Anterior Cord Syndrome

Original Editor - Rochelle Dsouza Top Contributors - Rochelle Dsouza

Introduction[edit | edit source]

Anterior Cord Syndrome

Anterior cord syndrome is referred to as Anterior spinal artery syndrome (ASAS) or ventral cord syndrome (VCS)[1]. ASAS is an incomplete spinal cord injury (SCI) that is often related to flexion injuries of the cervical region that result in infarction of the anterior two thirds of the cord and/or its vascular supply from the anterior spinal artery[2]. They present with impairments in the pain and temperature sensations while the vibratory and proprioceptive sensations are preserved. Motor deficits are observable both at and below the level of injury.

Clinically Relevant Anatomy[edit | edit source]

ASAS is caused by ischemia within the anterior spinal artery (ASA), which supplies blood to the anterior 2/3rd of the spinal cord. The anterior spinal artery, with a few radicular artery contributions, supplies blood to the bilateral anterior and lateral horns of the spinal cord, as well as the bilateral spinothalamic tracts and corticospinal tracts. For better understanding of the clinical presentation and pathological process, it is necessary to have know about somatotopic arrangement of tracts in the spinal cord. The anterior horns and corticospinal tracts control the somatic motor system from the neck to the feet. The lateral horns span T1-L2 of the spinal cord and sheathe the neuronal cell bodies of the sympathetic nervous system. The spinothalamic tracts carry pain and temperature sensory information.[3]

Aetiology[edit | edit source]

  • Iatrogenic (most common): Cross-clamping of the aorta during thoracic and abdominal aortic aneurysm repair.[4]
  • Direct injury/trauma[2]:
    • Crush injury
    • Burst fracture
    • Gunshot/knife injury
  • Indirect injury: Occlusion/hypo perfusion of the anterior spinal artery (ASA) and ischemia to the area the ASA supplies[3][4]:
    • Severe hypotension
    • Atherothrombotic disease
    • Vasculitis

Pathological process[edit | edit source]

The ventral two-thirds of the cord contains essential tracts for the proper functioning of the central nervous system (CNS); injury impairs the actions of these tracts.  Damage to the efferent corticospinal tract results in impairment of motor function whereas damage to the spinocerebellar and spinothalamic tracts cause sensory deficits.

Mechanisms of injury[edit | edit source]

  • Occlusion of the Anterior Spinal Artery results in:
    • Disruption of the blood flow through spinal artery causes → spinal cord tissue ischemia and infarction from the level of disruption of flow leading to →Infarction of the corticospinal and spinothalamic pathways[4]
  • Vertebral/burst fractures :
    • Resulting in forces coming from above or below the vertebral body (depending on the injury)
    • Nucleus pulposus of the intervertebral disc is forced into the vertebral body → shatters (burst) fracture → spinal cord injury related to the force and direction of the traumatic event.

Physiological Sequelae[edit | edit source]

The occlusion/hypo-perfusion of the artery results in:

  • Ischemic and reperfusion injuries→causes damage to the spinal cord by activation of the glial cells, disruption of the blood-spinal cord barrier (BSCB) disruption, tissue edema, and influx of neutrophils.
  • Additional neuronal death results from the associated inflammatory response, oxidative stress, and activation of apoptosis pathways, which, together, are also termed ‘reperfusion injury'[3].

The mechanical trauma to the spinal cord occurs in injury during two phases:

  • The initial direct trauma results in→ acute compression and disruption of vasculature and axons.
  • In the second phase, a cascade of events triggers as a result of the injury, including haemorrhage, edema, inflammation, demyelination, pathologic changes in the neurons and oligodendroglia, as well as microglial and astrocyte activation in an early stage.
  • A later stage consists of scar formation, Wallerian degeneration, development of cysts and syrinx, and schwannosis [1][3].

Clinical Presentation[edit | edit source]

The clinical presentation of ASA syndrome differs with the level of ischemia. There are varying degrees of muscle weakness and dissociated sensory loss: pain sensation is decreased or absent while proprioception is relatively or completely spared. Due to the anatomical proximity of the pyramidal and spinothalamic tracts in the cord, the loss of motor power usually mirrors that of pain. Other signs of the syndrome will depend on the location where the cord was injured. Broadly, there is a chance for autonomic dysreflexia , movement and sexual impairments, neuropathic pain, and bladder and bowel dysfunction[1].

Motor[edit | edit source]

  • Below the spinal cord level of injury, there is bilateral motor dysfunction since both halves of the anterior spinal cord receive vascular supply from one midline anterior spinal artery. Rare cases of ASA have been reported with unilateral symptomatology this could be due to collateralization from one posterior spinal artery or occlusion of unilateral sulcal arteries.
  • The clinical onset of ASA is abrupt, with pain. Depending upon the area of the infarct, the severity of dysfunction varies from flaccid paraplegia or tetraplegia below the lesion.
  • Early motor deficits due to spinal shock consist of flaccidity with absent reflexes, followed by a gradual return of the reflexes and increased tone or spasticity. Typically, the first presenting symptom is acute back pain, the area mostly corresponds with the level of the injury in the spinal cord[4].

Sensory[edit | edit source]

  • Alterations in temperature and pain sensation present two to three dermatomal segments below the level of the injury since the spinothalamic tract ascends at least two to three segments prior to decussating at the anterior commissure[5].
  • Vibration, fine touch, and proprioception sensory modalities are spared, as these are carried by the dorsal columns which are supplied by the two posterior spinal arteries and located in the posterior one-third of the cord[1].

Diagnostic Procedures[edit | edit source]

ASAS is generally suspected with a detailed history and the physical findings. Neuro-imaging studies can rule out and confirm the diagnosis of ASAS.[3]

Imaging studies[edit | edit source]

  • (MR) imaging is the modality of choice for visual assessment of spinal cord ischemia, which should include axial and sagittal diffusion-weighted MR imaging examinations. These diffusion weighted images help distinguish between inflammation and ischemia.[3]
  • Characteristic MR imaging features of acute spinal cord ischemia include thin "pencil-like" hyper-intensities on sagittal T2-weighted images, with or without cord enlargement. [4]
  • While, axial MR images show a two central T2-hyperintense signals on either side of the anterior horn, appearing as two bright dots resembling "owls eyes"[3][4].

Laboratory tests[edit | edit source]

  1. Lumbar puncture with cerebrospinal fluid (CSF) analysis - assists to rule out multiple sclerosis, infection, or inflammatory disease.
  2. Echocardiogram- rule out sources of embolism, such as infective endocarditis.
  3. Blood and urine laboratory studies- infection (borreliosis, Lyme disease, syphilis, human immunodeficiency virus, herpes virus), hypercoagulable disorders, atherosclerotic disease, inflammatory disorders, rheumatological diseases, or drug-related.[3]

Outcome Measures[edit | edit source]

While assessing a patient with SCI, it is important to determine the extent of neurologic injury (ie, incomplete versus complete). Incomplete injuries have a higher chance for neurologic recovery.

The neurological level and determining whether it's complete-incomplete spinal cord injury level can be done with the help of American Spinal Cord Injury (AISA) Impairment Scale [AIS].

A detailed history alongside clinical neurologic assessment and recording influences treatment decisions and provides prognostic information. For further details about outcome tools in SCI, please look into these pages:

Management/Interventions[edit | edit source]

Management is mainly supportive and follows guidelines for acute traumatic spinal cord injury, cerebral ischemia, atherosclerotic vascular disease. Treatment is mostly limited to improvement of symptoms and prevention of future complications. Limitations in mobility and activities of daily living, bladder, bowel and sexual dysfunction including impairments during hospitalization and after discharge should be addressed. Post discharge, patients should be accessible and able to safely use the required adaptive equipment so that they can enhance their functional independence. Particularly, the patient's psychosocial function and participation to achieve increased independence, quality of life, and ultimately a better prognosis should taken into consideration[1].

Non-surgical[edit | edit source]

The primary focus is the underlying cause, which includes

  1. Management of Anticoagulation
  2. Antiplatelet and Thromboprophylaxis
  3. Fever and Glycemic control

It is also important to maintain blood pressure support and protect the airways. If the patient is hypotensive, then blood pressure must be raised by using phenylephrine, norepinephrine and high-dose dopamine,if the patient is hypotensive. While, for blood pressure reduction, medications such labetalol, esmolol, and nicardipine must be used.

Tetraplegia and paraplegia are amongst the most deleterious consequences of anterior cord syndrome. These movement impairments result in a significant medical, social, and financial loss to both the individual and society. Patients must receive rehabilitation focused on improving independence and quality of life all while preventing secondary complications of spinal cord injury.

For physiotherapy management, please look into these pages:

Prognosis[edit | edit source]

The prognosis for ASAS is multifactorial. Various factors have correlations with better or worse prognosis. [1][3][4]

  • Primarily the etiology is an important tool to determine the prognosis: aortic dissection/rupture and high cervical lesions have a greater risk of death.
  • Symptom severity at initial presentation: Severe initial presenting symptoms have the poor outcomes.
  • Lack of improvement in the initial 24 hours have the poor outcomes.
  • Female sex and old age correlates with poorer outcomes.

Differential Diagnosis[edit | edit source]

  • Central cord syndrome
  • Dorsal cord syndrome
  • Brown-Séquard syndrome
  • Conus medullaris syndrome
  • Cauda equina syndrome
  • Transverse myelitis
  • Guillain-Barré syndrome
  • Multiple sclerosis
  • Spinal epidural abscess
  • Epidural hematoma

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Santana JA, Dalal K. Ventral Cord Syndrome.In: StatPearls [Internet]. 2021 Jan.
  2. 2.0 2.1 Deutsch JE, O’Sullivan SB. Stroke. In: O'Sullivan SB, Schmitz TJ, Fulk G, editors.Physical Rehabilitation.7th edition. Philadelphia: FA Davis; 2019. p. 480.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Sandoval JI, De Jesus O. Anterior Spinal Artery Syndrome. In: StatPearls [Internet]. 2021 Jan.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Pearl NA, Dubensky L. Anterior Cord Syndrome. In: StatPearls [Internet].2021 Jan.
  5. Klakeel M, Thompson J, Srinivasan R, McDonald F. Anterior spinal cord syndrome of unknown etiology. Proc (Bayl Univ Med Cent). 2015;28(1):85-7.