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Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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Related Experiment Video

Updated: Jun 9, 2026

Interictal High Frequency Oscillations Detected with Simultaneous Magnetoencephalography and Electroencephalography as Biomarker of Pediatric Epilepsy
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Interictal High Frequency Oscillations Detected with Simultaneous Magnetoencephalography and Electroencephalography as Biomarker of Pediatric Epilepsy

Published on: December 6, 2016

Familial hemiplegic migraine.

Jakob Møller Hansen1

  • 1Department of Neurology, Glostrup Hospital, Copenhagen, Denmark. jmh@dadlnet.dk

Danish Medical Bulletin
|September 7, 2010
PubMed
Summary

Familial hemiplegic migraine (FHM) genetic mutations do not cause hypersensitivity to common migraine triggers. This suggests FHM and common migraine forms have different underlying neurobiological mechanisms.

Area of Science:

  • Neurology
  • Genetics
  • Molecular Biology

Background:

  • Familial hemiplegic migraine (FHM) is a rare, inherited migraine subtype characterized by hemiplegia during aura.
  • Mutations in FHM genes affect ion transport proteins, potentially disrupting ion homeostasis and neuronal excitability.
  • FHM serves as a genetic model to study migraine pathophysiology and genotype-phenotype correlations.

Purpose of the Study:

  • To investigate if FHM mutations are associated with hypersensitivity to known migraine triggers.
  • To determine if FHM shares pathophysiological pathways with common migraine forms (MO and MA).

Main Methods:

  • Studied genotyped FHM patients and healthy controls.
  • Assessed the response to two known migraine-provoking substances.

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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

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Main Results:

  • Two common migraine triggers did not induce more aura or headache in FHM patients compared to controls.
  • The FHM genotype does not confer hypersensitivity to these specific migraine triggers.

Conclusions:

  • The hypothesis that FHM mutations are associated with hypersensitivity to common triggers is disproven.
  • FHM appears genetically and pathophysiologically distinct from common migraine forms (MO and MA).
  • The role of FHM genes in ion homeostasis may not be directly extrapolated to common migraine pathogenesis.