pressure, suspected neurocysticercosis workup can also include lumbar puncture and CSF evaluation in order to rule out other potential life-threatening infections, especially if imaging is not typical of NCC.15 The location of neurocysticerci (parenchymal versus extra-parenchymal, intraventricular versus extra-ventricular) and presentation on imaging (calcified versus non calcified, enhancing versus non-enhancing), and the size of the lesions will dictate treatment course moving forward.14
Patients should also be screened for latent tuberculosis and Strongyloides stercoralis prior to initiation of treatment.12 Initial treatment for the infection should begin with albendazole for at least 14 days and patients should be monitored for hepatotoxicity and leukopenia.14 Additional therapy with praziquantel can be added for stronger coverage.14 The household contacts should also be screened for tapeworm carriage.14
NCC presenting with psychiatric symptoms is unusual. A literature review found various case reports reporting similar instances of psychotic symptoms with eventual diagnosis of NCC. A case series found 21 other similar presentations among patients from India, Brazil, Portugal, Nepal and Africa.16 However, a literature review did not reveal any similar cases originating from patients in the United States.
Key Takeaways for Urgent Care Providers
- Consider organic causes of psychiatric symptoms in patients with concurrent somatic symptoms and/or no prior history of behavioral health diagnoses.
- NCC should be included in the differential diagnosis for patients with acute psychiatric and/or neurologic complaints, especially if they have a history travel or residence in endemic regions, such as Central and South America.
- NCC is considered a neglected parasitic disease by the CDC and further attention should be given to its prevention, detection, and treatment.
- Early clinical suspicion of NCC can minimize development of high risk complications and reduce morbidity.
Ethics Statement
The patient presented in this case was lost to follow-up, and therefore unable to give consent. All patient demographics were anonymized in the interest of patient privacy.
Manuscript submitted June 2, 2023; accepted September 9, 2023
Author Affiliations: Naail Tariq, MD, DeBusk College of Osteopathic Medicine, Lincoln Memorial University. Cavan Scheetz, student, Heritage College of Osteopathic Medicine, Ohio University. Michael Weinstock, MD, Adena Health System, Wexner Medical Center at The Ohio State University, The Journal of Urgent Care Medicine. The authors have no relevant financial relationships with any commercial interests.
References
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Michael B. Weinstock, MD
