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Related Concept Videos

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...
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
Herniated Intervertebral Disc l: Introduction01:29

Herniated Intervertebral Disc l: Introduction

Intervertebral disc herniation refers to the displacement of the nucleus pulposus (the gel-like inner core of the disc) through a tear or weakened area in the annulus fibrosus (the outer fibrous ring). The displaced disc material extends beyond the normal boundaries of the disc space and may compress or irritate nearby spinal nerve roots or, less commonly, the spinal cord.Etiology and Risk FactorsHerniation commonly results from degeneration, in which aging reduces disc hydration and...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Spinal Cord: Gross Anatomy01:15

Spinal Cord: Gross Anatomy

The spinal cord resides within the protective confines of the vertebral column. It is the main pathway for information traveling between the brain and the body. It plays a fundamental role in nearly all bodily functions, from simple reflexes to complex motor movements. The spinal cord begins at the medulla oblongata at the base of the brainstem and extends downward, terminating at the conus medullaris near the first and second lumbar vertebrae. The spinal cord's length in adults is...
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...

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Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review
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Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review

Published on: November 8, 2024

Cauda equina syndrome

Chris Lavy1, Andrew James, James Wilson-MacDonald

  • 1Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, Oxford OX3 7LD. christopher.lavy@ndos.ox.ac.uk

BMJ (Clinical Research Ed.)
|April 2, 2009
PubMed
Summary

No abstract available in PubMed .

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