Cysticercosis in Emergency Medicine Medication

Antihelminthic agents are the mainstay of definitive treatment. Controversy exists as to whether antiparasitic treatment of cysticercosis is necessary in most cases. Some authors claim that patients do well without antiparasitic therapy since symptomatology is produced by pericystic inflammation, which portends imminent involution of the parasite. This suggests that the presence of clinical symptoms is predictive of a subsequent self-limited disease course.

In addition, the calcific lesions of "inactive" disease may not be clinically silent but rather epileptogenic and can thereby confer significant morbidity. A randomized controlled study of 300 patients with neurocysticercosis over several years found that those treated with a course of albendazole plus corticosteroids and anticonvulsants developed significantly more lesional calcification on follow-up imaging than those treated with anticonvulsants alone.^[4] During the first year, this treatment group also had a significantly higher incidence of seizures and thereafter displayed a trend toward such. These investigators concluded that antihelminthic treatment may result in more long-term seizure activity since complete resolution of lesions may be more likely when cysts are allowed to spontaneously resolve. They therefore recommend treatment with anticonvulsants alone, with careful clinical and radiologic follow up.

Despite lively controversy surrounding the matter, a preponderance of the literature positively supports treatment with antihelminthics.^{[5, 6]} Several randomized controlled trials have demonstrated benefit of antihelminthic therapy, particularly in reducing the number of active cysts. Benefit seems to be greatest during the first weeks of therapy. As mentioned previously, treatment with antihelminthic medication will initially worsen clinical symptoms as faltering parasite defenses lead to increasing perilesional inflammation. Therefore, in nearly all trials, antiparasitic medication has been combined with steroid therapy. In addition, patients are usually maintained on concomitant anticonvulsant therapy for an indefinite period of time.

Caution is particularly warranted in patients with significant pretreatment encephalitis, hydrocephalus, or vasculitis, since treatment may cause increasing inflammation as cysts involute, leading to worsening clinical states. CSF shunting may be indicated before medical treatment begins since intracranial hypertension may worsen upon administration of antiparasitics.

Class Summary

Parasite biochemical pathways differ sufficiently from those of the human host so as to allow selective interference by chemotherapeutic agents in relatively small doses. Many patients may require more than one course of treatment to entirely eliminate active cysts.

The more effective agent, albendazole, has upstaged praziquantel as the traditional therapeutic agent. Subarachnoid and intraventricular neurocysticercosis (NCC) may be relatively more resistant to treatment. In these cases, repeat courses of medication are usually needed, and there is limited evidence that higher-dose albendazole treatment (30 mg/kg/d) may be beneficial.^[7]

Praziquantel (Biltricide)

Increases cell membrane permeability in susceptible worms, resulting in a loss of intracellular calcium, massive contractions, and paralysis of their musculature. In addition, produces vacuolization and disintegration of the schistosome tegument. This is followed by attachment of phagocytes to the parasite and death.

Albendazole (Albenza)

Broad-spectrum anthelmintic that decreases ATP production by the worm causing energy depletion, immobilization, and finally, death.

Class Summary

A temporary increase in pericystic inflammation often is observed during treatment of NCC, as the dying parasite no longer can escape host defenses. For this reason, it is often recommended that corticosteroids be administered in combination with, or instead of, antihelminthics. This practice is controversial and should be tailored to the individual patient according to the number and location of cysticerci. Steroids are more likely indicated in cases involving extraparenchymal cysts.

Prednisone (Orasone, Meticorten, Deltasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dexamethasone (Decadron, Dexone)

For various allergic and inflammatory diseases. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Class Summary

Anticonvulsant therapy should proceed as in other epileptiform states. Benzodiazepines are first-line agents for active prolonged or repeated seizures. They should generally be followed by a more definitive anticonvulsant such as phenytoin. Barbiturates may be needed in more refractory cases.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor blood pressure after administering dose. Adjust as necessary.

Phenytoin (Dilantin)

May act in motor cortex, where it may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Dose to be administered should be individualized. Administer larger dose before retiring if dose cannot be divided equally.

Phenobarbital (Solfoton, Luminal, Barbita)

Elevates seizure threshold, limits the spread of seizure activity, sedative.