et al. 2000b; Lewallen 1998; Tripathi et al. 1995). Retinal manifestations may be noted months or years after the acute malaria infection (Biswas et al. 1996).
Malaria-associated chronic ophthalmologic disorders include side effects of the chronic prophylactic use of antimalarial drugs, such as hydroxychloroquine and chloroquine (Balo et al. 1996; Easterbrook 1999; Lozier and Friedlaender 1989; Niemeyer and Fruh 1989; Portnoy and Callen 1983; Ruiz and Saatci 1991; Tzekov 2005; Wei et al. 2001). The associations have been recognized for decades (Begue 1964; Bernstein 1967; Giles and Henderson 1965; Rubin 1968; Sugiyama et al. 1967). Chloroquine-based prophylaxis is not being used for US troops deployed to OEF and OIF. Oxidative stress has been cited as a possible contributing etiology (Toler 2004). Rynes and Bernstein (1993) highlight the relative rarity of the retinal complications and the need for long-term administration of the drugs.
The committee concludes that there is sufficient evidence of a causal relationship between malaria infection and ophthalmologic manifestations, particularly retinal hemorrhage and scarring, recognized for the first time months or years after the infection.
Neurologic complications, particularly cerebral malaria due to P. falciparum, are characterized by confusion, clouding of consciousness progressing to coma, and seizures. Cerebral malaria is due largely to sequestration of infected red blood cells in the cerebral circulation (Renia et al. 2006), but coma can also be caused by such other malaria complications as hypoglycemia, uremia, or hypoxia due to pulmonary edema (Idro et al. 2005). Cerebral malaria is fatal in 15-20% of cases, and residual neurologic deficits have been reported in 1-3% of adults and 10% of children (Bajiya and Kochar 1996). It is notable that over 97% of afflicted adults who survive the cerebral episode of falciparum malaria are left without detectable chronic sequelae.
A postmalaria neurologic syndrome has been described in people who were treated for malaria due to P. falciparum (Falchook et al. 2003). The manifestations include confusion, psychosis, seizures, and a fine tremor (Malviya et al. 2005; Meier et al. 2004). There may be an associated magnetic resonance imaging finding of enhancement of nonspecific white-matter lesions (Dey et al. 2001).
Two other postmalaria neurologic complications have been described in case reports and case series. Acute inflammatory demyelinating polyneuropathy and Guillain-Barré syndrome have been reported after falciparum malaria and less frequently after vivax malaria (Chakravarty et al. 2004; Shubhakaran and Sharma 2003). Onset of neurologic symptoms can occur during the acute stage of the illness or days to weeks after the end of the acute illness (Shubhakaran and Sharma 2003; Kanjalkar et al. 1999). Cerebellar ataxia, often with tremors, has also been described after falciparum malaria, possibly resulting from demyelinating lesions in the cerebellum (Metha et al. 1996; Senanayake and de Silva 1994). All reports of patients who experienced acute inflammatory demyelinating polyneuropathy and cerebellar ataxia described complete recovery within months of onset (Chakravarty et al. 2004; Kanjalkar et al. 1999), although the natural history of these disorders after other conditions has been associated with slow recovery and persistent neurologic deficits in some of those affected (Kanjalkar et al. 1999).
One report dealt with neurologic deficits among veterans who had experienced cerebral malaria from P. falciparum during the Vietnam War (Varney et al. 1997). Veterans with a self-reported history of cerebral malaria were found to have a greater frequency of neuropsychiatric