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Secondary Spinal Cord Injury llI: Pathophysiology

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...

Spinal Cord Injury ll: Pathophysiology

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...

Spinal Cord

Spinal Cord

The spinal cord, a critical component of the central nervous system, extends from the base of the brainstem to the lumbar region of the vertebral column. It is essential for maintaining physical stability and facilitating communication between the brain and peripheral parts of the body.

Spinal Cord: Cross-sectional Anatomy

Spinal Cord: Cross-sectional Anatomy

The cross-sectional anatomy of the spinal cord offers a detailed view of its complex structure and function within the central nervous system. At the core of the spinal cord lies the gray matter, characterized by its butterfly or "H"-shaped appearance in cross-section. This central region is enveloped by white matter, with the overall structure divided into symmetrical halves by the dorsal median sulcus and the ventral median fissure.
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The Spinal Cord

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The spinal cord is the body’s major nerve tract of the central nervous system, communicating afferent sensory information from the periphery to the brain and efferent motor information from the brain to the body. The human spinal cord extends from the hole at the base of the skull, or foramen magnum, to the level of the first or second lumbar vertebra.

Spinal Cord: Gross Anatomy

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...

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Contusion Spinal Cord Injury via a Microsurgical Laminectomy in the Regenerative Axolotl

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Spinal cord involvement in Balo's concentric sclerosis.

Karim L Kreft¹, S Jouke Mellema, Rogier Q Hintzen

¹Erasmus MC, University Medical Center, Department of Neurology, Rotterdam, The Netherlands.

Journal of the Neurological Sciences

|February 3, 2009

Summary

A rare case of Balo concentric sclerosis developed in a patient with CNS inflammatory demyelinating disease after plasma exchange. Mitoxantrone stabilized the patient, highlighting treatment options for refractory multiple sclerosis.

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Area of Science:

Neuroimmunology
Neurology
Demyelinating Diseases

Background:

Central nervous system (CNS) inflammatory demyelinating diseases are a group of neurological disorders.
Multiple sclerosis (MS) is a common form of CNS inflammatory demyelinating disease.
Balo concentric sclerosis is a rare, distinct variant of MS.

Observation:

A patient with a history of myelitis experienced a steroid-refractory CNS inflammatory demyelinating disease attack.
The condition progressed to Balo concentric sclerosis following plasma exchange therapy.
The acute inflammatory disease involved the spinal cord, a rarely documented occurrence.

Findings:

Plasma exchange (plasmapheresis) provided no significant benefit to the patient.
The patient met the McDonald criteria for multiple sclerosis.
Mitoxantrone treatment led to stabilization of the patient's condition, albeit at a high Expanded Disability Status Scale (EDSS) score.

Implications:

This case highlights the potential for rare presentations of CNS inflammatory demyelinating diseases.
It underscores the limited efficacy of plasma exchange in certain refractory cases.
Mitoxantrone emerged as a stabilizing treatment option for this severe form of MS, even at advanced disability levels.