This is a five year old Latin American female who 
presented to the emergency department (ED) after 
having a presumed seizure.  She was playing in the 
school yard when she suddenly lost consciousness and 
developed generalized tonic-clonic movements of the 
upper and lower extremities for approximately five 
minutes.  EMS was called and she was brought to the 
ED in a post-ictal state.  In the ED, she was noted to 
develop a two-minute episode of right sided tonic-clonic 
movements of the upper and lower extremities with 
eyes deviating to the left.  She was incontinent of urine.  
There were no associated symptoms of fever, cough, or
upper respiratory illness.
     Past medical history was significant for an 
appendectomy six months prior because of abdominal 
pain.  The pathology report described a slightly inflamed 
appendix with the incidental finding of enterobius 
vermicularis within the lumen of the appendix.  She also 
had a subsequent emergency department visit for 
abdominal pain and fever.  Her work-up included a 
complete blood count, electrolytes, urinalysis, and 
abdominal films.  She was subsequently discharged 
with a diagnosis of benign abdominal pain and fever, 
probably due to a viral syndrome.  Her travel history 
included a trip to Mexico earlier in the year.
     Exam:  VS T37.6C, HR 110, RR 30, BP 128/62.  
The patient appeared sleepy but arousable and 
responded appropriately to family members.  Her pupils 
were equal and reactive.  Both tympanic membranes 
had good light reflexes, and her neck was supple.  Her 
breath sounds were clear and equal.  She had a regular 
heart rate and rhythm with no murmurs.  Peripheral 
pulses were brisk, with good capillary refill.  The 
abdomen was soft and non-tender with normal bowel 
sounds.  There was an appendectomy scar on the right 
lower quadrant.  No neurological deficits could be 
detected.  She had no clonus.  Her reflexes were 
normal.
     Because of the presentation of a focal seizure, a CT 
scan of the head was obtained.

View Head CT image.

     A high cut is shown here.  The image on the left is 
without contrast.  The view on the right is obtained after 
IV contrast is administered.  This CT scan shows a 
small intraparenchymal ring-enhancing lesion in the left 
parietal lobe near the vertex, with a fair amount of 
surrounding edema consistent with neurocysticercosis.  
There is no mass effect on the ipsilateral ventricular 
system, no hemorrhage, and no extra-axial fluid 
collection.  This appearance is not specific, as a brain 
abscess, tumor, or other lesions may also have this 
appearance.
     She was hospitalized overnight and started on oral 
carbamazepine.  Electroencephalography was 
abnormal, showing diffuse slowing, which was greater 
in the left hemisphere.  Her eye exam showed no 
evidence of cysticercosis.  She was not treated with 
anti-cysticercal drugs but was continued on oral 
carbamazepine.  She has subsequently remained 
seizure-free. 

Teaching Points: 
     1.  Onset of a focal, non-febrile seizure, which 
subsequently generalizes, suggests a focal CNS lesion.  
The use of imaging studies, CT scan in particular, is 
warranted to rule out a mass lesion or a bleed which 
could be life threatening.
     2.  Cysticercosis is the most common parasitic 
infection of the human central nervous system, mainly 
occurring in developing countries.  The increasing 
number of immigrants from endemic areas in Latin 
America, Asia and Africa has resulted in a higher 
prevalence of neurocysticercosis in the United States.  
Neurocysticercosis affects males and females of all 
ages, with a peak incidence between 30 and 50 years 
of age.  Sixty to ninety percent of patients with 
cysticercosis have CNS lesions.
     3.  Poorly cooked or raw pork is the only source of 
human infection for the development of the adult worm 
(Tinea solium).  Human infection with cysticerci can 
involve thousands of organisms obtained from various 
sources:  ingestion of T. solium eggs in contaminated 
food or water; self-infection from the presence of the 
adult worm in the intestine; and possibly internal 
autoinfection, in which the eggs come in contact with 
the stomach acid, thus possibly allowing hatching and 
penetration of the larvae into the tissues.  Stools of the 
patient and the immediate family should be examined 
for ova and proglottid of T. solium and treated 
accordingly.  Prevention involves awareness of the 
infection route and the use of good sanitary and 
personal hygiene measures.
     4.  The presence of the adult worm in the GI tract 
usually causes no problems other than slight irritation at 
the site of attachment or vague abdominal symptoms 
(hunger pains, indigestion, diarrhea, and/or 
constipation).  There may be a low-grade eosinophilia, 
usually under 15%.  This patient initially presented with 
several episodes of abdominal pain, which on one 
occasion led to the removal of the appendix.  Parasitic 
infections may certainly present as abdominal pain, and 
further studies on the stool (ova and parasites) may 
reveal other ongoing infestations.
     5.  The brain parenchyma is the most common 
location for neurocysticercosis, followed by the 
ventricles and subarachnoid spaces.  The cysts may be 
located anywhere in the brain, most commonly in the 
cerebral gray matter, followed by the brain stem, 
cerebellum, and spinal cord.  When the cysticercus 
dies, it sets up an antigenic stimulus resulting in a local 
inflammatory process and breakdown of the blood-brain 
barrier; as a consequence, contrast enhancement is 
seen.  The completely calcified lesions of cysticercosis 
represent the dead cysticercus larvae and do not 
enhance or elicit edema.  It is estimated that it takes 
4-7 years for the dead larvae to calcify, which may 
explain why calcification is much less commonly seen in 
the pediatric age group than in adult patients with 
cysticercosis.  The differences between adults and 
children with cysticercosis include:  (1) calcifications 
being more commonly seen in adults, and (2) diffusely 
homogeneous enhancing lesions being more commonly 
seen in children.  Hydrocephalus may also develop in 
25% of patients with neurocysticercosis secondary to 
obstruction of CSF outflow or cysts in the basal 
cisterns.  Occasionally, the parasite may lodge in the 
eye, most commonly under the retina in the posterior 
pole, often over the macular area.  The inflammatory 
reaction that ensues may lead to visual loss. 
     6.  It may be difficult to confirm the diagnosis, even 
using CT or MRI techniques.  Serologic testing can be 
helpful; however, there may be cross-reactivity between 
cysticercosis and other parasitic infections.  The 
enzyme-linked immunotransfer blot assay to detect 
antibody to T. solium, for serum and cerebrospinal fluid, 
is the antibody test of choice.  It is available through the 
Centers for Disease Control and Prevention.  The 
antibody assays, however, are rarely positive in children 
with solitary parenchymal lesions, but are often positive 
in those with inflamed lesions in contact with the 
subarachnoid space. 
     7.  The CSF in neurocysticercosis is abnormal in 
about fifty percent of cases.  The most common finding 
is a lymphocytic pleocytosis (>10 wbc/cu mm).  The 
presence of eosinophils (detected by Wright's stain) in 
the CSF is rare and increases the probability of the 
diagnosis.  It is seen in fifteen percent of cases of 
neurocysticercosis.  Other laboratory findings in the 
CSF that may be associated with neurocysticercosis 
include elevated opening pressure in 40% of cases, 
elevated protein in 40%, and low glucose in 25% of 
cases (2). 
     8.  Therapy for the different forms of 
neurocysticercosis must be individualized according to 
the level of disease activity, the number of lesions, the 
location of the parasite and  the presence or absence of 
inflammation as determined by CT or MRI of the brain.  
Patients with active disease or with multiple uninflamed 
cysts can be treated with praziquantel at 50 mg/kg/day 
in three divided doses for 15 days.  The use of 
corticosteroids is recommended for two to three days 
before and during drug therapy to minimize the strong 
inflammatory reaction of the host to acute destruction of 
parasites in the brain.  They may however reduce the 
effectiveness of the anti-cysticercal drug.  Another drug, 
albendazole, appears to have the same efficacy as 
praziquantel but is not yet approved by the FDA.  The 
drug is usually given at an oral dose of 15 mg/kg/day in 
three divided doses for 28 days; however, shorter 
courses for 3-8 days also appear effective.  Intraocular 
or ventricular cysts may require surgical resection.
     9.  Patients with inactive disease or calcification 
alone do not need anti-cysticercal therapy since these 
lesions represent previous cysts destroyed by the host's 
immune reaction.  Treatment with antiepileptic drugs, 
such as carbamazepine and/or phenytoin, is advised 
when calcifications are associated with seizures.  
Seizures may recur for months and will require 
anticonvulsant medication until patients have been 
seizure-free for 1 to 2 years.

References
     1.  Del Brutto OH, Sotelo J, and Roman GC.  
Therapy for Neurocysticercosis:  A Reappraisal.  
Clinical Infectious Disease 1993;17: 730-5.
     2.  Davis LE and Kornfeld M.  Neurocysticercosis:  
Neurologic, Pathogenic, Diagnostic and Therapeutic 
Aspects.  Eur Neurol 1991;31:229-240.
     3.  Garcia LS and Bruckner DA.  Diagnostic Medical 
Parasitology.  Amer. Society for Microbiology.  
Washington, DC. 2nd edition. 1993;266-280.
     4.  Peter G (ed). The 1994 Red Book:  Report of the 
Committee on Infectious Diseases.  American Academy 
of Pediatrics, Elk Grove Village, IL. 23rd edition.  
1994:455-457.