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Related Concept Videos

Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
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...
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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...
Parkinson Disease ll: Pathophysiology01:24

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Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Cerebral Edema ll: Pathophysiology01:22

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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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Related Experiment Video

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A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy
10:02

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Published on: November 3, 2016

Defining cerebral palsy: pathogenesis, pathophysiology and new intervention.

M Longo1, G D V Hankins

  • 1Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX 77555-0587, USA.

Minerva Ginecologica
|September 15, 2009
PubMed
Summary

Cerebral palsy (CP) is linked to antenatal factors like preterm birth and infection, not just birth asphyxia. Improved neonatal care may increase CP incidence, highlighting the need to understand its causes and prevention strategies.

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Area of Science:

  • Neurology
  • Obstetrics
  • Neonatology

Background:

  • Cerebral palsy (CP) affects approximately 2 in 1,000 live births.
  • Antenatal factors such as preterm delivery, low birth weight, infection, multiple gestations, and pregnancy complications are associated with CP.
  • Improved neonatal and obstetric care has increased the survival of very preterm and very low birth weight infants, potentially increasing CP incidence.

Purpose of the Study:

  • To review the pathogenesis and pathophysiology of cerebral palsy.
  • To explore antenatal antecedents as etiologies of CP.
  • To discuss the impact of obstetric care on CP prevention.

Main Methods:

  • Review of established criteria for defining intrapartum hypoxic events causing CP.
  • Discussion of four essential criteria for diagnosing CP secondary to intrapartum hypoxic-ischemic insult.
  • Exploration of antenatal factors and their contribution to CP etiology.

Main Results:

  • Four criteria are essential to attribute CP to intrapartum hypoxic-ischemic insult: metabolic acidosis, neonatal encephalopathy, specific CP types (spastic quadriplegic or dyskinetic), and exclusion of other causes.
  • Other criteria suggesting intrapartum timing are also considered.
  • Antenatal factors are significant contributors to CP development.

Conclusions:

  • Understanding the pathogenesis and pathophysiology of CP is crucial for prevention.
  • Obstetric care plays a vital role in preventing CP.
  • Focusing on antenatal antecedents and refining diagnostic criteria can aid in CP prevention efforts.