Neurological sequelae in survivors of cerebral malaria

Isaac Oludare Oluwayemi1, Biobele Joackim Brown, Olusola Adetunji Oyedeji

  • 1Department of Paediatrics, Ekiti State University Teaching Hospital, Ado-Ekiti, Nigeria.

Insights

Neurological deficits can persist for up to 24 months in children surviving cerebral malaria (CM). This study found no link between common risk factors and the persistence of these long-term neurological impairments.

Area of Science:

  • Pediatric Neurology
  • Infectious Diseases
  • Global Health

Background:

  • Cerebral malaria (CM) is a significant cause of childhood mortality and long-term neurological disability.
  • Data on the persistence of neurological sequelae after hospital discharge and their associated risk factors in pediatric CM survivors are limited.

Purpose of the Study:

  • To prospectively document persistent neurological impairments in children treated for cerebral malaria post-discharge.
  • To determine the frequency of persistent neurological deficits and identify risk factors associated with their persistence.

Main Methods:

  • Prospective study involving 160 children treated for CM between January 2004 and November 2006.
  • Review of case records for initial CM treatment and subsequent follow-up of survivors to assess neurological sequelae.
  • Analysis of potential risk factors including hypoglycemia, anemia, age, sex, and convulsion multiplicity.

Main Results:

  • Of 160 admitted children, 131 (81.9%) survived CM.
  • Neurological sequelae were observed in 13.7% at discharge and 4.6% at follow-up.
  • Persistent deficits included memory impairment (1.5%), seizure disorders (0.8%), visual impairment (0.8%), speech impairment (0.8%), monoparesis (0.8%), and hyperactivity (0.8%), with the longest lasting up to 24 months. No significant associations were found between risk factors and persistence.

Conclusions:

  • Neurological deficits are common complications of childhood cerebral malaria.
  • Neurological sequelae can persist for extended periods, up to 24 months or longer, in CM survivors.
  • Identified risk factors for CM did not correlate with the persistence of neurological sequelae.
Abstract

Related Concept Videos

Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
68
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
45
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
27
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
31
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
31
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
30