CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY 27

Due to the onion-skin or Déjerine pattern oftopographic representation, a perioral distribu-tion of sensory loss denotes a lesion in the lowermedulla and upper cervical cord, whereas amore peripheral facial distribution of sensoryloss involving the forehead, ear, and chin denotesa lesion in the cord at C3-4. Cervicomedullaryinjuries often mimic the central cord syndromebecause of a greater weakness in the arm thanthe leg.

Acute Central Cord SyndromeSchneider21,22 described the acute central cer-

vical cord injury syndrome characterized by adisproportionally greater loss of motor power inthe upper extremities than the lower extremitieswith varying degrees of sensory loss. He hypoth-esized that acute compression was an etiologicalfactor in many cases such as cord compressionbetween bony bars or spurs anteriorly and in-folded ligamenta flava posteriorly (Figure 3).Table 5 shows the similarities and differencesbetween the central cord syndrome and the syn-drome of cruciate paralysis. Clinically, it may bevery difficult to make this distinction. Fortu-nately, the combination of plain films, computed

Figure 3: Central cord syndrome. The drawingdepicts a case of cervical spondylosis withosteoarthritis of the cervical spine including ante-rior and posterior osteophytes and hypertrophy ofthe ligamentum flavum. Superimposed is an acutehyperextension injury that has caused rupture ofthe intervertebral disc and infolding of the liga-mentum flavum. The spinal cord is compressedanteriorly and posteriorly. The central portion ofthe cord shown in rough stippling sustained thegreatest damage. The damaged area includes themedial segments of the corticospinal tracts pre-sumed to subserve arm function. Reprinted withpermission from Tator.23

TABLE 5

CENTRAL CORD SYNDROME VS. CRUCIATE PARALYSIS WITH ARMS WEAKER THAN LEGS

Central Cord Syndrome Syndrome of Cruciate Paralysis

Site of Lesions Mid to lower Lower medulla and upper cervical cord,Anterior horn cells anterior aspectLateral corticospinal tract Corticospinal decussation caudal to the pyramids

(medial part)

Clinical Arms weaker than legs Arms weaker than legsManifestations Flaccid arms acutely Flaccid arms acutely

Legs normal or variably weak Legs normal or variably weakLower motor neuron deficits Upper motor neuron deficits in upper limbs develop

in upper limbs persist ± Trigeminal sensory deficit (onion skin, spinal tract of 5th cranial nerve)

± Cranial nerve dysfunction (9th, 10th, or 11th cranial nerve)

Prognosis for Variable Usually goodNeurological Recovery

CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION28

tomography (CT), and magnetic resonanceimaging (MRI) can usually accurately localizethe lesion to either the mid to lower cervicalspine in the central cord syndrome or to the cer-vicomedullary junction in the syndrome of cru-ciate paralysis.7

There is recent evidence that syndromescharacterized by greater weakness of the armthan leg are not based on previously enunciatedmechanisms such as the presumed differing lo-cations of the arm and leg fibers in the corti-cospinal tract.13 In contrast, the new explanationis derived from careful clinical-pathological-MRI correlations17 and of cases of SCI. The newunderstanding is based on the finding that thecorticospinal tract subserves mainly distal limbmusculature and, thus, the functional deficitwould be more pronounced in the hands whenthe tract is the primary site of damage.

It is of interest that Schneider initially ad-monished against operating on individuals withcentral cord syndrome because of their goodprognosis for spontaneous recovery. Indeed, insome instances, his patients showed very rapidspontaneous clinical recovery. Furthermore,Schneider reported deterioration following lam-inectomy in some patients. Although it is truethat a considerable number of patients with cen-tral cord syndrome make a substantial recoverywithout surgery, many remain with significantdeficits,3 especially with serious impairment ofthe hands due to a combination of severe weak-ness and severe proprioceptive loss. When there ispersistent compression, instability, or neurologi-cal deterioration, a patient with central cord syn-drome should be considered a surgical candidate.

Anterior Cord SyndromeAnterior cord syndrome was originally de-

scribed in the setting of acute cervical trauma bySchneider,20 who presented two patients with“immediate complete paralysis with hyperesthe-sia at the level of the lesion and an associatedsparing of touch and some vibration sense.”Both patients, one of which was a young footballplayer, had a ruptured disc (the football playeralso had bone fragments in the canal), and bothmade a substantial recovery following surgicalremoval of the intracanalicular space-occupyinglesions (Figure 4). This syndrome, in Schneider’s

view, was “a syndrome for which early operativeintervention is indicated.” The anterior aspect ofthe cord is damaged and, in severe cases, theremay only be sparing of the posterior columns(Figure 4). In less severe cases, there may besome retention of motor function due to sparingof some fibers in the lateral corticospinal tracts.

Posterior Cord SyndromePosterior cord syndrome is a rarely seen type

of incomplete SCI syndrome. Many researchers,including the author, have doubted its existence.It supposedly occurs after major destruction ofthe posterior aspect of the cord but with someresidual functioning spinal cord tissue anteriorly(Figure 5). Thus, clinically, the patient has re-tained spinothalamic function but lost move-ment and proprioception due to damage to theposterior half of the cord, including the corti-cospinal tracts and posterior columns.

Brown-Séquard SyndromeThe Brown-Séquard syndrome is caused by a

lesion of the lateral half of the spinal cord (Fig-

Figure 4: Anterior cord syndrome. A large discherniation is shown compressing the anterioraspect of the cord and resulting in damage (roughstippling) to the anterior and lateral white mattertracts and to the grey matter. The posteriorcolumns remain intact. Reprinted with permissionfrom Tator.23

CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY 29

ure 6) and is characterized by ipsilateral motorand proprioceptive loss and contralateral painand body temperature loss. The syndrome canbe associated with a variety of mechanisms ofinjury, but in the series of Braakman and Pen-ning4 was most often observed with hyperexten-sion injuries; also reported were cases with flex-ion injuries, locked facets, and compressionfractures.

The Brown-Séquard syndrome may be pres-ent at the onset of injury in some patients; inothers, it may become apparent only several daysafter injury as a gradual evolution from a bilat-eral incomplete injury. Hybrid combinations of Brown-Séquard and other incomplete syn-dromes may occur. For example, the author hasseen examples of central cord injuries that arequite asymmetric, with the more severely dam-aged side of the cord showing features of aBrown-Séquard syndrome. The Brown-Séquardsyndrome occurs most often following cervicalinjuries and less frequently in the thoracic cordand conus medullaris. In milder cases, there maybe no sphincter deficit.

Conus Medullaris SyndromeAlmost all of the lumbar cord segments are

opposite the T12 vertebral body, and almost all ofthe sacral cord segments are opposite the L1 ver-tebral body with the cord ending opposite theL1-2 disc space (Figure 7). Because injuries atT11-12 and T12-L1 are relatively common due tothe mobility of these segments compared withthe relatively immobile thoracic segments, in-juries to the conus medullaris are frequent. Theseinjuries usually produce a combination of lowermotor neuron deficits with initial flaccid paraly-sis of the legs and anal sphincter. This is followedin the chronic phase by a combination of somedegree of muscle atrophy and spasticity or reflexhyperactivity with, possibly, an extensor plantarresponse. The sensory picture may be variable,and in some cases the only evidence of incom-pleteness is retention of some perianal sensation,which is an example of sacral sparing. In themore severe conus lesions, bowel and bladderdeficits may be profound with the ultimate devel-opment of a low-pressure, high-capacity neuro-genic bladder.

Figure 5: Posterior cord syndrome. A laminar frac-ture is depicted with anterior displacement of thefractured bone and compression of the posterioraspect of the spinal cord. The damaged area of thecord (roughly stippled in the upper diagram)includes the posterior columns and the posteriorhalf of the lateral columns including the corti-cospinal tracts. Reprinted with permission fromTator.23

Figure 6: Brown-Séquard syndrome. A burst frac-ture is depicted, with posterior displacement ofbone fragments and disc, resulting in unilateralcompression and damage (rough stippling) to one-half of the spinal cord. Reprinted with permissionfrom Tator.23

CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION30

CAUDA EQUINA INJURIES

With the spinal cord normally terminatingopposite the L1-2 disc space (Figure 7), injuriesat this level or below involve the roots of thecauda equina, although injuries one or two levelsabove also involve the origins of some of theroots comprising the cauda equina. Clinically,these injuries may be complete (Grade A on thenew ASIA/IMSOP scale), whereas incompleteinjuries vary in severity and range from GradesB to D. Similar to SCI, the motor fibers tend tobe more susceptible to trauma so that incom-plete cases always have sensory preservation withor without some motor preservation. Cases withonly motor preservation are extremely rare. Thedegree of bowel and bladder deficits parallelsthose found with cord injury. It is believed thatcauda equina injuries have a much better prog-nosis for neurological recovery compared withSCI because the lower motor neuron inherentlyhas more resilience to trauma, with fewer sec-ondary injury mechanisms and greater regener-ative capacity than the upper motor neuron andits tracts.

One interesting and dangerous cauda equinasyndrome is associated with acute central discherniation at L4-5 or L5-S1 and results in majordamage to the sacral roots that lie centrallywithin the dural sac (Figure 8). Partial or com-plete sparing of the lumbar roots and often the

S1 roots may be present as well. Thus, these pa-tients may have total preservation of leg strengthbut complete bowel and bladder paralysis as wellas perineal anesthesia. The sacral roots are verydelicate and sometimes may not recover, evenwhen decompressed reasonably expeditiously.

REVERSIBLE OR TRANSIENTSYNDROMES

There are a number of complete or incom-plete SCI syndromes that are reversible or tran-sient (Table 4). One of the most interesting is the“burning-hands syndrome,” which frequentlyoccurs in athletes.28 The syndrome is character-ized by transient paresthesiae and dysesthesiae inthe upper limbs, especially the hands. It mayexist with or without long-tract signs, which, ifpresent, are usually evanescent. Biemond2 foundpathological changes in the posterior horn ofone case and termed the condition “contusiocervicalis posterior.” Braakman and Penning5

found that hyperextension was the most fre-quent mechanism of injury. Intramedullary le-sions may be demonstrable by MRI.28 Torg et al26

described a transient incomplete spinal cordsyndrome with sensory and motor deficits thatlasted up to 48 hours in football players and usedthe inappropriate term “neurapraxia.” Theyfound that all of the patients had radiological

Figure 7: Conus medullaris syndrome. A burst fracture of T12 is depictedwith posterior dislocation of bone fragments from the vertebral body intothe spinal canal resulting in compression of the conus medullaris. Almostall the lumbar cord segments are opposite the T12 vertebral body, so that asevere compression injury at this level could affect all lumbar and sacralsegments of the cord. Reprinted with permission from Tator.23

CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY 31

spinal abnormalities such as ligamentous insta-bility, disc disease, or spinal stenosis. These tran-sient cord injury syndromes are usually bilateral,which distinguishes them from the other syn-drome of “stingers” or “burners” in athletes dueto unilateral nerve root or brachial plexus lesions(especially traction injury), most of which arealso transient.28

Spinal cord concussion is a transient loss ofmotor or sensory function of the spinal cord,with recovery of function usually within min-utes but always within hours. In most instances,the patient reports that the symptoms are rap-idly diminishing and a normal neurologicalexamination is found. The exact pathophysiol-ogy of spinal cord concussion is unknown, butmost likely is caused by a biochemical abnor-mality in the cord such as leakage of potassiumfrom the intracellular to the extracellular spacedue either to direct mechanical injury or sec-ondary to a vascular mechanism. The latter pos-sibility was suggested by Schneider et al.21

Acute Spinal Cord Syndrome without Radiological Evidence of Trauma

The syndrome of SCI without radiologicalabnormality (SCIWORA) is more common in

children than in adults and represents a signifi-cant percentage of pediatric SCIs.16 Childrenwith SCIWORA tend to be less severely injuredthan those with definite evidence of bony injury,although complete injuries have been described.By definition, the negative radiological examina-tion includes only plain films and tomography,either conventional or CT. If a negative MRI wasincluded in the definition, the number of caseswould diminish dramatically, because of theextreme sensitivity of MRI in detecting mildcord injury and spinal column injuries such astorn ligaments and ruptured discs. Children aremore susceptible to these injuries, presumablybecause of the laxity of their spinal ligamentsand the weakness of their paraspinal muscles.

True SCIWORA can also occur in adults, butis much less frequent than the syndrome of SCIwithout radiological evidence of trauma (SCI-WORET). In patients with SCIWORET, radio-logical examinations are abnormal but x-raysshow no evidence of trauma. Prior to the use ofCT in spinal trauma, the incidence of SCI-WORET in adults was approximately 14%.24 Theaddition of CT has reduced the reported inci-dence of SCIWORET to about 5%. There hasbeen a recent analysis of the incidence of SCI-WORET in a Japanese study of acute SCI18 whichshows that many of these patients have demon-strable compression by myelography or MRI andshould be considered for early surgical decom-pression. It is likely that very few SCIs will re-main undetected by MRI, because of its highsensitivity for detecting mild SCI and nonbonyspinal column lesions. Cervical spondylosis is themost common associated condition in adultswith SCIWORET, but other arthropathies (e.g.,spinal stenosis, ankylosing spondylitis, and discherniation) may on rare occasion be associatedwith SCI and not show radiological evidence oftrauma.

Trauma Patients with an AcuteSpinal Cord Syndrome but WithoutDirect Trauma to the Spine

In some trauma patients, there is an acutespinal cord syndrome but no direct trauma tothe spine. This relatively rare syndrome differsfrom SCIWORET and SCIWORA in that these

Figure 8: Cauda equina syndrome. The drawingshows an acute central disc herniation of L4-5 withmajor compression of the central aspect of thecauda equina. The medially placed sacral rootsfrom S2 downward sustain the maximal compres-sion, whereas the more laterally located L5 and S1roots are completely or partially spared. Reprintedwith permission from Tator.23

CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION32

patients sustain a lesion of the spinal cord thatmanifests as an acute spinal cord syndrome andis associated with trauma although the trauma is not to the spine. The syndrome can occur inboth children and adults and produces the clini-cal findings known as the “anterior spinal arterysyndrome.” Keith11 described several cases inchildren with major abdominal, thoracic, orlimb trauma and concluded that many had sus-tained an aortic injury that caused occlusion ofintercostal or lumbar arteries with subsequentocclusion of medullary arteries and spinal cordinfarction. Rarely, penetrating injuries such asgunshot wounds can interrupt major arterialfeeders to the cord without direct trauma to thespine. Severe hypotension and systemic shock intrauma patients can also result in spinal cordischemia and infarction, even without causingconcomitant cerebral ischemia.

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