What are the symptoms of neurocysticercosis?

Symptoms of Neurocysticercosis

The two most common clinical presentations of neurocysticercosis are seizures and increased intracranial pressure, with seizures occurring in 70-90% of patients and representing the leading cause of late-onset epilepsy in endemic areas. 1, 2

Primary Clinical Manifestations

Seizures (Most Common)

• Seizures are the predominant symptom, accounting for approximately 29% of seizures in endemic areas and about 2% of seizure presentations in US emergency rooms 1, 3
• Seizure types include focal seizures, focal with secondary generalization, or generalized seizures 1
• More than 80% of children with neurocysticercosis present with seizures, particularly partial seizures 4
• Status epilepticus can occur in some cases 5

Increased Intracranial Pressure (Second Most Common)

• Approximately 20% of cases present with increased intracranial pressure, mainly from obstructive hydrocephalus 1, 3
• Symptoms include headache and vomiting, which occur in about one-third of cases 5, 4
• Life-threatening acute intracranial hypertension can develop when cysticerci lodge within the ventricular system 2

Additional Neurologic Symptoms

Headaches

• Headaches are a common symptom, including migraine-type headaches 1, 3
• Headaches occur in conjunction with other symptoms in approximately one-third of patients 6

Less Common Manifestations

• Spinal radiculopathies 1
• Cerebrovascular accidents, including lacunar infarctions, thrombotic strokes, and hemorrhagic strokes 1
• Visual changes 1
• Mass lesions 1
• Focal neurological deficits, including hemiparesis when giant cysts invade the Sylvian fissure 2, 6

Location-Specific Presentations

Ventricular and Basal Cisternal Disease (Malignant Forms)

• Racemose cysts in the basal cisterns cause intense inflammatory reaction, fibrosis, and progressive leptomeningeal thickening 2
• In approximately 60% of cases with basal cisternal involvement, CSF circulation obstruction results in hydrocephalus 2
• Mortality rate is high (50%) when hydrocephalus secondary to cysticercotic meningitis is present, with most patients dying within 2 years after CSF shunting 2

Subarachnoid Space Involvement

• Cysts may grow to large sizes (giant cysts) causing intracranial hypertension with hemiparesis, partial seizures, or other focal neurological signs 2

Clinical Polymorphism Determinants

The wide variability in symptoms depends on: 7

• Number of lesions (single versus multiple cysticerci)
• Location of CNS lesions (subarachnoid, intracerebral, intraventricular, intramedullary)
• Type of cysticercus (Cysticercus cellulosae versus Cysticercus racemosus)
• Stage of parasite development (vesicular/viable, necrotic, fibrocalcified nodule)
• Intensity of host immune-inflammatory response

Important Clinical Caveat

There is typically a latent period of years (months to decades) between infection and onset of symptoms, so exposure history should not be limited to recent periods but should include queries about access to safe water, contact with tapeworm carriers, and contact with pork-raising areas throughout the patient's lifetime 1