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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...

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...

Ischemic Stroke ll: Pathophysiology

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

Ischemic Stroke l: Introduction

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Hemorrhagic Stroke ll: Pathophysiology

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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...

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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...

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Related Experiment Video

Updated: Jul 16, 2026

Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice

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Published on: July 16, 2015

Spinal cord infarction with multiple etiologic factors.

John J Millichap¹, Bernard T Sy, Rodney O Leacock

¹Department of Internal Medicine, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA. millichapj@mail.ecu.edu

Journal of General Internal Medicine

|March 14, 2007

Summary

Spinal cord infarction is rare, often causing sudden paralysis and sensory loss. This case highlights multiple contributing factors and unusual symptoms, emphasizing preventive therapy for at-risk individuals.

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Area of Science:

Neurology
Vascular Neurology
Spinal Cord Medicine

Background:

Spinal cord infarction (SCI) is an uncommon neurological emergency.
It typically presents with acute paralysis and sensory deficits.
Multiple underlying causes exist, but cases involving several factors are rare.

Observation:

A 63-year-old male with diabetes mellitus, hypertension, and osteoarthritis presented with acute chest pain, numbness, and weakness.
He experienced episodic hypotension and developed incomplete tetraplegia with areflexia.
Neurological examination revealed sensory deficits in pain, temperature, proprioception, and vibration below specific cervical and thoracic dermatomes.

Findings:

Magnetic resonance imaging confirmed spinal cord infarction spanning the C6-T3 segments.
Severe degenerative changes were noted in the cervical and lumbar spine.
The patient's presentation included atypical symptoms and multiple comorbidities.

Implications:

This case underscores the diverse and sometimes unusual clinical presentations of spinal cord infarction.
Identifying multiple, concurrent risk factors is crucial for accurate diagnosis and management.
Optimal preventive strategies are essential for patients susceptible to spinal cord vascular events.