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Related Concept Videos

Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
Bacterial Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
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...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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...

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Related Experiment Video

Updated: Jun 27, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
09:04

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging

Published on: June 8, 2017

[Post-malaria neurologic syndrome].

Gonçalo Matias1, Nuno Canas, Isabel Antunes

  • 1Serviço de Neurologia, Hospital de Egas Moniz, Lisboa.

Acta Medica Portuguesa
|December 20, 2008
PubMed
Summary
This summary is machine-generated.

Post-malaria neurologic syndrome (PMNS) is a rare complication occurring after Plasmodium falciparum malaria treatment. This case highlights successful methylprednisolone treatment for PMNS-induced encephalopathy.

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Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
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Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice

Published on: January 2, 2013

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Last Updated: Jun 27, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
09:04

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging

Published on: June 8, 2017

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
12:48

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice

Published on: January 2, 2013

Area of Science:

  • Neurology
  • Infectious Diseases
  • Immunology

Background:

  • Neurologic symptoms in malaria are typically linked to severe Plasmodium falciparum infection.
  • Hypoglycemia or anti-malarial drug toxicity can cause neurologic deficits, but post-malaria neurologic syndrome (PMNS) is a rare, distinct complication.
  • PMNS presents as encephalopathy days to weeks after parasite clearance, with unclear pathogenic mechanisms, possibly immunological.

Observation:

  • A 61-year-old man developed severe encephalopathy (delirium, cerebellar ataxia, ophthalmoparesis) two days after recovering from Plasmodium falciparum malaria.
  • Initial diagnostic tests, including peripheral blood smears, were negative for malaria parasites.
  • Magnetic Resonance Imaging (MRI) revealed extensive multifocal white matter abnormalities during the acute phase.

Findings:

  • The patient experienced complete resolution of neurological deficits following treatment with high-dose methylprednisolone.
  • Follow-up MRI at 9 months showed minimal residual white matter lesions, indicating significant recovery.
  • This case supports an immunological basis for PMNS and demonstrates therapeutic efficacy of corticosteroids.

Implications:

  • Early recognition and prompt corticosteroid treatment may be crucial for managing post-malaria neurologic syndrome.
  • Further research into the immunological mechanisms of PMNS is warranted to improve patient outcomes.
  • This case contributes to understanding rare neurologic complications following malaria treatment.