Differential diagnosis includes:-
2. Disseminated TB into brain
3. Tumors etc.
But here with the specific symptom a chief complaint of only seizures and specific imaging study indicates that it is Neurocysticercosis.
Neuroysticercosis is the most common helminthic infection of the nervous system, and a leading cause of acquired epilepsy worldwide. The disease occurs when humans become intermediate hosts of Taenia solium by ingesting its eggs from contaminated food or, most often, directly from a taenia carrier by the fecal-to-oral route. Cysticerci may be located in brain parenchyma, subarachnoid space, ventricular system, or spinal cord, causing pathological changes that are responsible for the pleomorphism of neurocysticercosis. Seizures are the most common clinical manifestation, but many patients present with focal deficits, intracranial hypertension, or cognitive decline. Seizures respond well to a single antiepileptic, and the seizure recurrence rate is low in cases with single lesions; those with multiple, persistent or calcified lesions usually have recurrent seizures. Extraparenchymal NCC is often associated with intracranial hypertension, hydrocephalous and chronic meningitis; it has a guarded prognosis; surgical intervention is required in many cases. Management of NCC needs to be individualized. NCC is potentially eradicable; proper sanitation, hygiene and animal husbandry are warranted.
Two hosts are involved in the life cycle of this cestode, humans and pigs. Humans are definitive hosts for the adult tapeworm, whereas both pigs and humans may be intermediate hosts for the larval form (cysticercus). In the usual cycle of transmission, a few gravid proglottids from the adult tapeworm—attached to the intestinal wall of humans—are passed every few days with feces. Each proglottid liberates thousands of infective eggs to the environment. In areas where feces disposal is deficient and swine husbandry is poor, pigs have access to human feces containing T solium eggs. Once in the intestinal tract of the pig, eggs liberate oncospheres that cross the intestinal wall and enter the bloodstream, from where they are carried to the tissues to mature into metacestodes and then into larvaes (cysticercus). The life cycle is completed when humans ingest improperly cooked infected pork and cysticerci—by action of digestive enzymes—are released, their scolices evaginate, attach to the intestinal wall, and proglottids begin to multiply until the adult tapeworm is formed.
Humans can also become intermediate hosts of T solium after ingesting its eggs. Under this circumstance, human cysticercosis develops. Recent epidemiological evidence showing clustering of patients with cysticercosis around tapeworm carriers has changed previous concepts crediting the environment as the main source of human contamination with T solium eggs. Therefore, human cysticercosis must be seen as a disease mostly transmitted from person to person and the role of infected pigs is to perpetuate the infection only
Most cysticerci lodge in the brain parenchyma (parenchymal NCC) particularly at the grey–white cortical junction. In general, cysticerci live asymptomatically within host tissues for prolonged periods because of various protective mechanisms.
The immune response in symptomatic human NCC is thought to be of the Th1 phenotype predominantly, which is responsible for severe neuropathology including the formation of granulomas. Toll-like receptors (TLRs), particularly TLR 4 polymorphisms, have been reported to be significantly associated with symptomatic NCC.
In the brain parenchyma, the cyst evolves through four stages. In the vesicular stage, the cyst is filled with clear fluid, has a thin semitransparent wall and an eccentric opaque 4–5 mm scolex. Vesicular cysts are viable, produce scarce inflammatory changes and are usually asymptomatic. When the host immune system overcomes the protective mechanisms of the cyst, the cyst starts degenerating and an inflammatory response is elicited, the larva undergoes hyaline degeneration and the clear cyst fluid is replaced with gelatinous material; this is termed the colloidal stage. The cyst then contracts, the walls are replaced by focal lymphoid nodules and necrosis, and the scolex is transformed into coarse mineralized granules forming the granular nodular stage. Finally the granulation tissue is replaced by collagenous structures and calcification giving rise to the nodular calcified stage. At this time the oedema subsides but there are perilesional astrocytic changes. When cysts lodge outside the brain parenchyma (extraparenchymal NCC), such as in the ventricles, subarachnoid space, or cisterns, they tend to grow irregularly depending on the space available and usually elicit a strong inflammatory response. Occasionally the cysts enlarge considerably, become racemose without scolices and cause mass effects. Hydrocephalous can result either because of direct obstruction of cerebrospinal fluid (CSF) pathways by intraventricular cysts or secondary to inflammatory obstruction.
The clinical presentation of NCC is variable and ranges from asymptomatic cases to cases with severe neurological problems. The clinical manifestations are determined by the location, number and viability of the cysts, and the host immune response. In many cases, the infection is asymptomatic as has been demonstrated in population-based studies in areas where cysticercosis is endemic, where a sizable proportion of persons with neurocysticercosis only have evidence of the disease in neuroimaging studies.
Seizures are the most common clinical form of presentation of neurocysticercosis, occurring in up to 80% of symptomatic infections. Neurocysticercosis typically is first seen either with seizures (70% to 90% of acutely symptomatic patients) or headache. Headache usually indicates the presence of hydrocephalus, meningitis, or increased intracranial pressure. When hydrocephalus is present, the use of antiparasitic drugs is relatively contraindicated, unless a shunt is placed before administration. The mortality rate of patients with hydrocephalus or increased intracranial pressure is higher than the mortality rate of patients with seizures.
- Histologic demonstration of the parasite from biopsy of a brain or spinal cord lesion
- Evidence of cystic lesions showing the scolex on neuroimaging studies
- Direct visualization of subretinal parasites by fundoscopic examination
- Evidence of lesions highly suggestive of neurocysticercosis on neuroimaging studies
- Positive serum immunoblot for the detection of anticysticercal antibodies
- Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel
- Spontaneous resolution of small single enhancing lesions
- Evidence of lesions suggestive of neurocysticercosis on neuroimaging studies
- Presence of clinical manifestations suggestive of neurocysticercosis
- Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens
- Evidence of cysticercosis outside the central nervous system
- Individuals coming from or living in an area where cysticercosis is endemic
- History of frequent travel to disease-endemic areas
- Evidence of a household contact with Taenia solium infection
Degrees of diagnostic certainty
- Presence of 1 absolute criterion
- Presence of 2 major plus 1 minor or 1 epidemiologic criteria
- Presence of 1 major plus 2 minor criteria
- Presence of 1 major plus 1 minor and 1 epidemiologic criteria
- Presence of 3 minor plus 1 epidemiologic criteria
Single cyst: albendazole 15 mg/kg/d for 3 days or praziquantel 30 mg/kg in 3 divided doses every 2 hours. Corticosteroids rarely needed. AED for seizures
Mild to moderate infections: albendazole 15 mg/kg/d for 1 week or praziquantel 50 mg/kg/d for 15 days. Corticosteroids may be used when necessary. AED for seizures
Heavy infections: albendazole 15 mg/kg/d for 1 week (repeated cycles of albendazole may be needed). Corticosteroids are mandatory before, during, and after therapy. AED for seizures
Single cyst: albendazole 15 mg/kg/d for 3 days or praziquantel 30 mg/kg in 3 divided doses every 2 hours. Corticosteroids may be used when necessary. AED for seizures
Mild to moderate infections: albendazole 15 mg/kg/d for 1 week. Corticosteroids are usually needed before and during therapy. AED for seizures
Cysticercotic encephalitis: cysticidal drugs are contraindicated. Corticosteroids and osmotic diuretics to reduce brain swelling. AED for seizures. Decompressive craniectomies in refractory cases
Granular and calcified cysticerci
Single or multiple: no need for cysticidal drug therapy. AED for seizures. Corticosteroids for patients with recurrent seizures and perilesional edema surrounding calcifications
Small cysts over convexity of cerebral hemispheres
Single or multiple: albendazole 15 mg/kg/d for 1 week. Corticosteroids may be used when necessary. AED for seizures
Large cysts in Sylvian fissures or basal CSF cisterns
Racemose cysticercus: albendazole, 15 to 30 mg/kg/d for 15 to 30 days (repeated cycles of albendazole may be needed). Corticosteroids are mandatory before, during, and after therapy
Other forms of extraparenchymal neurocysticercosis
Hydrocephalus: no need for cysticidal drugs therapy. Ventricular shunt. Continuous corticosteroid administration (50 mg 3 times a week for up to 2 years) may be needed to reduce the rate of shunt dysfunction
Ventricular cysts: endoscopic resection of cysts. Albendazole may be used only in small lesions located in lateral ventricles. Ventricular shunt only needed in patients with associated ependymitis
Angiitis, chronic arachnoiditis: no need for cysticidal drug therapy. Corticosteroids are mandatory
Cysticercosis on the spine: surgical resection of lesions. Anecdotal use of albendazole with good results