Cerebral malaria is a rapidly developing encephalopathy, but much pathology of is not clearly understood. Malaria occurs in millions of people, but only 20-50 % of the cases develop into cerebral malaria. It is unclear why some people develop it and others do not.
Cerebral malaria develops when parasitized red blood cells (PRBCs) adhere to the cerebral microvasculature, causing blockage of the blood's pathway (see photos 6-8). This blockage stops blood flow, leading to a shortage of oxygen and nutrients those areas of the brain. The occlusion of the small vessels occurs diffusely throughout brain. This phenomenon seems to occur in all patients with cerebral malaria, although there are numerous other complications that occur as a result of this disease.
Approximately half of the patients with cerebral malaria have elevated intercranial pressure and seizures. Patients in the Gambia, in West Africa, had rings of PRBCs form around the normal RBCs, which will also lead to microvasculature occlusion.
On rare occations, the parasite causes cerebellar ataxia, but no loss of consciousness. The ataxia can occur up to 4 weeks after a malaria attack occurs, but will disappear after 1-2 weeks.
Physical manifestations of the disease may be an abnormal EEG resulting from the lack of oxygen, loss of sulci, and a MRI may show hemorrhagic lesions and infarction.
A common cause of death for patients with cerebral malaria is acute respitory arrest, which may be a result of the intracranial pressure causing a fatal brain stem herniation.
Most people who survive cerebral malaria have no residual neurologic problems. Only about 10 % of patients surviving cerebral malaria suffer from neurologic deficits such as hemiparesis, hypotonia, or spasticity.
We know we have an unclear understanding of the disease because so many people survive the disease without any neurologic problems. This fact leads us to believe it is unlikely that there is complete obstruction of blood flow.
One hypothesis is that the parasite indirectly causes an abnormally high release of nitric oxide in the brain, which changes brain function in the same way as ethanol. This would result in a unconscious state. However, this state would be reversible without residual neurologic probelms.
This hypothesis explains the reversability of the coma state, however, it does not explain many of the other problems associated with the disease, such as the blocked microvasculature.
[ 07-20-2009, 08:51 AM: Message edited by: Momfromtexas ]
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