Spinal Shock, Neurogenic shock, and Autonomic Dysreflexia Explained

Kia ora team! In this video, we're breaking down the three key consequences of a spinal cord injury — Spinal shock, Neurogenic shock, and Autonomic Dysreflexia, also known as Autonomic Hyperreflexia. We'll explain how they’re different, when they occur, what they look like, and why they matter.. Let’s get into it, happy studying! 00:00 Introduction 00:15 Autonomic nervous system 02:05 Spinal shock 04:14 Neurogenic shock 05:52 Autonomic dysreflexia 14:21 Recap 14:25 Spinal shock 15:04 Neurogenic shock 16:27 Autonomic dysreflexia Spinal Shock and Neurogenic Shock Spinal Shock After an acute spinal cord injury, the person will experience some degree of spinal shock. This occurs shortly after injury and is characterised by a temporary loss of all neurological function below the level of injury, including: Spinal reflexes Autonomic function Motor control Sensation This state may last up to 6 weeks, although in many cases it resolves within days to weeks. The return of reflexes marks the end of spinal shock. Neurogenic Shock If the spinal cord injury is at or above T6, the injury can disrupt sympathetic outflow, resulting in: Hypotension Bradycardia Peripheral vasodilation This hemodynamic state is known as neurogenic shock, caused by the loss of sympathetic tone and unopposed parasympathetic (vagal) function. It is a medical emergency that requires immediate recognition and management. Important: Although spinal shock and neurogenic shock can occur simultaneously, spinal shock does not cause neurogenic shock. They are distinct processes triggered by the same injury, not by each other. Time Period Post-Injury Spinal shock begins immediately after the injury and resolves over days to weeks. Autonomic dysreflexia (AD) typically develops after spinal shock has resolved, during the chronic phase of spinal cord injury. Autonomic dysreflexia is most commonly seen in individuals with injuries at or above T6. Pathophysiology of Autonomic Dysreflexia Triggering Stimulus Autonomic dysreflexia is triggered by noxious stimuli below the level of injury: *Bladder-related* • Distended bladder (urinary retention) • Blocked or kinked catheter • Urinary tract infection (UTI) *Bowel-related* • Constipation • Fecal impaction • Digital rectal examination • Enemas or suppositories *Skin-related* • Pressure injuries • Ingrown toenails • Burns/scalds • Tight clothing or medical devices *Other triggers* • Sexual activity or stimulation • Menstruation • Labor and delivery • Fractures or injuries below the lesion • Sudden temperature changes --- Afferent Signal Transmission Sensory receptors detect the noxious stimulus and send afferent impulses to the spinal cord below the lesion. These impulses cannot ascend past the spinal injury to the brain for proper interpretation and control. --- Autonomic Nervous System Activation A reflex sympathetic response occurs at the spinal cord level: Diffuse vasoconstriction below the injury Massive increase in blood pressure (BP) due to unregulated vasoconstriction --- Baroreceptor Response Baroreceptors in the aortic arch and carotid sinuses detect the dangerously elevated blood pressure. The brainstem initiates compensatory actions: ✅ Activates the parasympathetic nervous system via the vagus nerve, causing a decrease in heart rate (bradycardia). ✅ Inhibits sympathetic outflow above the level of injury, which leads to vasodilation in those areas. --- Flushing and Sweating Above the Injury Vasodilation above the lesion causes a local increase in skin temperature. This warming is sensed by thermoreceptors in the skin, which activate the central thermoregulatory response (via the hypothalamus). The hypothalamus then stimulates sympathetic cholinergic fibers (which are still intact above the lesion) to produce sweating. ✅ This sweating is a response to skin warming, not increased sympathetic tone. It is a thermoregulatory mechanism, not a sign of sympathetic activation. --- 🚫 Disrupted Regulation Below the Injury Although the vagus nerve can slow the heart rate, it cannot reverse the sympathetic vasoconstriction below the lesion. Parasympathetic nerves do not innervate most blood vessels, and vasodilation normally occurs via withdrawal of sympathetic tone, which the brain can no longer send below the injury. The result is persistent vasoconstriction, sustaining severe hypertension despite bradycardia. --- Symptoms and Complications of Autonomic Dysreflexia Common Symptoms: Severe, pounding headache Flushing and sweating above the level of the lesion Cool, pale skin below the level of the lesion Nasal congestion Visual changes (blurred vision, spots) Potential Complications (if untreated): Stroke (risk increased 3–4x) Seizures Myocardial infarction (heart attack) Pulmonary edema Retinal hemorrhage Death