Introduction
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease. Tanae Solium.
Clinical Features:
History
NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.
•Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
•The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:
◦Epilepsy
■Epilepsy is the most common presentation (70%)
■Seizures secondary to NCC may be generalized or partial.
◦Headache
■Chronic headaches associated with nausea and vomiting (simulating migraines)
■Headaches associated with intracranial hypertension and indicative of hydrocephalus
■Headaches due to meningitis
◦Intracranial hypertension
■Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
■These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
◦Strokes5
■Ischemic cerebrovascular complications of NCC include lacunar infarcts6 and large cerebral infarcts due to occlusion or vascular damage.
■Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
■Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.
◦Neuropsychiatric disturbances
■These range from poor performance on neuropsychological tests to severe dementia.
■These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.
◦Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
◦Hydrocephalus
■Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
■Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
•Other forms of neurocysticercosis
◦Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.
◦Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.
Physical
Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:
•Cognitive decline
•Dysarthria
•Extraocular movement palsy or paresis
•Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
•Hemisensory loss
•Movement disorders
•Hyper/hyporeflexia
•Gait disturbances
•Meningeal signs
Causes
NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.
Laboratory Studies
•CSF analysis
◦Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.
•Stool examination
◦Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
◦Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.
•Immunological tests
◦Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.
Imaging Studies
•CT scan
•MRI
considering biopsy.
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease. Tanae Solium.
Clinical Features:
History
NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.
•Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
•The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:
◦Epilepsy
■Epilepsy is the most common presentation (70%)
■Seizures secondary to NCC may be generalized or partial.
◦Headache
■Chronic headaches associated with nausea and vomiting (simulating migraines)
■Headaches associated with intracranial hypertension and indicative of hydrocephalus
■Headaches due to meningitis
◦Intracranial hypertension
■Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
■These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
◦Strokes5
■Ischemic cerebrovascular complications of NCC include lacunar infarcts6 and large cerebral infarcts due to occlusion or vascular damage.
■Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
■Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.
◦Neuropsychiatric disturbances
■These range from poor performance on neuropsychological tests to severe dementia.
■These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.
◦Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
◦Hydrocephalus
■Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
■Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
•Other forms of neurocysticercosis
◦Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.
◦Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.
Physical
Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:
•Cognitive decline
•Dysarthria
•Extraocular movement palsy or paresis
•Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
•Hemisensory loss
•Movement disorders
•Hyper/hyporeflexia
•Gait disturbances
•Meningeal signs
Causes
NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.
Laboratory Studies
•CSF analysis
◦Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.
•Stool examination
◦Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
◦Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.
•Immunological tests
◦Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.
Imaging Studies
•CT scan
•MRI
considering biopsy.
Medical Care
Treatment of neurocysticercosis depends upon the viability of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite.
•If the parasite is dead, the treatment is directed primarily against the symptoms (eg, anticonvulsants for management of seizures). Monotherapy is usually sufficient. Duration of the treatment remains undefined, and depends neither on the type of seizure at presentation nor on other risk factors for recurrence, such as age at onset and number of seizures before diagnosis. Calcification remains an epileptogenic focus. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice.
•If the parasite is viable or active and the patient has vasculitis, arachnoiditis, or encephalitis, a course of steroids or immunosuppressants is recommended before the use of anticysticercal drugs. Antiparasitic treatment8 with albendazole is also useful in cysticercosis of the racemose type. If only parenchymal, subarachnoid, or spinal cysts are present without the complications mentioned, anticysticercal treatment can be considered, with the concomitant use of steroids, even in patients with massive brain infection. Reports indicate that multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts.
•A recent double-blind, placebo-controlled study has shown that in patients with seizures due to viable parenchymal cysts, antiparasitic therapy decreases the burden of parasites and is safe and effective, at least in reducing the number of seizures with generalization.
Surgical Care
•In the presence of hydrocephalus due to intraventricular cyst, placement of a ventricular shunt is recommended, followed by surgical extirpation of the cyst and subsequent medical treatment.
•In cases of multiple cysts in the subarachnoid space (ie, the racemose form), surgical extirpation, on an urgent basis, is recommended.
•If the obstruction is due to arachnoiditis, placement of a ventricular shunt should be followed by administration of steroids and subsequent medical therapy.
•Because of frequent shunt dysfunctions due to entry of inflammatory tissue as well as parasitic debris inside the ventricular cavities, Sotelo designed a device that functions at a constant flow without the valvular mechanism of Pudenz-type shunts.
•Neuroendoscopy is a new tool with great potential for use in the management of ventricular cysticercosis.
•Surgical treatment in the particular case of medically refractory epilepsy due to a single lesion has been reported. Evaluation in an epilepsy center is indicated.
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