Guide
If you've seen Dr. House, you'll remember the episode that opened with neurocysticercosis. Although this disease is rare now, it still requires doctors to be vigilant, especially for patients with a corresponding medical history. In this paper, a patient with neurocysticercosis who presents with seizures is used as an example to detail the imaging manifestations of each stage of neurocysticercosis. Let's take a look.
overview
Neurocysticercosis is transmitted by human faeces-oral transmission of tapeworm-carrying tapeworm, while taeniasis is transmitted by ingestion of infected pork. Most of the transmission routes of neurocysticercosis are human-to-human transmission, rather than pig-to-human transmission, as is commonly believed. With frequent international movements, clinicians who encounter epilepsy, particularly those who have lived in developing countries, should consider suspecting that epilepsy, headache, and focal neurological deficits are due to neurocysticercosis, and should determine the staging of the disease by identifying the imaging characteristics of neurocysticercosis.
The patient in the case in this article is a young man who presents with generalized tonic-clonic seizures. He was diagnosed with epilepsy in Malawi and immigrated to the UK from Malawi two years before the onset. Here he did his first MRI examination, which showed multiple cystic lesions that characterize neurocysticercosis.
Life history of cerebral cysts
Neurocysticercosis is a parasitic infection of the nervous system caused by pregnancy nodes or eggs produced by adult pig tapeworms. It is a terroir disease in developing countries, but is becoming more common in developed countries with frequent international movements of people [1].
The life history of tapeworms is complex and requires two kinds of hosts: humans and pigs. The route of infection in humans is divided into two types according to the different stages of life history of tapeworms at the time of infection.
Taeniasis: Tapeworm disease is infected by eating undercooked pork containing cysticercosis. Once ingested, the cephalic segment (the head of the parasite) adsorbs into the mucosal layer of the small intestine, giving birth to several sodomes (segments) and developing into adults [2]. This is taeniasis. Eventually, the segment containing the eggs will fall off the worm body and be excreted with the feces. After eating feed contaminated with the feces of an infected person, pigs are parasitic. These ingested larvae are absorbed through the intestines and spread into the pig's muscles, forming cysticercosis, thus completing the life history.
➤ Cysticercosis: This patient is transmitted in the same form as pigs in the form of infection, which is transmitted by contact with larval faeces excreted by human carriers. Once ingested, the larvae lose their embryonic membrane under the action of stomach acid and become a larval-containing sac called a six-hooked larvae. They are absorbed and migrated through the intestines, often parasitizing the brain, eyeballs, and muscles, and forming cysts [3].
Imaging presentation
Cysticercosis is formed when the central nervous system is infected with cysticercosis. When the brain parenchyma is affected, the disease can be divided into four separate stages: the vesicle phase, the gel phase, the granulomatous nodule phase, and the calcification phase.
1
Vesicle phase
The capsule membrane of the parasite in this phase is intact, and the host immune response is mild. In this staging, there is only liquid in the bag. The imaging characteristics of the CT and MRI sequences of fluids are similar to cerebrospinal fluid[4]. (Figure 1)
Figure 1: Brain MRI scan (axial T2-weighted image) showing lesions in two different stages. First, a simple liquid can be seen in the sac, which is the vesicle phase (indicated by the black arrow). Images also show that this patient has a mixed type of nodular granulomatous lesion that presents as a high-signal fluid with a calcified cephalic segment and a low signal (indicated by a white arrow).
2
Gel period
When the capsule ruptures, the fluid in the capsule becomes proteinic and penetrates into the surrounding tissues, causing a strong immune response, which is the gelatinous phase. In MRI images, lesion areas appear as thickened, strengthened envelopes in contrast to surrounding tissue edema (Figures 2 and 3), and high-density envelopes under CT [5].
Figure 2: Brain MRI scan (axial T1-weighted image, flat scan, and enhanced scan image) shows the strengthening of the enveloping membrane in the gelatinous phase.
Figure 3: Brain MRI scan (coronary FLAIR [left] and T2-weighted image [right]) shows edema secondary to right occipital lobe lesions in the colloidal phase.
3
Granulomatous nodules
At this stage, the sac is further degenerated and the edema is reduced. MRI shows that these cysts are converted into nodules or mixed tissues. The surroundings of the nodular lesion are hyperinsified under MRI, and the signal intensity in the center of the nodule is the same as that of the white matter. Mixed-type lesions are high-signal, with the center of the nodule showing a low signal due to calcification of the head segment (figure 1); CT shows a "bull's eye sign" [6] (figure 4).
Figure 4: Head CT scan (axial flat scan) showing two different stages of the lesion. The "bull's eye sign" (indicated by the white arrow) may be seen in the granulomatous stage of the nodule. Calcified lesions (indicated by black arrows) may be seen during calcification of nodules.
4
Calcification phase
At this stage, the capsules are calcified and granulomas form within the nodules [7]. CT shows lesions that calcified in the brain parenchyma (Figure 4). Appears as a nodular lesion under MRI, with isosignals under T1-weighted images and low signals under T2-weighted images (Figure 5) [5].
Figure 5: Brain MRI scan (axial T2-weighted image) showing low-signal calcified small nodules during the calcification phase of nodules.
Summary of diagnosis and treatment
Common symptoms of cerebrocysticers include seizures, headache, and focal neurological deficits. Neurocysticercosis is the most common cause of acquired epilepsy. Sequelae include hydrocephalus, intracranial hypertension, and dementia [8].
Treatment of neurocysticercosis should be individualized according to patient presentation, disease stage, and presence or absence of inflammation. As common anthelmintics, propylthiazole and praziquantel are effective in reducing the number of cysts in the brain parenchyma and even reducing the frequency of long-term seizures of epilepsy [9]. Sometimes symptoms worsen after 48 hours of medication due to cystic degeneration and edema, at which point high doses of glucocorticoids are recommended. Antiepileptic drugs are the primary means of controlling seizures in patients with neurocysticercosis [10]. Surgical treatment can be used in complex cases, including insertion of a drainage tube, removal of the cyst with a neuroendoscope, etc. [11].
bibliography
[1] Sotelo J, Del Brutto OH. Review of neurocysticercosis. Neurosurg Focus 2002;12:e1.
[2] García HH, Gonzalez AE, Evans CA, et al.; Cysticercosis Working Group in Peru. Taenia solium cysticercosis. Lancet 2003;362:547–56.
[3] Garcia HH, Gonzalez AE, Tsang VCW, et al. Neurocysticercosis: some of the essentials. Pract Neurol 2006;6:288–97.
[4] Lerner A, Shiroishi MS, Zee CS, et al. Imaging of neurocysticercosis. Neuroimaging Clin N Am 2012;22:659–76.
[5] Dumas JL, Visy JM, Belin C, et al. Parenchymal neurocysticercosis: follow-up and staging by MRI. Neuroradiology 1997;39:12–18.
[6] Kramer LD, Locke GE, Byrd SE, et al. Cerebral cysticercosis: documentation of natural history with CT. Radiology 1989;171:459–62.
[7] Giorgio CM, Medina MT, Durón R, et al. Neurocysticercosis. Epilepsy Curr 2004;4:107–11.
[8] Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. Nat Rev Neurol 2011;7:584–94.
[9] Baird RA, Wiebe S, Zunt JR, et al. Evidence-based guideline: treatment of parenchymal neurocysticercosis: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2013;80:1424–9.
[10] García HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747–56.
[11] Rajshekhar V. Surgical management of neurocysticercosis. Int J Surg 2010;8:100–4.
医脉通编译自：Dhesi, B., Karia, S. J., Adab, N., & Nair, S. (2015). Imaging in neurocysticercosis. Practical neurology, 15(2), 135-137.
Source: Medical Pulse
Welcome to Weibo: Daily Medical News