Neurocysticercosis

Neurocysticercosis is infection of the central nervous system by the larval (cysticercus) stage of the pork tapeworm Taenia solium, acquired by ingesting T. solium eggs (from fecal-oral contamination, typically from a human tapeworm carrier, rather than from eating undercooked pork itself, which instead causes intestinal taeniasis, see the separate Cysticercosis entry for the broader disease and the distinction between these transmission routes).

It is the most common parasitic infection of the central nervous system worldwide and a leading cause of acquired epilepsy in endemic regions (much of Latin America, sub-Saharan Africa, and parts of Asia).

Presentation depends heavily on the number, location, and stage (viable, degenerating, or calcified) of the cysts, and the accompanying host inflammatory response.

Seizures are the most common presenting feature, typically occurring as cysts begin to degenerate and provoke a surrounding inflammatory response (viable cysts themselves are often relatively asymptomatic, provoking less host reaction).

Other features include headache, features of raised intracranial pressure (particularly with intraventricular or large cysts obstructing CSF flow, causing hydrocephalus), and, less commonly, focal neurological deficits depending on lesion location.

Racemose neurocysticercosis (cysts within the subarachnoid space or ventricles, often lacking a scolex and capable of substantial growth) tends to cause more significant mass effect and hydrocephalus than the more common parenchymal form.

MRI is the imaging investigation of choice, more sensitive than CT for detecting the scolex within a cyst (pathognomonic when seen) and for characterizing lesion stage; CT is more sensitive for detecting calcified lesions (the burnt-out, inactive stage) and remains useful and more widely available, particularly in resource-limited settings
Imaging findings are staged: vesicular (viable, cyst with visible scolex, minimal surrounding inflammation), colloidal/degenerating (surrounding edema and enhancement as the host immune response intensifies, often the stage provoking seizures), nodular-calcified (granular, calcified remnant, often still epileptogenic even in this "inactive" stage)
Serology (enzyme-linked immunoelectrotransfer blot, EITB, the preferred test where available) supports diagnosis, particularly useful with multiple lesions, though sensitivity is lower with a single lesion or purely calcified disease
Diagnostic criteria (Del Brutto criteria) combine imaging findings, serology, epidemiological exposure, and clinical features into absolute, major, minor, and epidemiological categories to standardize diagnosis given the absence of a single definitive non-invasive test in all cases
Ophthalmological examination is performed before starting antiparasitic treatment where intraocular cysts are a possibility, given the risk of a damaging inflammatory response to treatment within the eye if unrecognized

Antiparasitic treatment is not appropriate for all presentations and requires careful case selection: it is generally avoided or used with extreme caution for calcified, inactive lesions (already dead, treatment offers no benefit and provoking further inflammation could worsen seizures), and is more clearly indicated for viable (vesicular) parenchymal cysts causing symptoms
Albendazole 15 mg/kg/day PO in divided doses (typically bd), maximum 800 mg/day, for 8 to 30 days depending on cyst burden and location, is generally preferred over praziquantel for parenchymal disease given superior CSF penetration; praziquantel (50 mg/kg/day in 3 divided doses) is an alternative or adjunct, particularly favored for certain subarachnoid or ventricular disease patterns per specialist guidance
Corticosteroids (commonly dexamethasone or prednisolone, dosed per severity and specialist protocol) are given concurrently with antiparasitic treatment, both to manage the inflammatory response provoked by dying cysts (which can transiently worsen symptoms, including seizures and raised intracranial pressure) and, in some regimens, to increase antiparasitic drug levels through reduced first-pass metabolism
Antiparasitic treatment is contraindicated in the presence of significant raised intracranial pressure, active hydrocephalus, or a large cyst burden with significant mass effect without first addressing these, given the risk of provoking a dangerous inflammatory surge; ventriculoperitoneal shunting or other neurosurgical management of hydrocephalus takes priority in this situation
Anticonvulsant therapy for seizures follows standard epilepsy management principles (see Epilepsy and Status Epilepticus entries), often continued for a prolonged period even after successful antiparasitic treatment given ongoing seizure risk from residual calcified lesions
Surgical management (including endoscopic removal) is indicated for intraventricular cysts causing obstructive hydrocephalus, or large cysts causing significant mass effect not amenable to medical management alone
Prevention at a public health level centers on identifying and treating human tapeworm carriers (intestinal taeniasis, see the Cysticercosis entry), improved sanitation, and food safety/hygiene education, given the fecal-oral transmission route for the eggs causing neurocysticercosis specifically

Referral: neurology for seizure management and treatment planning; neurosurgery for hydrocephalus or significant mass effect; infectious disease or tropical medicine for antiparasitic treatment guidance, particularly for complex or heavy infections.

Viral Encephalitis

Inflammation of brain parenchyma from viral infection, with HSV-1 as the most common identifiable sporadic cause in immunocompetent adults (see dedicated entry).

Other causes include arboviruses (Japanese encephalitis, West Nile virus, tick-borne encephalitis, per regional epidemiology), enteroviruses, VZV, and, in the immunocompromised, CMV and HHV-6. A substantial proportion remain of unidentified cause despite thorough workup.

Fever, headache, altered consciousness, seizures, and focal neurological signs, with the specific pattern sometimes suggesting a cause (temporal lobe involvement favoring HSV; movement disorder or flaccid paralysis favoring certain arboviruses; cerebellar signs favoring VZV).

Distinguishing encephalitis from meningitis rests on the presence of altered brain function (confusion, seizures, focal deficit) beyond meningism alone.

CSF typically shows a lymphocytic pleocytosis with normal or mildly elevated protein and normal glucose.

PCR panels for HSV, VZV, enterovirus, and other regionally relevant pathogens; specific arbovirus serology (IgM) where endemic exposure is relevant.

MRI to assess pattern and severity, and EEG to characterize seizure activity and support diagnosis where PCR is negative but the syndrome is compatible.

Empirical IV aciclovir 10 mg/kg every 8 hours started immediately in any suspected encephalitis pending PCR results, given HSV is the most treatable and most catastrophic-if-missed cause; stopped once HSV PCR (and, where relevant, a repeat sample at 3 to 7 days) is confirmed negative and an alternative diagnosis is more likely
Supportive care: seizure control, management of raised intracranial pressure, ICU support for significant reduction in consciousness
Most arboviral and enteroviral encephalitides have no specific antiviral treatment and are managed supportively
CMV encephalitis (immunocompromised): ganciclovir or foscarnet, per specialist guidance

Referral: neurology and infectious disease for all cases; ICU for significant compromise.

Neurocysticercosis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management