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Related Concept Videos

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...
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...
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...
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...
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 barrier loses...

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Translational Orthotopic Models of Glioblastoma Multiforme
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Published on: February 17, 2023

[Glioblastoma multiforme mimicking limbic encephalitis].

Joana Nunes1, Sílvia Carvalho, Paula Gouveia

  • 1Serviço de Neurorradiologia, Centro Hospitalar de Coimbra, Coimbra, Portugal.

Acta Medica Portuguesa
|November 27, 2012
PubMed
Summary

This study presents a rare case of glioblastoma multiforme selectively invading the bilateral limbic system, initially mimicking limbic encephalitis. This rare presentation highlights the importance of considering tumors in differential diagnoses for limbic system dysfunction.

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Area of Science:

  • Neuro-oncology
  • Neuropathology
  • Neuroradiology

Background:

  • Gliomas rarely involve the limbic system bilaterally and selectively.
  • Limbic system dysfunction can present with symptoms like memory loss.
  • Differentiating neoplastic from inflammatory processes in the limbic system can be challenging.

Observation:

  • A 58-year-old male presented with acute short-term memory loss.
  • Initial MRI showed bilateral limbic system abnormalities (hippocampus, amygdala, parahippocampus, fornix) with right mesial temporal contrast enhancement.
  • Initial diagnosis of limbic encephalitis was made, and steroid therapy was initiated.

Findings:

  • Follow-up imaging revealed a tumor consistent with glioblastoma multiforme.
  • Neuropathologic examination confirmed glioblastoma multiforme in the right temporal lesion.
  • Glioblastoma's ability to spread via white matter tracts, including the corpus callosum, is known, but selective bilateral limbic invasion is uncommon.

Implications:

  • Selective bilateral limbic system gliomas are rare and can mimic limbic encephalitis.
  • This case underscores the need for thorough diagnostic workup in suspected limbic encephalitis, including consideration of neoplastic etiologies.
  • Advanced neuroimaging and neuropathology are crucial for accurate diagnosis and management of limbic system tumors.