|Central Cord Syndrome | American Association of Neurological Surgeons|
Central cord syndrome (CCS) is an incomplete traumatic injury to the cervical spine resulting in more extensive motor weakness in the upper extremities than the lower extremities. The mechanism of injury occurs from a forceful hyperextension neck injury with prior existence of degenerative ligamentous and osteophytic spinal column disease. There is usually no obvious associated spinal column fracture or evidence of spinal instability.
Mechanism and Causes of Injury
CCS typically occurs in patients with hyperextension injuries where the spinal cord is squeezed or pinched between pre-existing anterior cervical spondylotic bone spurs and a thickened posterior intraspinal canal ligament, the ligamentum flavum. The ligamentum flavum is a strong ligament that connects the laminae of the vertebrae.
It serves to protect the neural elements and the spinal cord and stabilize the spine so that excessive motion between the vertebral bodies does not occur. Pictured left is a sagittal, or lateral cervical MRI, showing bone spurs (degeneratove spondylotic bone spurs) narrowing the cervical spinal canal and compressing the cervical spinal cord in a CCS patient.
The injury occurs as a result of anterior and posterior compression of the spinal cord, leading to edema, hemorrhage or ischemia to the central portion of the spinal cord. The site of most injuries is in the mid-to-lower cervical cord.
Due to the anatomical lamination of the corticospinal tract with the arm fibers medially and the leg fibers laterally, the arms are affected more so than the legs, resulting in a disproportionate motor impairment (see the illustration below). Typical patients with CCS regain use of their legs and can often walk, but cannot effectively use their arms and hands.
Symptoms and Incidence
Patients are typically left with more profound motor weakness of the upper extremities and less severe weakness of the lower extremities. A varying degree of sensory loss below the level of the lesion and bladder symptoms (urinary retention) may also occur.
This syndrome more commonly affects patients age 50 and older who have sustained a cervical hyperextension injury. CCS affects males more frequently than females.
It is anticipated that the incidence and prevalence of CCS will increase proportionately with an aging population that tends to remain physically exertive much later in life than in past generations.
CCS may occur in patients of any age and is seen in athletes who present with not only hyperextension injuries to their neck but associated ruptured disc(s) with anterior cord compression.
Evaluation of the patient includes a complete history, thorough general and neurological examinations, cervical magnetic resonance imaging (MRI), computed tomography scan (CT) and plain cervical spine X-rays including supervised flexion and extension views.
- MRI: A diagnostic test that produces three-dimensional images of body structures using powerful magnets and computer technology; can show direct evidence of spinal cord impingement from bone, disc or hematoma. MRI can also show ligamentous and soft tissue injuries that might be missed by other imaging tests.
- CT or CAT scan: A computer enhanced X-ray imaging device that shows boney detail superior to any other imaging device. It also shows shape and size of the spinal canal, its contents and the structures around it. It is usually performed prior to MRI scanning. Combined with MRI scans it provides a more comprehensive diagnostic data set for treatment decision making.
- X-ray: Application of radiation to produce a film or picture of a part of the body can show the structure of the vertebrae and the outline of the joints. X-rays of the spine delineate fractures and dislocations, as well as the degree and extent of spondylitic changes. Flexion/extension views assist in evaluation of ligamentous stability. Both the MRI and CAT scan images are static images. Flexion / extension plain X-rays can provide a simple means of determining dynamic stability or instability of the spinal column. These views can help determine whether or not a cervical collar or stabilizing cervical spine surgery is necessary or not.
Acute surgical intervention is not usually necessary unless there is significant cord compression. Prior to the CT/MRI era, surgical intervention was thought to be more harmful because of the risk of injuring a swollen cervical cord and worsening the deficit.
However, with advanced imaging technology, patients with compression of the spinal cord secondary to traumatic herniated discs and other structurally compressive lesions can be quickly diagnosed and surgically decompressed. In cases with anterior bony ridges and spinal canal narrowing secondary to ligamentous thickening and or stenosis, acute surgery is usually not performed until the patient has made significant recovery that has stabilized clinically.
Reassessment at that time may lead to surgery depending on the underlying cause. If there is a surgically treatable lesion with significant residual motor weakness after a period of recovery, or if there if new neurological deterioration is observed, then surgical intervention may be considered. Additional pre-surgical re-evaluation with pre-surgical CAT scan and/or MRI scan will usually be necessary beforehand.
Observed neurological improvement is the most compelling reason not to proceed with surgical treatment in favor of non-surgical management of CCS. Nonsurgical treatment consists of immobilization of the neck with a rigid cervical collar, steroids unless contraindicated and rehabilitation with physical and occupational therapy.
Many patients with CCS make spontaneous recovery of motor function while others experience considerable recovery in the first six weeks post injury.
If the underlying cause is edema, recovery may occur relatively soon after an initial phase of motor paralysis or paresis. Leg function usually returns first, followed by bladder control and then arm function. Hand movement and finger dexterity improves last. If the central lesion is caused by hemorrhage or ischemia, then recovery is less likely and the prognosis is more devastating.
The prognosis for CCS in younger patients is more favorable than older patients. Within a short time, a majority of younger patients recover and regain the ability to ambulate and perform daily living activities. However, in elderly patients the prognosis is not as favorable, with or without surgical intervention.
Journal of Neurosurgery: Spine
July 2002 / Vol. 97 / No. 1 / Pages 25-32
Traumatic central cord syndrome: results of surgical management
Illustration Credit: Bernard Robinson, MD, FAANS
The AANS does not endorse any treatments, procedures, products or physicians referenced in these patient fact sheets. This information is provided as an educational service and is not intended to serve as medical advice. Anyone seeking specific neurosurgical advice or assistance should consult his or her neurosurgeon, or locate one in your area through the AANS’ Find a Board-certified Neurosurgeon”online tool.
Central Cord Syndrome
The Central Cord Syndrome (CCS) was initially described by Schneider et al (1954). It is the most common type of incomplete spinal cord injury (Shaw 1995).
The American Spinal Injury Association (ASIA) define this syndrome as: 'a lesion, occurring almost exclusively in the cervical region, that produces sacral sparing and greater weakness in the upper limbs than in the lower limbs' (ASIA 1994).
The acute central cord spinal syndrome is commonly stated to arise from an injury which affects primarily the central part of the spinal cord and is frequently haemorrhagic (Morse 1982, Maroon et al 1991). However, Quencer et al (1992) found no evidence of haemorrhage into the substance of the cord and concluded that central cord syndrome was not primarily a grey matter lesion but that the neurological disability, at least in part, was due to damage to the white matter tracts. They suggested that the most common mechanism of injury may be direct compression of the cord in an already narrowed spinal canal. This would explain the predominance of axonal injury in the white matter of the lateral columns.
Roth et al (1990), in a study of 81 traumatic central cord syndrome patients, found that more than 90% of patients had neurological recovery of both upper and lower limbs, neurological recovery being defined as an increase in strength of one muscle grade. This recovery generally occurred in the order of lower limbs, bladder function, upper limbs and finally the hands. The extent of recovery is greatest in younger patients, who have a better prognosis for recovery in activities of daily living and in becoming functional walkers (Penrod et al1990, Roth et aI1990).
It is possible that arteriosclerosis may compromise blood supply to the cord in older subjects and that the initial damage may be more severe due to cervical spondylosis (Scher 1995).
Progressive neurological deterioration, characterized by spasticity, has been identified in older patients with central cord syndrome, whereby patients who were initially functionally ambulant became wheelchair-dependent (Maroon et al1991).
This type of lesion usually affects older people with cervical spondylosis who sustain hyperextension injuries in falls or in motor vehicle accidents. Older men, over the age of 40, with predisposing narrow cervical canals and osteoarthritis of the cervical spine have also been identified to be at risk of central cord syndrome following body surfing accidents (Scher 1995).
However, central cord syndrome may occur in people of any age and be associated with other aetiologies, injury mechanisms or predisposing factors. (Roth et aI1990). In older age groups, fracture of the cervical spine is less common than in younger subjects (Penrod et al 1990), and in the absence of a fracture, this lesion may be difficult to diagnose.
Computerized tomography or magnetic resonance imaging will provide confirmation and additional information.
Clinical Picture of Central cord syndrome
The general clinical picture is of:
- disproportionately more motor impairment of the upper than lower extremities
- bladder dysfunction, often with urinary retention
- varying degrees of sensory loss. Spasticity, shoulder pain, hand oedema and dysaesthetic pain are noted complications (Roth et al1990, Maroon et al1991).
Motor deficit. At the level of the lesion, there will be damage to the anterior horn cells resulting in a flaccid paralysis of those muscles supplied from this level (Scher 1995). For example, a lesion occurring at the C5 level will give rise to flaccidity, most notably of deltoid and biceps. The gradual wasting of these muscles gives rise to the fairly typical picture of the central cord lesion.
Hand dysfunction is an outstanding feature of cervical myelopathies (Nakajima & Hirayama 1995) but this is variable in central cord syndrome. The hands may be relatively uninvolved, but without the background of proximal stability, selective upper limb function cannot be achieved.
In other cases, the hands may be paralysed. The predominant loss of muscle function in distal muscles may be explained by axonal damage. Disruption of axons, particularly in the lateral columns in the region occupied by the corticospinal tracts, reflects their importance for hand and finger function (Quencer et al1992).
Paralysis of the hands may lead to the development of stiff and painful joints or cervical hand syndrome and swelling may occur compounded by the effect of gravity.
The development of contractures and / or painful joints of the upper limbs will remain a very real danger throughout all stages of rehabilitation. Roth et al (1990) found that the number of patients with shoulder pain and dysaesthetic pain increased over time to be greater at discharge than during rehabilitation.
Many patients with CCS will achieve an independent gait with or without the use of walking aids. In a sense, these patients differ from virtually all other patients with neurological disability, in that use of the arms in gait re-education is recommended. All too often, these patients walk independently before they have significant recovery of the upper limbs. The importance of the use of the arms while learning how to walk again cannot be overemphasized. Once the patient is able to walk independently, there may be little if any opportunity for the arms to be involved in function.
Depending on the severity of the lesion, the patient will demonstrate some degree of motor deficit in the trunk and lower limbs which is invariably characterized by the presence of spasticity.
Sensory deficit. This is extremely variable, ranging from severe sensory loss to virtually no impairment.
The disability of these patients is often underestimated. Those who are ambulant may appear less disabled, and yet, without the use of their upper limbs they are invariably more impaired than the chair bound paraplegic.
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