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Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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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...
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Encephalitis l: Introduction01:19

Encephalitis l: Introduction

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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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Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

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Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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Hepatic Encephalopathy01:29

Hepatic Encephalopathy

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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
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Arboviral Encephalitis01:25

Arboviral Encephalitis

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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...
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Bacterial Meningitis II: Pathophysiology01:26

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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...
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Related Experiment Video

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Simultaneous Flow Cytometric Characterization of Multiple Cell Types Retrieved from Mouse Brain/Spinal Cord Through Different Homogenization Methods
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Neuro-Behçet syndrome.

Sabahattin Saip1, Gulsen Akman-Demir2, Aksel Siva1

  • 1Department of Neurology, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey.

Handbook of Clinical Neurology
|December 25, 2013
PubMed
Summary

Behçet syndrome (BS) involves the nervous system in 5-10% of cases, presenting as either central nervous system inflammation or venous sinus thrombosis. Understanding these neuro-Behçet syndrome (NBS) subtypes is crucial for managing this complex vascular-inflammatory condition.

Keywords:
Behçet’s diseasecerebral venous sinus thrombosisdifferential diagnosisnervous system involvementneuro-Behçet syndrometreatment

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Area of Science:

  • Neurology
  • Immunology
  • Vascular Medicine

Background:

  • Behçet syndrome (BS) is a chronic, relapsing, multisystem vascular-inflammatory disorder of unknown etiology.
  • Nervous system involvement, termed neuro-Behçet syndrome (NBS), affects 5-10% of patients, presenting with diverse clinical manifestations.
  • BS is characterized by a wide range of organ involvement, necessitating its classification as a syndrome due to its heterogeneity.

Purpose of the Study:

  • To subclassify primary neurologic involvement in Behçet syndrome.
  • To differentiate between intra-axial and extra-axial forms of neuro-Behçet syndrome.
  • To discuss the clinical characteristics, pathogenesis, and treatment challenges of neuro-Behçet syndrome.

Main Methods:

  • Clinical and imaging evidence analysis to identify distinct patterns of neurological involvement.
  • Review of histopathological findings to understand the underlying disease mechanisms.
  • Assessment of current treatment strategies and their limitations in neuro-Behçet syndrome.

Main Results:

  • Neuro-Behçet syndrome (NBS) can be subclassified into two main forms: intra-axial (vascular-inflammatory CNS disease) and extra-axial (cerebral venous sinus thrombosis with intracranial hypertension).
  • Intra-axial NBS often presents with subacute brainstem syndromes and hemiparesis, while extra-axial NBS typically involves fewer symptoms and has a better prognosis.
  • Vascular-type headaches are common in BS, independent of neurological involvement, and rare manifestations include isolated behavioral syndromes and peripheral nervous system issues.

Conclusions:

  • Neuro-Behçet syndrome is a heterogeneous condition with distinct intra-axial and extra-axial subtypes, likely differing in pathogenesis.
  • The diverse nature of NBS complicates prediction of its course, prognosis, and response to treatment.
  • Current treatment options for NBS, including immunosuppressants and anti-TNF agents, lack robust evidence for efficacy, highlighting the need for further research.