Anterior cord syndrome is injury to the anterior two-thirds of the spinal cord, the territory of the anterior spinal artery, so below the lesion the patient has bilateral weakness and bilateral loss of pain and temperature sensation, while vibration, joint position sense and fine touch are preserved because the dorsal columns are fed by the posterior spinal arteries. The classic cause is anterior spinal artery infarction, most often after aortic surgery or with aortic dissection or atherosclerosis; the stem gives paraplegia on waking from aortic repair, or sudden back pain followed within minutes by paraplegia (quadriplegia with a cervical lesion) and urinary retention. It has the poorest functional outcome of the spinal cord syndromes; only about 10–20% of patients regain functional motor recovery.
What is lost and what is spared
A quick hook: anterior = action and agony. The front of the cord carries movement (corticospinal tracts) and pain (spinothalamic tracts), so both are lost; the back of the cord (dorsal columns) keeps working.
| Structure | Blood supply | What it does | Finding in anterior cord syndrome |
|---|---|---|---|
| Lateral corticospinal tracts | Anterior spinal artery | Voluntary movement | Weakness on both sides below the lesion: flaccid and areflexic during spinal shock, later spastic with brisk reflexes and Babinski signs |
| Anterior horn cells | Anterior spinal artery | Lower motor neurons of the infarcted segments | Lower motor neuron signs (flaccid weakness, absent reflexes, later wasting) at the level of the lesion |
| Spinothalamic tracts | Anterior spinal artery | Pain and temperature | Lost on both sides; the sensory level typically sits two to three segments below the motor level |
| Lateral horns, T1–L2 | Anterior spinal artery | Sympathetic outflow | Hypotension, bradycardia, neurogenic bladder and bowel, sexual dysfunction |
| Dorsal columns | Posterior spinal arteries | Vibration, position sense, fine touch, two-point discrimination | Preserved |
A high cervical infarct can also knock out phrenic motor neurons and cause respiratory failure.
Blood supply: why the front of the cord infarcts
The anterior spinal artery forms at the foramen magnum from a branch of each vertebral artery and runs down the anterior median sulcus to the conus medullaris. It supplies the anterior two-thirds of the cord: both anterior and lateral horns and both corticospinal and spinothalamic tracts. The two posterior spinal arteries supply the posterior third, which is why the dorsal columns survive.
One artery cannot fill the whole cord from the top, so it is reinforced along the way by radiculomedullary feeders, 7 to 8 on average. The largest is the artery of Adamkiewicz (arteria radicularis magna). It arises from an intercostal artery, on the left in 70–80% of people and most often at T9–T12 (about 75%). Two features make the thoracic cord fragile: the anterior spinal artery is narrowest in its thoracic segment, and some segments, such as those around T2–T4, have sparse collateral supply. Injury to a feeder or to the aorta itself (atherosclerosis, dissection, clamping during surgery) causes cord infarction more often than disease of the spinal arteries themselves. For where each tract runs, see the spinal cord tracts visual hack.
Causes
| Cause | What to know |
|---|---|
| Aortic surgery | Iatrogenic injury is the most common cause; risk rises with hypotension, prolonged aortic cross-clamping and raised spinal cord pressure |
| Aortic dissection | Dissection frequently occludes the feeders of the anterior spinal artery |
| Atherosclerosis and emboli | Thrombus or emboli from atheroma or the heart; cardiac arrest and hypotensive shock cause global hypoperfusion |
| Fibrocartilaginous embolism | Nucleus pulposus material embolizes into spinal vessels |
| Other vascular causes | Vasculitis, sickle cell disease, hypercoagulable states, cocaine (vasospasm, vasculitis or thrombosis), arteriovenous malformations |
| Trauma and compression | Direct injury to the front of the cord from fracture fragments, a herniated thoracic disc or cervical spondylosis |
| Spine procedures | Minimally invasive procedures such as vertebroplasty and balloon kyphoplasty |
Smoking, hypertension, diabetes and dyslipidemia raise the risk. Spinal cord infarction is rare, about 1% of all strokes, but anterior spinal artery syndrome is the most common ischemic cord syndrome. The aortic side of the story is covered in the aortic dissection (Stanford A vs B) Q-bank breakdown.
How it shows up in a question stem
- Onset: abrupt. The first symptom is usually sudden back pain, often with a band of tightness around the trunk, followed within minutes by bilateral weakness and sensory loss.
- Setting: waking from aortic surgery, an aortic dissection, cardiac arrest or shock, or an older patient with vascular risk factors.
- Motor: flaccid, areflexic weakness at first (spinal shock); tone and reflexes return over time as spasticity.
- Sensation: a dissociated loss. Pinprick and temperature are gone; vibration and toe position sense are intact.
- Autonomic: urinary retention, bowel dysfunction, hypotension or bradycardia.
Anterior cord syndrome vs the other cord syndromes
| Syndrome | What is damaged | Motor | Pain and temperature | Vibration and position | Classic cause |
|---|---|---|---|---|---|
| Anterior cord | Anterior two-thirds (anterior spinal artery territory) | Lost on both sides below the lesion | Lost on both sides below the lesion | Preserved | Anterior spinal artery infarction (aortic surgery, dissection, atherosclerosis); anterior compression |
| Posterior cord | Dorsal columns | Spared | Spared | Lost; positive Romberg | B12 deficiency, tabes dorsalis, compression |
| Brown-Séquard | One half of the cord | Lost on the same side | Lost on the opposite side | Lost on the same side | Hemisection, classically penetrating trauma |
| Central cord | Central cervical cord | Arms weaker than legs | Variable | Variable | Hyperextension injury in a narrowed cervical canal |
Anterior and posterior cord syndromes are mirror images, as the posterior cord syndrome overview shows, and a one-sided, crossed pattern belongs to Brown-Séquard syndrome.
Diagnosis
- MRI of the spine is the key test. It excludes compression that needs surgery and shows the infarct, but it can be normal in the first 24 hours; repeat it within 24–48 hours if suspicion stays high.
- What the infarct looks like: restricted diffusion in the anterior spinal artery territory on diffusion-weighted imaging, a thin "pencil-like" T2-bright stripe spanning several levels on sagittal images, and on axial images a bright spot on each side of the midline, the "owl's eyes" or "snake eyes" sign (present in only 4–35% of cases).
- Look for the cause: CT or MR angiography of the aorta and spinal vessels, plus labs for vascular risk, coagulation and infectious or inflammatory mimics.
- Mimics: transverse myelitis (onset less abrupt), multiple sclerosis (can look similar on MRI) and compressive lesions.
Treatment and prognosis
- No treatment reverses the infarct. Care is supportive and aimed at the cause, such as repair of an aortic dissection.
- Protect perfusion: secure the airway and treat hypotension with fluids and vasopressors such as phenylephrine or norepinephrine.
- Traumatic cord injury: many experts keep the mean arterial pressure at 85–90 mm Hg or higher for 5 to 7 days.
- Steroids: high-dose corticosteroids are ineffective for anterior spinal artery syndrome and are not routinely recommended after traumatic cord injury.
- Prevention in high-risk aortic repair: raise the mean arterial pressure and drain cerebrospinal fluid through a lumbar drain.
- Supportive care: bladder catheterization, DVT prophylaxis, pressure-injury prevention (lifetime risk about 50% after spinal cord injury) and rehabilitation.
- Prognosis: the poorest functional outcomes of the cord syndromes, with mortality of 9–23%. Initial severity is the most reliable predictor, and no improvement within 24 hours is a bad sign.
Exam traps
- Normal vibration and position sense do not clear the cord. That is exactly what anterior cord syndrome spares, so check pinprick and temperature.
- The posterior spinal artery is the wrong answer when the dorsal columns work; its territory carries vibration and position sense.
- Flaccid, areflexic legs right after the event mean spinal shock, not a peripheral nerve lesion; spasticity and Babinski signs come later.
- The pain and temperature level sits below the motor level, so do not place the lesion at the sensory level.
- Paraplegia on waking from aortic surgery is anterior spinal artery ischemia from lost flow through its feeders, classically the artery of Adamkiewicz.
- Steroids are the wrong answer for an ischemic anterior cord syndrome.
- The same losses on both sides argue against Brown-Séquard, which splits weakness and pain loss between the two sides; arms weaker than legs after a neck hyperextension injury is central cord syndrome.
Worked example
Vignette. A 71-year-old man with hypertension and a long smoking history undergoes open repair of a thoracoabdominal aortic aneurysm with a long cross-clamp time. On waking he cannot move either leg. Both legs are flaccid with absent knee and ankle reflexes. He cannot feel pinprick or cold below the umbilicus, but he feels a vibrating tuning fork at both ankles and correctly says whether his big toes are moved up or down. A bladder scan shows 900 mL of retained urine. Which artery's territory has infarcted?
Answer: The anterior spinal artery, in the thoracic cord, after loss of flow through its radiculomedullary feeders, classically the artery of Adamkiewicz.
Why the distractors are wrong:
- Posterior spinal artery: it supplies the dorsal columns, which are working here; its infarct would spare strength and pinprick.
- Brown-Séquard syndrome: a hemisection gives one-sided weakness and vibration loss with pain and temperature loss on the other side, not a symmetric bilateral pattern.
- Central cord syndrome: it follows a neck hyperextension injury and weakens the arms more than the legs.
- Cauda equina syndrome: partial, often asymmetric leg weakness and numbness with saddle anesthesia, not a truncal sensory level with preserved vibration.
- A lower motor neuron lesion because the reflexes are absent: early areflexia below a cord lesion is spinal shock, and spasticity with extensor plantar responses follows.
Key takeaways
- Anterior cord syndrome = anterior two-thirds of the cord, the anterior spinal artery territory.
- Lost on both sides below the lesion: strength, pain and temperature. Kept: vibration, position sense and fine touch.
- Classic cause: anterior spinal artery infarction after aortic surgery or with dissection or atherosclerosis; trauma and anterior compression also cause it.
- Artery of Adamkiewicz: the largest feeder, usually from a left intercostal artery at T9–T12.
- Early flaccid areflexia is spinal shock; bladder retention and hypotension are common.
- MRI (diffusion restriction, pencil-like T2 signal, owl's eyes) confirms it and excludes compression, but can be normal in the first 24 hours.
- Treatment is supportive, with blood pressure support; high-dose steroids do not help, and the prognosis is the worst of the cord syndromes.
Sources
Frequently Asked Questions
What is lost and what is spared in anterior cord syndrome?
Below the lesion, both sides lose voluntary strength (corticospinal tracts) and pain and temperature sensation (spinothalamic tracts), and damage to the anterior horns gives lower motor neuron signs at the level of the lesion. Vibration, joint position sense, fine touch and two-point discrimination are spared because the dorsal columns lie in the posterior third of the cord. Bladder, bowel and blood pressure control are often affected as well.
Why does anterior spinal artery infarction spare vibration and proprioception?
The anterior spinal artery supplies only the anterior two-thirds of the cord: the anterior and lateral horns and the corticospinal and spinothalamic tracts. The dorsal columns, which carry vibration, proprioception and fine touch, sit in the posterior third and are supplied by the two posterior spinal arteries, so an anterior spinal artery infarct leaves them working.
Why can aortic surgery cause paraplegia?
The anterior spinal artery depends on radiculomedullary feeders that branch off the aorta, and the largest, the artery of Adamkiewicz, usually arises from a left intercostal artery between T9 and T12. Prolonged cross-clamping, hypotension, raised spinal cord pressure or a dissection can cut flow through these feeders and infarct the anterior cord. Raising the mean arterial pressure and draining cerebrospinal fluid through a lumbar drain are used to protect the cord during high-risk repairs.
How is anterior cord syndrome different from Brown-Séquard and central cord syndrome?
Anterior cord syndrome is bilateral: strength, pain and temperature are lost on both sides below the lesion while vibration and position sense are preserved. Brown-Séquard syndrome is a hemisection, with weakness and loss of vibration and position sense on the same side and pain and temperature loss on the opposite side. Central cord syndrome follows a hyperextension injury in a narrowed cervical canal and weakens the arms more than the legs.
What is the prognosis of anterior cord syndrome?
It has the poorest functional outcome of the spinal cord syndromes. Only about 10–20% of patients regain functional motor recovery, and reported mortality is 9–23%. The severity of the initial deficit is the most reliable predictor of recovery, and complete paralysis at onset or no improvement within the first 24 hours points to a worse outcome.