Incomplete spinal cord syndromes

Last updated: January 3, 2023

Summary

Incomplete spinal cord syndromes are caused by lesions of the ascending or descending spinal tracts that result from trauma, spinal compression, or occlusion of spinal arteries. Central cord syndrome, anterior cord syndrome, posterior cord syndrome, and Brown-Séquard syndrome are the most common types of incomplete spinal cord syndromes. In contrast to a complete spinal cord injury, lesions only affect part of the cord, and patients present with a dissociated sensory loss. A spine MRI is the diagnostic modality of choice to determine the etiology, level, and extent of the lesion. Treatment depends on the underlying etiology. In some cases, surgery may be necessary to treat the underlying cause and to improve the patient's outcome. Spinal compression is a medical emergency and requires urgent treatment with steroids and decompressive surgery.

Overview

Basic neuroanatomy and function

Pyramidal tracts: lateral corticospinal tract and anterior corticospinal tract
- Descending tracts originate in the cerebral cortex and extend to the alpha motor neuron in the ventral horn of the spinal cord.
- About 90% of pyramidal neurons decussate as they pass through the medulla and descend further as the lateral corticospinal tract.
- The remaining 10% continue as the anterior corticospinal tract and decussate at the segmental level.
- Function: controls motor function
Posterior column: posterior funiculus consisting of gracile and cuneate fasciculi
- Decussation at the medulla oblongata
- Remains ipsilateral in the spinal cord
- Function
  - Conveys epicritic sensation: fine touch, vibration, pressure
  - Conveys proprioception: awareness of position in relation to one's body in space
Spinothalamic tract: anterior spinothalamic tract and lateral spinothalamic tract
- Decussation only at segmental level or shortly above
- Function: conveys protopathic sensation (contralateral temperature, pain stimuli, and crude touch)

Cross section of the spinal cord Dermatome map

Overview of incomplete spinal cord syndromes

Types of incomplete spinal cord syndromes
Syndrome	Affected spinal tracts	Etiology ^[1]^[2]	Clinical features*
Central cord syndrome (most common)	Bilateral central corticospinal tracts and lateral spinothalamic tracts	Hyperextension injury (e.g., car crash) associated with chronic cervical spondylosis Syringomyelia Spinal cord compression	Bilateral paresis: upper > lower extremities
Anterior cord syndrome	Corticospinal tracts and spinothalamic tracts	Trauma (e.g., penetrating injury, burst fracture of vertebra) Occlusion of anterior spinal artery	Bilateral motor paralysis, loss of pain and temperature sensation, and autonomic dysfunction below the level of the lesion
Posterior cord syndrome	Posterior columns	Trauma (e.g., penetrating injury) Occlusion of the posterior spinal artery Multiple sclerosis	Bilateral loss of proprioception, vibration, and touch sensation below the level of the lesion ^[3]
Brown-Séquard syndrome (hemisection syndrome)	Hemisection of the cord	Trauma (e.g., penetrating injury) Spinal cord compression	Ipsilateral Loss of proprioception, vibration, and tactile discrimination below the level of the lesion Segmental flaccid paresis at the level of the lesion Spastic paralysis below the level of the lesion, and ipsilateral Babinski sign Horner syndrome in lesions above T1 Contralateral: loss of pain and temperature sensation one or two levels below the lesion
*All syndromes present with dissociated sensory loss: a pattern of selective sensory loss (“dissociation of modalities”), which suggests a focal lesion of a single tract within the spinal cord (or brainstem). ^[4]

Spinal cord lesions Syringomyelia with lesion at C5-T2 Anterior spinal artery syndrome at T8 level Arterial supply of a spinal segment Brown-Séquard syndrome

Overview of incomplete spinal cord lesions

Spinal cord lesions
	Pathophysiology	Affected spinal tracts	Clinical features
Syringomyelia	Obstructed central canal of spinal cord → impaired CSF flow → dilated fluid-filled central canal of the spinal cord (syrinx) Usually cervical spine, the thoracic or lumbar spine are less commonly affected	Anterior white commissure of spinothalamic tract	Symmetrical loss of: Pain and temperature Sensation Bilateral, symmetrical dysesthetic pain Affects neck, shoulders, and arms (cape-like distribution) Other: Horner syndrome
Spinal muscular atrophy	Congenital motor neuron disease: autosomal recessive SMN1 mutation → defective snRNP assembly	Lower motor neurons (anterior horns of the spinal cord)	Symmetrical muscle weakness and hypotonia (flaccid paralysis) Hyporeflexia Tongue fasciculations
Amyotrophic lateral sclerosis	Gene mutation (e.g., defect in superoxide dismutase 1) → different mechanisms of cell damage (e.g., protein aggregation, mitochondrial dysfunction) → both upper and lower motor neuron degeneration	Upper motor neuron (precentral gyrus, prefrontal cortex, corticobulbar tract, and corticospinal tract) Lower motor neuron (anterior horns of the spinal cord and brainstem)	LMN damage Bilateral, asymmetrical flaccid muscle weakness, atrophy, and fasciculations Hyporeflexia UMN damage Bilateral, asymmetrical spastic muscle weakness and clonus Hyperreflexia Bulbar symptoms (e.g., dysarthria, dysphagia)
Multiple sclerosis	Autoimmune inflammation (via activation of autoreactive T-cells), demyelination, and axonal degeneration	White matter of spinal cord (cervical region is mostly affected) Pyramidal tract Dorsal columns Can also involve other structures (e.g., cerebrum, cranial nerves, cerebellum)	Asymmetric lesions UMN damage: muscle weakness, spasticity, hyperreflexia, positive Babinski sign Loss of vibration and fine-touch sensation (numbness, paresthesias) Other Optic neuritis, internuclear ophthalmoplegia Charcot neurological triad (scanning speech, nystagmus, intention tremors) Autonomic dysfunction (e.g., bladder incontinence) Cranial nerve palsies (e.g., facial nerve palsy)
Poliomyelitis	Poliovirus enters the bloodstream → invasion and inflammation of the brain and spinal cord	Gray matter of the spinal cord (particularly, the anterior horns)	Ascending, asymmetric flaccid paralysis: most commonly affects lower limbs (proximal > distal muscles) Muscle atrophy, hypotonia, fasciculations Hyporeflexia
Tabes dorsalis	Late sequelae of infection with Treponema pallidum → demyelination of the spinal cord	Dorsal columns Dorsal root ganglia	Impaired proprioception: progressive sensory broad-based ataxia (positive Romberg test) Absent deep tendon reflexes Loss of sensation (mainly in the lower extremities), dysesthesias Sharp, shooting pain in the legs and the abdomen Other: Charcot joint Argyll Robertson pupil
Vitamin B₁₂ deficiency	Dysfunctional methionine synthase → ↓ methionine → neuropathy Dysfunctional methylmalonyl CoA mutase → ↑ methylmalonyl CoA and its precursor propionyl CoA → propionyl CoA replaces acetyl CoA in neuronal membranes → demyelination	Dorsal columns Lateral corticospinal tracts Spinocerebellar tracts	Symmetrical Peripheral neuropathy (especially in the lower extremities) Paresthesia Loss of vibratory sensation and tactile sensation UMN damage: spastic paresis, hyperreflexia Impaired proprioception Spinal ataxia Autonomic dysfunction (e.g., incontinence) Other Signs of anemia Glossitis Jaundice Optic neuropathy
Cauda equina syndrome	Damage (e.g., trauma) to or compression (e.g., disk herniation) of the cauda equina with nerve fibers of L2 and below	Cauda equina	Unilateral, asymmetric: LMN damage: flaccid muscle weakness and muscle atrophy of the leg Severe radicular pain Hyporeflexia Absent knee jerk reflex and ankle jerk reflex Saddle anesthesia Loss of anal and bladder sphincter control
Conus medullaris syndrome	Damage (e.g., trauma) to the spinal cord segments T12–L2	Conus medullaris	Sudden, bilateral Symmetric, flaccid muscle weakness of lower limbs, possibly fasciculations Lower back pain Hyperreflexia Achilles reflex may be absent Symmetric, bilateral perianal numbness Sensory dissociation Bladder and fecal incontinence

Spinal cord lesions Spinal epidural hematoma

Central cord syndrome

Definition: injury to the central region of the spinal cord (central corticospinal tracts and decussating fibers of the lateral spinothalamic tract)
Epidemiology
- Most common type of incomplete cord syndrome
- Common in the elderly with preexisting degenerative changes in the cervical spine
Etiology
- Syringomyelia
- Degenerative spine disease
- Cervical spondylosis
- Traumatic disk herniation
- Various hyperextension injuries (e.g., whiplash injury in a person with long-standing cervical spondylosis)
Clinical features
- Bilateral motor paresis (upper > lower extremities; distally > proximally)
- Variable sensory impairment
  - Burning pain in the arms
  - Loss of pain and temperature in the arms
- Sacral sparing
Diagnostics: CT and/or MRI to determine location, cause, and extent of neurological damage
Treatment: See “Management of spinal cord injuries”.
Prognosis: relatively good prognosis

Syringomyelia with lesion at C5-T2

References:^[5]

Anterior cord syndrome

Definition

Damage to the anterior two-thirds of the spinal cord, usually as a result of reduced blood flow or occlusion to the anterior spinal artery (ASA) → anterior spinal artery syndrome (∼ 95% of cases) ^[6]

Etiology ^[7]

Systemic hypoperfusion (e.g., heart failure)
Iatrogenic (e.g., during aortic surgery, spinal angiography, or spinal anesthesia)
- Aortic repairs may result in lesions of the artery of Adamkiewicz: a thoracic radicular artery (branch of the intercostal vasculature) that supplies the lower two-thirds of the spinal cord
- Mid-thoracic ASA territory is a watershed area because the artery of Adamkiewicz is the only major vessel that supplies the spinal cord below the spinal level T8/T9. ^[8]
Arteriosclerosis, vasculitis (e.g., associated with diabetes)
Thrombosis, embolic occlusion
Aortic dissection, aneurysm
Severe hypotension (e.g., following hemorrhage)
Trauma (e.g., penetrating injury, burst fracture, hyperflexion injury with vertebral instability which is common in young athletes) ^[7]
Pathological compression (e.g., tumors, cervical spondylosis)

Clinical features

Acute (within hours)
- Back or chest pain ^[9]
- Spinal shock
  - Bilateral loss of temperature and pain sensation below the level of the lesion due to damage of the spinothalamic tracts
  - Lower motor neuron deficits (flaccid paralysis) at the level of and below the lesion
  - Autonomic dysfunction (bladder, bowel, and sexual dysfunction, orthostatic hypotension)
  - Absent bulbocavernosus reflex
Late (after days or weeks)
- Continued sensory and autonomic dysfunction
- Upper motor dysfunction (spastic paraparesis or quadriparesis) below the level of the lesion due to damage to the corticospinal tracts
- Lower motor neuron deficits (flaccid paralysis) at the level of the lesion due to damage to the anterior horn
- Hyperreflexia

Vibration and proprioception are typically spared because of an intact dorsal column.

Anterior spinal artery syndrome at T8 level

Diagnostics

Spinal MRI (best confirmatory test)
- Excludes soft-tissue lesions (e.g., tumors, hematomas) and bone lesions
- Detects spinal cord parenchyma abnormalities (e.g., infarction) in the anterior part of the spinal cord: Dorsal columns and Lissauer tract, which are located in the posterior part of the spinal cord, are intact.

Treatment

Treat the underlying condition (if possible)
- Consider surgical repair
- Aspirin for thrombotic occlusion
- Penicillin for syphilis
- Surgery for vascular abnormalities (e.g., aortic dissection) or tumors
- Control chronic comorbidities (e.g. diabetes mellitus)
See “Management of spinal cord injuries”.

Prognosis

10–15% functional recovery
If no recovery is evident and progressive after 24 hours, the prognosis is poor.

Posterior cord syndrome

Definition: injury of the posterior spinal cord affecting the posterior column (fine touch, vibration, pressure, and proprioception)
Epidemiology: very rare
Etiology ^[3]
- Occlusion of the posterior spinal artery
- Multiple sclerosis
- Tabes dorsalis
- Subacute combined degeneration
- Friedreich ataxia
Clinical features: bilateral loss of vibration, fine touch, and proprioceptive sensation below the lesion ^[3]
Diagnostics
- MRI showing infarction of the dorsal columns in the case of posterior spinal artery occlusion
- VDRL or RPR if syphilis suspected
Treatment: See “Management of spinal cord injuries”.
Prognosis: Patients show functional gain with rehabilitation. ^[10]

Arterial supply of a spinal segment

Brown-Séquard syndrome

Definition: hemisection of the spinal cord (often in the cervical cord)
Etiology
- Unilateral compression commonly through trauma (e.g., often penetrating injuries, or crush injury)
- Less commonly: disk herniation, spinal epidural hematoma, spinal epidural abscess (rare) or tumor, multiple sclerosis, complication of decompression sickness ^[11]
Clinical features
- Ipsilateral
  - Loss of all sensations at the level of the lesion
  - Loss of proprioception, vibration, and tactile (fine touch) discrimination below the level of the lesion due to an interrupted posterior column
  - Segmental flaccid paresis at the level of the lesion due to the affection of lower motor neurons at the level of the lesion
  - Spastic paralysis below the level of the lesion
  - Ipsilateral Babinski sign; due to the affection of upper motor neuron axons in the lateral corticospinal tracts
  - In lesions above T1, Horner syndrome occurs due to damage to ipsilateral sympathetic fibers (the oculosympathetic pathway).
- Contralateral: loss of pain, temperature, and non-discriminative touch (crude touch) sensation one or two levels below lesion due to an interrupted spinothalamic tract
Diagnostics
- Clinical diagnosis
- Consider CT if trauma has occurred or an MRI if a tumor is suspected.
Treatment: See “Management of spinal cord injuries”.
Prognosis: poor ^[12]

Autonomic symptoms are generally absent in Brown-Séquard syndrome because of unilateral involvement of the descending autonomic fibers.

Brown-Séquard syndrome

References

Central Cord Syndrome. https://www.ninds.nih.gov/Disorders/All-Disorders/Central-Cord-Syndrome-Information-Page. Updated: March 27, 2019. Accessed: December 3, 2020.
Mohassel P, Wesselingh R, Katz Z, Mcarthur J, Gailloud P. Anterior spinal artery syndrome presenting as cervical myelopathy in a patient with subclavian steal syndrome. Neurol Clin Pract. 2013; 3 (4): p.358-360.doi: 10.1212/CPJ.0b013e318296f217 . | Open in Read by QxMD
Vargas MI, Gariani J, Sztajzel R et al.. Spinal cord ischemia: practical imaging tips, pearls, and pitfalls. AJNR Am J Neuroradiol. 2015; 36 (5): p.825-830.doi: 10.3174/ajnr.A4118 . | Open in Read by QxMD
Hoehmann CL, Hitscherich K, Cuoco JA. The Artery of Adamkiewicz: Vascular Anatomy, Clinical Significance and Surgical Considerations. Int J Cardiovasc Res. 2016; 5: p.6.doi: 10.4172/2324-8602.1000284 . | Open in Read by QxMD
Purves D, Augustine GJ, Fitzpatrick D, et al. Neuroscience. Sinauer Associates ; 2001
Spinal Cord Compression. http://www.merckmanuals.com/professional/neurologic-disorders/spinal-cord-disorders/spinal-cord-compression. Updated: October 1, 2016. Accessed: March 2, 2017.
Ribas ES, Schiff D. Spinal cord compression. Curr Treat Options Neurol. 2012; 14 (4): p.391-401.doi: 10.1007/s11940-012-0176-7 . | Open in Read by QxMD
Kunam VK, Velayudhan V, Chaudhry ZA, Bobinski M, Smoker WRK, Reede DL. Incomplete Cord Syndromes: Clinical and Imaging Review. RadioGraphics. 2018; 38 (4): p.1201-1222.doi: 10.1148/rg.2018170178 . | Open in Read by QxMD
Campbell WW. DeJong's The Neurologic Examination. Lippincott Williams & Wilkins ; 2012
Tamori Y, Takahashi T, Suwa H, et al. Cervical Epidural Abscess Presenting with Brown-Sequard Syndrome in a Patient with Type 2 Diabetes. Internal Medicine. 2010; 49 (14): p.1391-1393.doi: 10.2169/internalmedicine.49.3419 . | Open in Read by QxMD
Scivoletto G, Di donna V. Prediction of walking recovery after spinal cord injury. Brain Res Bull. 2009; 78 (1): p.43-51.doi: 10.1016/j.brainresbull.2008.06.002 . | Open in Read by QxMD
McKinley W, Santos K, Meade M, Brooke K. Incidence and Outcomes of Spinal Cord Injury Clinical Syndromes. J Spinal Cord Med. 2007; 30 (3): p.215-224.

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Incomplete spinal cord syndromes

Summary

Overview

Basic neuroanatomy and function

Overview of incomplete spinal cord syndromes

Overview of incomplete spinal cord lesions

Central cord syndrome

Anterior cord syndrome

Definition

Etiology [7]

Clinical features

Diagnostics

Treatment

Prognosis

Posterior cord syndrome

Brown-Séquard syndrome

References

3 free articles remaining

Etiology ^[7]