Neurocysticercosis with the Transient Ischemic Attack as a Primary Symptom in a 34-Year-Old Male Patient

Sir, A 34-year-old male patient was admitted to the Neurology Department for the first time complaining of repeated episodes of transient left upper limb weakness 5 times, each time lasting for 1 minute, within a day. The patient’s vital signs, including body temperature, heart rate (HR), blood pressure (BP), and respiration rate, were normal at admission. During each episode, the patient was unable to raise his left hand and experienced weakness in clenching his fist, but no sensory impairment and no muscle twitches, indicating upper limb motor function impairment. However, there was no such problem in moving his left lower limb, facial deviation, or dysarthria. The patient had no risk factors for cerebrovascular disease, such as hypertension, diabetes, smoking, and hyperlipidemia, and was not taking statins. The patient also had no past medical history or family history. The physical examination of the central nervous system (CNS) revealed bilateral papilledema, suggesting an occurrence of intracranial hypertension [Figure 1]. The cerebrospinal fluid (CSF) pressure measured by lumbar puncture (LP) was 240 mmH2O, and laboratory examinations showed signs of lymphocytosis (leukocyte count: 115/μL; lymphocyte percentage: 97%) and eosinophilia (eosinophil percentage: 2%), and increase in total protein level (protein content: 1107 mg/L). Cranial magnetic resonance imaging (MRI) examinations revealed narrowing of the right lateral fissure cistern, and long T1- and T2-weighted signals were in the right temporal and insular lobes, respectively. Furthermore, contrast-enhanced MRI indicated irregular annular enhancement [Figure 2]. The magnetic resonance angiography (MRA) clearly showed stenosis of the M2 segment of the right middle cerebral artery [Figure 3], possibly explaining the reason for transient left upper limb weakness. Immunological examinations of CSF further showed immunoglobin G (IgG) antibody positivity for cysticercosis. Next-generation sequencing (NGS) and bioinformatic analysis demonstrated the presence of 116 Taenia solium-specific genomic sequences in the CSF, suggesting tapeworm infection-associated cysticercosis. The electroencephalogram showed no epileptic discharge.Figure 1: Fundus examination revealed bilateral papilledema in the (a) right eye and (b) left eyeFigure 2: Magnetic resonance imaging (MRI) examinations showing changes before and after the albendazole treatment. The MRI exhibited long T1- and T2-weighted signals (a and b) in the right insular and temporal lobes. The contrast-enhanced MRI further indicated irregular annular enhancement (c and e) in the right lateral fissure before treatment, which was significantly reduced after the treatment (d and f). There are also significant changes in FLAIR images before (g) and after treatment (h)Figure 3: Magnetic resonance angiography (MRA) examination indicates the changes before and after the albendazole treatment. (a) Right middle cerebral artery M2 segment stenosis (before treatment). (b) Local stenosis of the right middle cerebral artery disappeared 1 year after treatmentDuring the first admission, the patient was treated with oral albendazole (0.4 g each time, thrice a day) for 14 days, and no recurrence of the left upper limb weakness was observed. Five days after the first discharge, he was readmitted with a complaint of persistent and progressive headache, while his CSF pressure was recorded above 400 mmH2O. At this time, the patient was treated with a combination of oral albendazole (0.4 g each time, thrice a day), intravenous (i.v) dexamethasone (5 mg/day), and mannitol (250 mL, q6h). After the second discharge, the patient received a total of seven courses of oral albendazole, and the headache did not recur during the 1-year follow-up. One year later, the MRI showed significantly less irregular ring enhancement [Figure 2], and the MRA result did not show any stenosis of the right middle cerebral artery [Figure 3]. Cerebral cysticercosis is the most commonly occurring CNS-infected parasitic disease, and its clinical presentation depends on the number of cysticercosis granulomas, the location, and the host’s immune response to the parasite. Cysticercosis is an endemic disease in most developing countries. Notably, the Chinese National Surveys suggest a significantly decreasing incidence of cysticercosis in the country.[1] Cysticercosis is not rare in clinical practices and is often misdiagnosed or misinterpreted. The major clinical manifestations of CNS parasitic infections, in general, include headache, epileptic seizures, cognitive decline, visual impairment, and limb weakness,[2] which could be easily misdiagnosed as a symptom of cerebrovascular diseases. The cerebrovascular complications associated with cysticercosis commonly present transient ischemic attack (TIA), massive cerebral infarction (MCI), and lacunar cerebral infarction (LCI). The rate of incidence of stroke in cysticercosis patients is between 4% and 12%.[3] However, an estimated incidence rate of TIA is not exactly described in this literature. At the same time, case studies of cysticercosis-associated TIA have been rarely reported in this literature. The TIA pathology in cysticercosis patients includes compression of the infection site adjacent vessels, cerebral vasculitis-induced reversible vasospasm, and transient neurological dysfunctions. Interestingly, cysticercosis has also been identified previously as a risk factor for stroke in young adults.[4] Cerebrovascular involvement in cysticercosis pathology can be divided into two types—small vessel involvement (SVI) and large vessel involvement (LVI). SVI is the most common cerebrovascular complication, which shows lacunar infarcts, usually located in the basal ganglia, on MRI and computed tomography (CT) scanning. Cysticercosis-related LCI onset is usually caused by endarteritis secondary to an inflammatory response in the area of cysticercosis infection of the anterior or middle cerebral artery. Angiographic examination or transcranial Doppler ultrasound (TCD) can provide evidence of intracranial artery stenosis with LVI.[5] Moreover, cysticercosis granuloma can cause inflammation around cysts, resulting in the stenosis of the circle of Willis and its branches.[6] Cerebral arteritis is the most common manifestation of cerebrovascular diseases caused by cysticercosis that exhibits involvement of small and large vessels of the middle cerebral artery and posterior cerebral artery.[7] Notably, reversible vasospasm may be an important cause of TIA during cerebral vasculitis, which can induce immune-mediated vasospasm or thrombosis, leading to a hypercoagulable state.[8] Finsterer et al.[9] have reported a case of neurocysticercosis with TIA and headache as the initial symptoms, suggesting that this type of TIA may be caused by Takayasu’s arteritis. Hayes et al.[10] have also reported a case study of transient right-sided facial paralysis in a patient with transient dizziness and dysarthria. MRA examinations further revealed mild stenosis of the middle cerebral artery branches. A diagnosis of cerebral cysticercosis with TIA indicated that the patient might progress to cerebrovascular events (CVE) if left untreated. The patient received i.v doses of steroids and oral albendazole during the hospitalization and was discharged with a prescription of albendazole (0.4 g twice daily) and a tapering dose of prednisone. The patient had no recurrence after discharge. Some studies also support the notion that neurological dysfunctions observed in cerebral cysticercosis patients are very similar to those found in TIA patients, as well. These symptoms show tumor-like transient bulges caused by the mass effect of cysts.[3] In this case, MRA identified a right middle cerebral artery stenosis, which might explain the manifestation of TIA involving large arteries. In the1-year follow-up examination, MRA confirmed the disappearance of this pathology after the treatment, including smaller sizes of neurocysticercosis granulomas, reduced headache, and no recurrence of transient left limb weakness. This patient received a total of seven courses of oral albendazole treatment in two segments, each continued for 14 days. The patient is a subarachnoid neurocysticercosis patient, and the 2017 Clinical Practice Guidelines[11] recommend the use of antiparasitic drugs for treatment until the resolution of viable cysticerci on MRI and resolution of other evidence of cysticerci. At the same time, bilateral papilledema also disappeared following the treatment courses. Therefore, we hypothesized that the mechanism of TIA might have involved cysticercosis granulomas that oppressed the middle cerebral artery, resulting in cerebral arteritis. In conclusion, cerebral cysticercosis has a variety of clinical manifestations, and associated TIA is a rare clinical phenomenon that should not be ignored. Financial support and sponsorship Nil. Conflicts of interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflicts of interest.