8.1. Cysticercosis of the brain
Cysticercosis is the most common parasitic disease of the CNS; in endemic regions, neurocysticercosis can affect up to 4% of the population. It is found mainly in developing countries, in regions with grazing pig farming. The causative agent is pork, or armed, tapeworm (Taenia solium).
The life cycle of pork tapeworm takes place in the organisms of two hosts — human and pig, and includes three stages, i.e., oncosphere (larva), embryo and adult. The final host and source of the invasion becomes a human. Infection occurs when eating thermally insufficiently processed pork infected with encapsulated parasite embryos (cysticerci). In the small intestine, the shell dissolves, the scolex is fixed to the intestinal wall, and the parasite gradually grows to 1.5 m or more.
The disease (taeniasis) often goes undiagnosed. Proglottids (mature segments with a large number of eggs) and eggs are excreted with feces; when swallowed by a pig (intermediate host), the eggshell dissolves in the duodenum, oncospheres penetrate the intestinal wall, enter the bloodstream and spread throughout the body, where they are fixed in the connective tissue between muscle fibers, where they grow and after 4 months turn into embryos (cysticerci, or measles) ranging in size from 7 to 10 mm. In pigs, cysticerci usually remain viable throughout the entire (short) life of the animal.
Cysticercosis is a disease, in which a person becomes an intermediate host of a parasite. It develops when ingesting pork tapeworm eggs. Unlike pigs, human cysticerci mainly (in 70−80% of cases) affect the brain and only then skeletal muscles, eyes and subcutaneous fat; most human cysticerci die within 5−7 years.
The mechanism of infection is fecal-oral (with unwashed vegetables and fruits or auto-infection in case of non-compliance with personal hygiene), hypothetically, auto-infection is possible due to the ingestion of helminth eggs from the jejunum into the duodenum during vomiting.
Pathomorphology
Cysticercus in the CNS is a bubble filled with a clear liquid ranging in size from 5 to 15 mm; when located in the cavity of the cerebral ventricles, the diameter of the bubble can reach 50 mm. On the inner surface of the bubble, there is a measle, i.e., scolex head with two rows of hooks and four suction cups.
There are two variants of cysticercosis of the CNS: cystic and cluster-shaped (racemose).
- In the cystic variant, unconnected cysticerci are localized in the parenchyma of the brain or subarachnoid space at the base of the brain, less often in the cavity of the cerebral ventricles, where they can float freely. The inflammatory reaction of the surrounding tissues in this variant is usually insignificant, but in the case of death of the parasite is more pronounced.
- In the racemose variant, groups of bubbles resembling a bunch of grapes are formed, reaching 10−12 cm in maximum dimension, located in the subarachnoid space at the base of the skull. Bubbles grow rapidly, which is accompanied by a pronounced inflammatory reaction.
- By localization, the following types of cysticercosis are distinguished :
- parenchymal — 35% of cases (with clarification of the localization of parasites by lobes and parts of the brain);
- meningeal — 30% of cases:
- dorsolateral, usually cystic;
- basal, usually racemose;
- intraventricular (15%);
- mixed forms (20%).
Clinical presentation is determined by the extent of parasitic invasion, localization and variant structure of cysticerci. Due to the small size of the bubbles, the clinical picture is characterized mainly by symptoms of meningeal irritation (headaches) and the cerebral cortex (epileptic seizures). With massive invasion and/or occlusion of the CSF outflow tracts, ICH occurs. Intellectual and mental disorders develop, ranging from neurotic syndrome to hallucinations and delirium.
Clinically, parenchymal form of cysticercosis of the brain usually manifests as an encephalitis. This option develops more often in children and adolescents. In patients with basal meningeal variant of cysticercosis, there are signs of cranial nerve palsies (more often visual, abducens and facial).
With the localization of the cysticercus in the fourth ventricle and its displacement with the occlusion of the foramina of Luschka and Magendie, Bruns syndrome may occur, characterized by sudden severe headache, vomiting, forced head position, with possible respiratory and cardiac disorders.
The symptoms of cysticercosis of the lateral ventricles may resemble those of a frontal lobe tumor, there may be attacks of a sharp headache with impaired consciousness caused by intermittent occlusion of the interventricular foramen of Monro by a parasite. Cysticercosis can also cause damage to the spinal cord.
Diagnostic evaluation
In some patients, there may characteristic palpable nodules in subcutaneous tissue, which can be evaluated by a biopsy; occasionally, intraocular cysticerci are detected during ophthalmoscopy. Blood tests show eosinophilia (not always). Eggs of pork tapeworm in the feces are found in less than a third of patients. Diagnostic significance is the detection of antibodies to cysticercus in a titer of 1:64 in serum, and 1:8 in the CSF. The most informative is enzyme immunoassay, the specificity of which is close to 100% (with the exception of cases of single cysticerci of parenchymal localization).
Calcified parasites can be seen on an X-ray craniogram (Fig. 8.1), although today craniography is usually not included in the standard of neurosurgical diagnostics. On CT images, living parasites look like cysts of various diameters, the density of their contents corresponds to the cerebrospinal fluid (which makes CT diagnosis of intraventricular cysticercosis extremely difficult); sometimes, hyperintensive scolex is visible inside the cyst. The parasite does not accumulate contrast agent; the contrast agent accumulates along the periphery in the zone of reactive changes in the surrounding matter of the brain. Perifocal edema is also often detected. The dead parasites look like a small, usually point zone of increased density, often calcified (Fig. 8.2); the accumulation of contrast agent is uncommon.