The spinal cord is about 45 cm long in adults, roughly the diameter of a thumb, and runs from the brainstem down through the vertebral column to around the level of the first or second lumbar vertebra. Everything the brain tells the body below the neck travels through it. Everything the body below the neck tells the brain travels through it. When it is damaged, most of what it carried stops working permanently.
At a glance
What it does
Two jobs: signal conduction and reflex processing. Ascending tracts (dorsal columns, spinothalamic tracts, spinocerebellar tracts) carry sensory information up — touch, vibration, proprioception, pain, temperature. Descending tracts (corticospinal, rubrospinal, vestibulospinal, reticulospinal) carry motor commands down to the muscles and autonomic targets.
Reflex arcs live entirely inside the cord. When you touch something hot, the signal enters the dorsal root, synapses onto a motor neuron in the ventral horn (sometimes with one interneuron in between), and the hand withdraws before the brain is even aware of the stimulus. The patellar reflex — knee tap, leg kicks — is a textbook two-neuron arc. These reflexes exist because routing every protective response through cortex would be too slow.
The cord also contains central pattern generators for rhythmic motor output like walking. These circuits can produce coordinated stepping patterns in spinalized animals; the brain's job is more about initiating, modulating, and steering than generating the pattern from scratch.
How it works
Gray matter — H-shaped in cross-section — contains cell bodies and is organized into dorsal horns (sensory input) and ventral horns (motor output). White matter surrounds the gray and contains myelinated tracts running up and down.
Nerve roots exit at each spinal level. Dorsal roots carry sensory axons in; ventral roots carry motor axons out; they merge just outside the cord to form the mixed spinal nerve. Because the cord is shorter than the vertebral column in adults, lumbar and sacral nerves have to travel down as the cauda equina before exiting at their respective levels.
The autonomic nervous system has its preganglionic motor neurons in the cord too: sympathetic in the lateral horns from T1 to L2, parasympathetic in the sacral segments S2-S4. That is why spinal injuries above T6 disrupt blood pressure regulation and cause autonomic dysreflexia.
When it goes wrong
Traumatic spinal cord injury affects roughly 250,000-500,000 new people globally each year, most commonly from motor vehicle crashes, falls, violence, and sports (especially diving into shallow water). Level and completeness are the two numbers that matter.
Level determines what is lost. Cervical injuries (above C8) produce tetraplegia — arms, legs, trunk, and often diaphragm. C3-C4 injuries typically require ventilator support for life. Thoracic injuries produce paraplegia with preserved arm function. Lumbar and sacral injuries can spare walking but affect bowel, bladder, and sexual function.
Completeness determines how much is lost below the level. Complete injuries (ASIA A) wipe out all motor and sensory below the lesion. Incomplete injuries preserve some function, and prognosis improves with any preserved voluntary anal contraction or sacral sensation. Central cord syndrome, anterior cord syndrome, and Brown-Sequard syndrome are specific incomplete patterns with characteristic deficits.
Non-traumatic causes include tumor, multiple sclerosis, transverse myelitis, vascular malformation, spinal stenosis, and infection. Cauda equina syndrome — compression of the nerve roots below the cord — is a surgical emergency because delayed decompression leaves permanent bladder, bowel, and saddle sensation deficits.
Interactions
The cord is the bottleneck that autonomic and somatic signals pass through together. Cortisol, thyroid hormone, and sex hormones act on neurons within it and modulate pain processing — this is part of why chronic stress and hormonal states change pain perception. Opioids act strongly at dorsal horn receptors to dampen ascending pain; epidural and intrathecal injections exploit this for anesthesia and chronic pain management.
Regenerative medicine has been promising spinal cord repair for three decades. Progress is real but slow — stem cell trials, scaffolds, electrical stimulation, and combination approaches are producing measurable but still limited restoration of function in early trials. Anyone advertising a cure for complete SCI in 2026 is lying.
Honest take
The reason SCI is so devastating is not mysterious — it is that mature CNS axons do not regenerate across the injury site, scar tissue blocks any attempt, and the downstream neurons eventually die from disuse. That is an enormously hard biological problem, not one that a supplement or hyperbaric chamber will solve. Prevention is where most of the expected value sits: wear seatbelts, do not dive into unknown water, helmet up for cycling and skiing. Once an injury has happened, the best current care is aggressive early surgical decompression, intensive rehabilitation, and participating in legitimate clinical trials through a real SCI center — not paying out of pocket for stem cell tourism.
Sources
- Kirshblum et al., Journal of Spinal Cord Medicine — the International Standards for Neurological Classification of SCI.
- Ahuja et al., Nature Reviews Disease Primers (2017) — traumatic SCI review.
- Fehlings et al., Global Spine Journal — guidelines on early decompression.