This post-malaria neurological syndrome (PMNS) is characterized by neurological manifestations, including neurological deficit to encephalopathy. Cerebral malaria is a severe neurological condition after the individual has contracted malaria. This is seen after one to four months after the disease condition. The disease mortality is high, and there is long-term neurocognitive impairment in some surviving victims. In this article, you can read the effects of the disease and the causes to understand the neural defects and their treatment.
Where Is This More Predominant?
Malaria is a disease that causes health issues that cause neurological symptoms, which leads to death in many tropical countries. Children below five years in the African race are more affected the most. Severe malaria is manifested as anemia. Some symptoms are hypoglycemia, seizure, acidosis, coma, and multiple organ failure.
What Are the Symptoms of PMNS?
Clinically coma is the last stage for severe malaria infection.
Some other symptoms can be:
How Does PMNS Happen?
The mechanism of PMNS is not clearly understood but an idea of how this neurological damage can be explained from the postmortem bodies.
Parasite sequestration in the Brain: Parasite sequestration in cerebral microvasculature is the primary pathogenesis. Resulting in pathophysiological changes in cells and tissue and the sequestered parasites, which explains the intravascular parasite can cause neural dysfunction. The parasite adheres to the endothelial surface using parasite-derived proteins exposed on the erythrocyte surface. This attaches to host receptors which make intercellular adhesion. This causes brain necrosis and coma, also intracranial hypertension.
Cytokines, Chemokines, and Excitotoxicity: Cytokines and chemokines play a significant role in pathogenesis and have protective and harmful effects—parasite antigens released due to the multiplication of parasites this release both pro-and anti-inflammatory cytokines. Although the balance between these mediators is crucial for parasite control, their role in the pathogenesis of neuronal damage is unclear. Cytokine-mediated synaptic changes contribute to the syndrome of cerebral malaria. When this happens, it causes inflammation of brain cells and tissues, causing damage.
Epithelial injury, Apoptosis, BBB Dysfunction, and Intracranial Hypertension causes Cytoadherence of pRBCs to the endothelium, which initiates a chain of events beginning with the transcription of genes involved in inflammation, cell-to-cell signaling, and signal communication, which result in endothelial activation, the release of endothelial microparticles (EMPs), and apoptosis of host cells. There is widespread endothelial activation in vessels that contain pRBCs. Other complications of falciparum malaria, increases in circulating EMPs, are seen in patients in coma. interactions between RBCs and platelets cause more damage to endothelial cells through a direct cytotoxic effect
Cerebral Blood Flow and Perfusion: Patients with PMNS have an increased and profused cerebral blood flow. This increases the probability of an adaptive response to the high metabolic necessity for oxygen and nutrient delivery. Reduced local perfusion is associated with abnormal electroretinography. Suppose the retina mirrors events in the brain. Likewise, a similar obstruction can be present. A coma in PMNS may result from under-perfusion in multiple but small areas of the brain because these patches of the tiny brain are affected. With early treatment and relief of obstruction, there is less tissue necrosis. Early restoration of perfusion can completely recover the gross neurological function in most patients. Therefore this develops severe brain hypoxia, which leads to damage.
Seizures: Plasmodium falciparum is epileptogenic, increasing the risk and attacking parasitemia. Irreversible neural damage happens due to prolonged seizure activity; edema is recognized on MRI within days. Prolonged seizures may worsen this injury and create a vicious cycle of neural damage and more episodes.
Depth, Duration, and Cause of Coma: PMNS is not a single homogenous syndrome but rather four distinct groups: a prolonged state, covert status epilepticus, severe metabolic derangement, and a primary neurological syndrome. Patients with a long postictal condition can have coma secondary to seizures. The patients regain consciousness within six hours and have a good recovery. Patients with severe metabolic derangement regain consciousness a few hours after resuscitation. Impaired consciousness is a secondary phenomenon that is also common in this. Prolonged hypoglycemia or acidosis causes neuronal dysfunction or death. The outcome may depend on the duration of exposure among patients.
What Can Be Affected Due to PMNS?
What Are the Treatment and Management Options of PMNS?
Steroids, immunoglobulin, acetylsalicylic acid, heparin, anti-TNF agents, mannitol, iron chelation, micronutrients, and prophylactic anticonvulsants are used for therapy. Prophylactic Phenobarbital was associated with respiratory depression. The respiratory depressant prophylactic anticonvulsant, Fosphenytoin, and B5 complex provitamin pantethine prevented the development of the post-malaria neurological syndrome. Erythropoietin provides neuroprotection, infectious encephalopathy, and hypoxic-ischemic encephalopathy can also be reduced, and patients can have a better prognosis.
This is necessary for particular areas such as physical and occupational therapy, behavior and speech therapy, cognitive rehabilitation, and hearing aids. This can help the patient improve the condition and help to live a quality lifestyle.
Post-malaria neurological syndromes cause brain injury. Coma and brain damage develops through multiple mechanisms, and there are several reasons for brain injury. Therefore Combinations of adjuvant therapies are needed for specific mechanisms of brain injury to improve neurocognitive outcomes. Meanwhile, MRI can provide important insights into pathogenesis.
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