the syndrome of acute central cervical spinal

J. Neurol. Neurosurg. Psychiat., 1958, 21, 216.

THE SYNDROME OF ACUTE CENTRAL CERVICALSPINAL CORD INJURY

BY

RICHARD C. SCHNEIDER, JOHN M. THOMPSON, and JOSE BEBINFrom the Departments of Surgery and Sections of Neurosurgery of the University of Michigan Hospital, U.S.

Veterans Hospital, and St. Joseph's Mercy Hospital, Ann Arbor, Michigan, and the Wayne County General Hospital,Eloise, Michigan, and the Department of Neuropathology, University Hospital, Ann Arbor

Any discussion of the diagnosis and treatment ofspinal cord injuries inevitably involves controversialmatters. Among the foremost of these are the indica-tions for (Schneider, 1951, 1955) and the contra-indications for (Schneider, Cherry, and Pantek, 1954)surgical intervention. It seems highly important,therefore, to establish criteria which will assist indetermining whether an operation should or shouldnot be undertaken. In 1955, a paper was publishedon " The Syndrome of Acute Central CervicalSpinal Cord Injury" (Schneider et al., 1954), asyndrome the presence of which contraindicated anysurgical procedure. At that time, nine of theauthors' cases which exhibited this neurologicalpattern were described in detail, and six others wereabstracted from the literature. There was no patho-logical material presented, however, which wouldsubstantiate firmly the clinical thesis which had beenadvanced.

This paper is written to present 12 additionalpatients who exhibited the syndrome. In one casethe post-mortem examination confirms the assump-tions previously made on the basis of clinicalexamination. A study of this group of cases permitsfurther consideration of the mechanisms involved inthis type of injury.The description of the syndrome reads:

" In acute cervical spinal cord injuries, there is asyndrome that suggests acute central cervical spinalcord involvement. It is characterized by dispropor-tionately more motor impairment of the upper thanof the lower extremities, by bladder dysfunction,usually by urinary retention, and by varying degreesof sensory loss below the level of the lesion. If thefindings are caused by central cord destruction withbleeding, hematomyelia, there may be caudad orcephalad extension of the lesion with further progres-sion of symptoms, perhaps culminating in completetetraplegia or death. But if the symptoms are causedby concussion or contusion, with an edematous typeof central cord involvement, there may be gradualreturn of function in a definite sequence. The amountof recovery depends on the degree of edema presentcompared to the extent of true destruction of nervous

tissue. The lower extremities tend to recover motorpower first, bladder function returns next, and finallystrength in the upper extremities reappears, with thefiner finger movements coming back last. The varyingdegrees of sensory impairment do not follow any setpattern of recovery."

It was first thought that the acute central cervicalspinal cord injury was found only in severe hyper-extension injuries. The importance of suspectingsuch an injury of the cervical spine in the presenceof facial lacerations or contusions of the foreheadhas been emphasized by Taylor and Blackwood(1948). When the hypertrophic arthritic cervicalspine is hyperextended, there may be simultaneouslycompression of the anterior cord caused by aposteriorly placed bony spur and a posterior im-pingement upon the cord caused by a wrinkling ofthe ligamentum flavum. This mechanism waseffectively demonstrated in myelography on cadaversby Taylor (1951). In younger specimens there wasno distortion of the pantopaque column in thecervical spinal canal when the head was placed in aflexed or neutral position. When the cervical spinewas forcibly hyperextended, however, there wasdefinite encroachment posteriorly upon the pant-opaque column in the spinal canal. Taylor suggestedthat this was probably caused by a bulging forwardof the ligamentum flavum. When a cervical myelo-gram was made similarly in hyperextension in anelderly patient with posterior hypertrophic spurringof the cervical vertebral bodies, the bony spuranteriorly and the wrinkled ligamentum flavumposteriorly encroached simultaneously in the canal.

There are other mechanisms which may result ina squeezing of the cervical spinal cord. The acutecentral cervical spinal cord injury syndrome mayoccur in severe cervical compression fractures andin some cervical fracture-dislocations. It is difficult topostulate in cervical compression fractures whetherthe cervical spinal cord is squeezed in hyperextensionor in flexion of the cervical spine.

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ACUTE CENTRAL CERVICAL CORD INJURY

Cases of cervical fracture-dislocation, however,are a different matter. The acute central cervicalcord injury syndrome may occur in an acute flexioninjury accompanied by fracture-dislocation. Thecervical spinal cord is acutely squeezed anteriorly bythe lower involved, or caudad, vertebral body of a

cervical fracture-dislocation and posteriorly by thelamina of the upper, or cephalad, involved vertebra.The 12 patients presented here were admitted to

four different hospitals in the year following thepublication of the article on the acute centralcervical cord injury syndrome (Schneider et al.,1954).

Case ReportsCase 1.-On May 3, 1955, S. B., a 63-year-old woman,

fell headlong downstairs, striking upon her face. Thepatient developed complete tetraplegia accompanied bynumbness of the lower extremities. Within two hoursafter the fall she was examined at Wayne County GeneralHospital, and the following positive findings were noted:a large contusion on the left forehead, slight paresis ofthe lower extremities, marked weakness of the upperextremities, and complete paralysis of the hands. Therewas a complete areflexia with no pathological reflexes.Hypaesthesia was noted from the shoulder downward.Position sense was intact. A radiograph of the cervicalspine showed hypertrophic spurring at the C3-C4, C4-C5,and C5-C6 interspaces.

Several hours after she was admitted, her legs beganto move readily, and on the following day they were

strong. The upper extremities, however, showed almostcomplete paralysis of the forearm and hand musclegroups. Twenty-four hours after admission the hypaes-thesia which had been present below C7 bilaterally beganto diminish gradually in the lower extremities. It was

necessary to insert an indwelling catheter in the bladder.A lumbar puncture on May 5, 1955, produced cerebro-

spinal fluid with 21 R.B.C.s per high-power field and a

total protein value of 83 mg. per 100 ml. The bloodKahn test was 3 plus, but the spinal fluid Kahn test was

negative. A jugular vein compression test showed no

block. Twelve days after the injury movements in thepatient's hands began to improve. By May 18, bladdercontrol was good. A myelogram performed three weeksafter injury with the patient in a steep Trendelenburgposition showed that the pantopaque did not pass thelevel of C6 until the neck was flexed. A defect was presentat the C3-C4 interspace on the lateral view with a " stepladder " pattern on the anterior-posterior view.By July 7, 1955, the patient moved her hands only

weakly, but all other muscles of the extremities were

normal. Pyramidal tract signs were observed in the leftlower and upper extremities.

Case 2.-J. D., 55 years old, fell headlong down 23steps on January 22, 1955. He remembered striking uponhis forehead and left temple so that his neck was throwninto marked hyperextension. He was completely numband paralyzed from the neck downward at the time whenhe was admitted to a local osteopathic hospital. Twenty-

four hours after he was injured he could move thethumbs and toes. It was necessary to insert an indwellingcatheter into the bladder. The strength in the lowerextremities increased much more rapidly than in theupper, so that within a period of two weeks he couldmanipulate his lower extremities quite well. He couldraise his arms to a certain extent. All forearm movementswere poor, however; and, although his thumbs could bewiggled slightly, he could not move his fingers.The patient was treated with intermittent halter

traction until the time of his transfer to the U.S. VeteransHospital, Ann Arbor, Michigan, on February 10, 1955.When he was admitted, a disproportionately better move-ment was noted in the lower extremities than in theupper, and his hands were very weak. Hypalgesia andhypaesthesia were observed over the upper extremitiesand, in a lesser degree, over the trunk and lower ex-tremities. The deep reflexes were symmetrically hyper-active and no pathological reflexes were apparent. Vinketongs were inserted. Radiographs of the cervical spinedemonstrated a hypertrophic arthritis with spurring atall the interspaces but no evidence of fracture-dislocation.A follow-up examination was made on March 4, 1956.

His gait was impaired because of weakness in dorsi-flexion of the right great toe and foot. Strength was lessin the upper extremities than in the lower ones. Thesmall hand muscles on the right side were atrophied.Vibration and position sensations were intact. Theremainder of sensation had returned in patches. Therewas a zone of hyperaesthesia from T1o through T12 derma-tome bilaterally. Hypalgesia was demonstrated over thedorsum of the right foot, leg, and knee, and bilaterallybelow the T12 dermatome. The deep tendon reflexeswere more hyperactive in the right upper and lowerextremities than in those on the left. There were definitepathological reflexes in both upper extremities and in theright lower, with equivocal abnormality in the left lowerextremity.

Case 3.-L.R., 61-year-old farmer, was working on hismanure spreader on Friday, April 13,1956, when he fellheadlong to the ground forcing his neck into extremehyperextension. He could not move his arms or legs.After a short time he found he could move his legs weaklyand attempted to roll over, but he was unable to do so.Four hours later the patient was taken to the hospital.He felt sharp shooting pains in his arms and legs. Uponsensory examination, however, there was a complete lossof sensation in both upper extremities. He could flex andextend his lower extremities and could move his shouldersbut he could not move his forearms, wrists, or fingers.He had no pathological reflexes. Position sense wasabsent in both upper and lower extremities. Vibrationsense was present in the left upper extremity, but absentover the remainder of the body. Complete thermanaes-thesia was demonstrated below the level of T1 derma-tome bilaterally. He had hypalgesia over the left C6and C7 dermatone and hypalgesia to L3 on the left andT12 on the right side.

Radiographs of the cervical spine showed extensivedegenerative and hypertrophic changes. No evidence ofany fracture-dislocation was observed. Dr. Adam

217

RICHARD C. SCHNEIDER, JOHN M. THOMPSON, AND JOSE BEBINMcClay, the orthopaedic consultant, made a diagnosisof acute central cervical cord injury and stated that theprognosis was good. He advocated conservative treat-ment.An examination on April 15 showed that the sensory

pattern was essentially unchanged. The patient hadpowerful quadriceps and flexor movement in the lowerextremities but still no detectable movement in theupper ones.

Case 4.-On March 23, 1956, H. S., a 51-year-old man,fell head first down a long flight of stairs while under theinfluence of alcohol. He regained his senses six hourslater in a Detroit hospital, suffering from numbness andtingling from the neck downward over his body, markedweakness of his arms, paralysis of his hands, and slightparesis in his right leg. He had right-sided hyperactivedeep tendon reflexes and a right extensor plantar reflex.A lumbar puncture was made within the first 24 hoursafter his injury, and the cerebrospinal fluid contained60 red blood cells and 3 white blood cells per high-powerfield. The protein content of the fluid was 117 mg. per100 ml. He had no bladder control during the first 48hours in hospital. The motor power in his legs improvedmarkedly within the first 24 hours, but he still hadmarked paresis in the right arm and moderate weaknessof the left hand. A diagnosis was made of " conversionhysteria, possibly superimposed on some cord damage".On the sixth day after injury, the patient was trans-

ferred to Wayne County General Hospital. Radiographsof the cervical spine demonstrated posterior hypertrophicspurs on CA, C5, and C6 vertebral bodies, with no apparentevidence of fracture-dislocation.On April 6, 1956, two weeks after he sustained the

injury, the patient had only 5% normal strength in themuscle groups of the right arm. He had only minimalmotion of the right thumb and fingers. The muscle groupsof the left arm showed about 75% normal strength, incontrast to the lower extremities, where there was mini-mal paresis bilaterally. With the exception of thehypalgesia below the left knee, a sensory examinationdemonstrated normal responses. He had no bicepsreflexes, but triceps reflexes were present, the left beingmore active than the right. The lower extremities hadhyperactive deep tendon reflexes, the right quadricepsreflex being more active than the left. There werebilateral extensor plantar reflexes. After four days, heshowed marked improvement in the strength of the rightarm, although the hand grip was still weak.

Case 5.-E. B., a 52-year-old lumberman, fell 12 feetfrom a loaded pulp truck on the morning of March 2,1956. He was unconscious for about an hour and didnot recall in what position he had struck the ground.Upon regaining consciousness he found that he wastemporarily unable to move all four extremities; his toemovements returned almost immediately, however.Within four hours he recovered motor power, first in theleft leg, then in the right, so that he was able to standerect four hours after injury. He could move his armsbut they were much weaker than his legs. Finally, he wasable, with assistance, to walk 250 feet to a car in which

he was taken to a local hospital. Radiographs of thespine were taken and he was put to bed. No lumbarpuncture was made.During the first seven weeks in hospital the patient

felt numb from the neck downward over his body, andwas unable to use his arms, although he moved his legsslightly. Three and a half months after his injury henoted a generalized tingling sensation below the levelof TIo dermatome anteriorly and T. dermatome pos-teriorly. He began to walk unassisted about four monthsafter the accident. His chief complaint was that he felthot, prickly, and swollen sensations in the right leg. Anindwelling catheter had to be used during the first twomonths of his stay in hospital until the bladder regainedits function.The patient was transferred to the University of

Michigan Hospital, where the following neurologicalfindings were noted: weakness in the legsand trunk, moremarked paresis in the upper extremities, and maximalimpairment of strength in the hands. There was hypaes-thesia along the ulnar aspect of the right hand and ahypalgesic level at T, segment bilaterally. Dysaesthesiawas found over the right leg. He had no vibratorysensation over the ankles, but position sense was presentin both feet. With the exception of the Achilles reflexes,all deep reflexes were symmetrically hyperactive. Bilateralpyramidal tract signs were demonstrated in both upperextremities and he had an equivocal extensor plantarreflex in the right lower extremity. Radiographs of thecervical spine showed hypertrophic vertebral body spur-ring at C3-C4 and CQ-C, interspaces.

Case 6.-At 11.30 p.m. on October 11, 1955, J. H., a72-year-old man, fell from a wagon, striking on his head.He was not unconscious but he was immediately paralyzedin all four extremities with numbness from the neckdownward. While in transit to the University Hospitalin the ambulance, he began to move his toes and legs.When he was admitted to the hospital, the patient wasalert and cooperative. He had no movement in the upperextremities or in the intercostal musles, but there wassome motion in the hamstrings, quadriceps, adductorsof the hips, and dorsiflexor muscles of the feet. On theleft side from the T. to L, dermatome, he had a zone ofloss of sensation to pinprick and dysaesthesia of tem-perature, and a loss of all sensory modalities of theremainder of the trunk and extremities. The deepreflexes in the extremities were equal, although sym-metrically hyperactive in the legs. He had no patho-logical reflexes. A diagnosis was made of acute centralcervical cord injury at C3-C, or C4-C5 interspaces. Haltertraction was applied.

Radiographs of the cervical spine demonstrated afracture of the C, and C, spinous processes, and showedalso some mild evidence of hypertrophic spurring of thevertebral bodies at C4-C5 and C,-C, interspaces, withslightly more lipping at the C6-C7 interspace (Fig. 1).A lumbar puncture was performed and when jugularcompression was applied, the cerebrospinal fluid roseand fell normally. Vinke tongs were substituted for thehalter traction and, within 10 hours after admission,intercostal function had returned. A cystometric

218


FIG. 1.-Case 6: Lateral radiographs of the cervical spine demon-strating fractures of C, and C, spinous processes and mildspurring at the C4-C, and C,-C, interspaces with more markedlipping at the C,-C, interspace.

examination demonstrated a 180 ml. capacity reflex typeof bladder on October 15, and the examining urologistconcluded that the patient might be experiencing some

return of function. Five days later there were uninhibitedcontractions suggesting a neurogenic reflex type ofbladder. On October 25 bladder sensation partiallyreturned. The bulbo-cavernous reflex was intact. Thestrength in the patient's legs improved but his armsremained paralyzed. On October 30, his temperature roseto 103° F. and his blood pressure fell. The chest radio-graph showed right atelectasis and pneumonia. Theelectrocardiograph was normal. The patient becameprogressively worse and died on November 9. He hadsustained a pulmonary embolus complicated by atelec-tasis and pneumonia.

Necropsy Examination.-This disclosed more markedbony ridges at the C4-C5 and Cs-C7 interspaces than weredemonstrable radiologically. The surface of the spinalcord appeared to be normal, but the cord was soft(Fig. 2). Cross sections of the cervical spinal cord takenat the upper C4 segment revealed, macroscopically, afairly normal cord, somewhat flattened transversely andsoft to palpation (Fig. 3). Cross section of the spinalcord just below this level exhibited necrosis of the centralportion which extended toward the posterior surface toinclude parts of the posterior and postero-lateral funiculi.Sections above and below this segment exhibited onlypallor of the funiculi.

Sections of the spinal cord were cut and preparedhistologically with haematoxylin and eosin, Massontrichrome, and Weil stains. The sections of the lowerfourth cervical segment of the spinal cord showed a largedestructive lesion, which, at its maximum, included thecentral portion of the grey commissure, the anteriorhorns, the posterior horns, and the posterior columns ofthe cord (Fig. 4). A few millimetres below this level, thelesion appeared well circumscribed in the central portionof the cord immediately behind the central canal (Fig. 5).The lesion included the more proximal portions of bothposterior horns and the medial parts of the posteriorcolumns and the postero-lateral columns.

Microscopic examination of these areas showed almostcomplete destruction of the substance of the cord withliquefaction and necrosis. This area was filled with

FIG. 2.-Case 6: The necropsy specimen showing that there was actually little evidence of gross external damage apparent to the dorsal surfaceof the cervical spinal cord. The three incisions A, B, and C through the involved area unfortunately were made before photographingthe specimens.

219

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debris and numerous macrophages (gitter cells). Thelimits of the lesion were not well delineated from sur-rounding areas. Numerous small arterioles and newly-formed blood vessels were seen in this area. Many ofthese had hyalinized walls and appeared markedlycongested. The blood vessels were more abundant inthe transition zone between the necrotic centre and thesurrounding cord tissue. The anterior horn cells werediminished in number and those remaining showedmarked retrogressive changes. In the area of maximuminvolvement the anterior horns had completely dis-appeared and had been replaced by a mass of gitter cells,debris, and newly-formed blood vessels. At the marginalzone of the cord there was some degeneration of themyelin sheaths in the posterior and postero-lateralcolumns. The myelin degeneration of the postero-lateral columns was more prominent in the deeper por-tions of the columns and merged into the gross lesion.The leptomeninges were thickened with fibroblastic

changes. The meningeal vessels, including the anteriorspinal artery, posterior spinal arteries and veins, appearedto be normal but congested. The dura was normal inappearance.

Sections of the cord one segment below and onesegment above the lesion showed marked congestion andmoderate oedema. There was some loss of myelin inboth postero-lateral columns, mostly in the deep por-tions. The anterior and posterior horns appeared wellpreserved in relation to the number of cells. The neuronesshowed changes compatible with ageing. The lepto-meninges likewise exhibited changes of marked conges-tion and moderate oedema.

Case 7.-R. D., a 36-year-old severely paranoidschizophrenic male patient at the Veterans Hospital inBattle Creek, Michigan, was assaulted by another patienton January 21, 1954, and, during the ensuing scuffle,struck his head on the floor. The physician who examinedhim shortly afterwards stated that the patient was livid,had an irregular, thready pulse, and was incontinentof faeces. As the patient gradually regained conscious-ness, he complained of headache and pain radiatingdown the neck. There was no abnormality noted whenthe neurological examination was made. About 2 a.m.on January 22, 1954, the patient stated that he could notmove, but he actually was seen moving his extremities.At 4 a.m., the patient could void only very small amounts,and later he was incontinent of a large amount of urine.On January 23, two days after the injury, he was unableto move either arm voluntarily. He also had a loss ofpain and temperature sensation in the left arm, hyper-active patellar and ankle jerks, and a temperature of104.80 F. By the next day he had marked weakness andflaccidity of the upper extremities but could move hislegs. A lumbar puncture disclosed a clear cerebrospinalfluid with no block shown by the jugular compressiontest. Cervical spine films made on January 26 demon-strated a "crown" compression fraction of the C5vertebral body.

The patient was transferred to the Veterans Hospitalin Ann Arbor, Michigan, and on admission was seen tohave flaccid paralysis of both upper extremities with

normal tendon reflexes, weakness in both legs, withspasticity and increased tendon reflexes and bilateralankle clonus. On February 6, 1954, a neurosurgical con-sultant made a diagnosis of hyperextension injury of thecervical spine with compression fraction of C5 vetrebralbody and central cord destruction or haematomyelia.By February 24, 1954, he walked with assistance. InMarch the patient had regained bladder control; andby May, 1954, he could feed himself.Two years after the accident he exhibited more weak-

ness in the upper than in the lower extremities, a spasticgait, a slight decrease in vibration sense in the rightupper and lower extremities, symmetrically hyperactivereflexes, and a left extensor plantar reflex.

Case 8.-At 8.30 p.m. on July 9, 1954, E. S., a 12-year-old boy, dived into two feet of water and sustained animmediate paralysis of the upper extremities, but retainedminimal movement in the legs. On admission to St.Joseph's Mercy Hospital, Ann Arbor, Michigan, he hadonly movements at the shoulders with no extension ofthe upper extremities or motion of the fingers. He hadslight internal rotation in the thighs and the toes of bothfeet moved slightly. A level of hypaesthesia and hypal-gesia was demonstrated extending to the T7 dermatomebilaterally but motion and position sense were preserved.He had equally hyperactive deep reflexes. No extensorplantar reflex could be demonstrated. Priapism waspresent.

Radiographs of the cervical spine revealed a fracture-dislocation of C2 vertebral body anteriorly on C3 andcompression fractures of C4, C5, and C6 vertebral bodieswith protrusion of the C, centrum posteriorly into thespinal canal. The posterior rim of the axis was in closeproximity to the occipital bone.A diagnosis of acute central cervical cord injury was

made. A guarded prognosis was given to the patient'sparents but the chance of recovery was considered goodwith the classical pattern of motor return predicted. Thesurgeon inserted Vinke tongs on the night of admission.By July 11, the priapism had subsided and there werebilateral extensor plantar reflexes. On July 12 a lumbarpuncture revealed a bloody fluid (traumatic tap) withoutevidence of block when the jugular vein compression testwas made. Five days later the patient had slightly betterdorsiflexion in the left foot than in the right. On July 26,the day before transfer to another city, a cystometricexamination revealed a reflex neurogenic bladder.

Reports from the Mary Free Bed Hospital in GrandRapids, Michigan, where the patient was observedduring his convalescence, indicated that he was able tomove his fingers on August 17. By January 25, 1955, hecould walk unassisted. At the time of his discharge onJuly 7, 1955, he had some slight residual weakness in hishands, but he performed all necessary functions readily.

Case 9.-C. L., a 52-year-old taxi driver, was examinedat St. Joseph's Mercy Hospital, Ann Arbor, Michigan,on August 21, 1955, having been transported 500 mileswithout the benefit of any type of cervical immobiliza-tion. He had sustained an injury in an automobileaccident five days before he was brought to the hospital.

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RICHARD C. SCHNEIDER, JOHN M. THOMPSON, AND JOSE BEBIN

He had been rendered unconscious immediately, had alucid interval, and then became semiconscious for24 hours. His lower arms and hands were totallyparalyzed, but he could move his lower extremitiesslightly. During the five days before his transfer, heimproved markedly. Upon arrival in Ann Arbor, therewas minimal strength in the grip and in the arms, buthe had good motor power in both legs. There washypalgesia over the C6, C7, and C8 dermatomes bilater-ally and the entire right side of the trunk. The deepreflexes were symmetrically hypoactive with no pyra-midal tract signs in the upper or lower extremities.Cystometric examination was normal. A diagnosis ofacute central cervical spinal cord injury was made, andthe prognosis was stated to be good.

Radiographs of the cervical spine showed a markedanterior fracture-dislocation of the C5 vertebral bodyanteriorly on the compressed vertebral body of C6.There were also fractures and posterior displacement ofthe laminae of C5 and C6 bilaterally, and a fracture ofthe C4 spinous process. Skeletal traction was applied.Decompressive laminectomy was deferred until August31, 1955, to permit improvement in the patient's generalcondition. At operation the laminae of C4, C5, and C6vertebrae were found to be fractured and displacedposteriorly. The dura was opened, the arachnoid wassectioned laterally, and after the dentate ligaments werecut, the cord pulsated readily. The dura was closedtightly and spinal fusion was performed. He was dis-charged from the hospital on December 11, 1955.Radiographs of the cervical spine after fusion showedthat the graft was calcifying nicely. Three months laterthe patient was able to return to his job as a taxi driverand was bothered only by some stiffness of the neck.

Case 10.-J. D., a 17-year-old student, was admittedto the University of Michigan Hospital on August 4,1955, one hour after diving into shallow water. He wasparalyzed immediately in all four extremities and had tobe carried from the water. On admission to the hospitalthe patient had diaphragmatic respirations. There was acomplete areflexic tetraplegia with a sensory level atthe C7 dermatome bilaterally and the patient was unableto void. Head halter traction was applied immediately,and radiographs demonstrated a subluxation of the C5vertebral body anteriorly on the slightly compressedC6 vertebra. Thirty minutes after the application of thecervical traction he experienced a complete return ofsensation. The halter traction was replaced by a Vinkeskeletal tractor. A lumbar puncture revealed a completeblock on the jugular vein compression test.Twelve hours after he was admitted to the hospital, the

patient had a decompressive laminectomy of C5 and C6vertebrae. The right C5-C, facet was locked. The durawas opened in the midline, the dentate ligaments cut, andthe subluxation reduced by traction and careful pryingwith an osteotome. The pulsating cord appeared slightlyhypaeremic and swollen. The dura was not closed.

Within 24 hours after the operation had been per-formed, the patient began to move his left foot and super-ficial as well as deep sensation returned on his right side.Four days after the injury he still had hypalgesia to the

C7 dermatome. Deep pain and position sensations wereintact in the lower extremities. He showed markedrecovery of motor power in the legs, but less in theupper and forearm muscles, and no return of functionin the fingers or triceps muscles. The deep reflexes wereequal and active and he had bilateral extensor plantarreflexes. The first finger movement appeared on August16, and cystometric examination showed a normalbladder. The patient left the hospital on October 18with his neck supported by a Forester collar. OnDecember 9, 1955, he walked readily without a cane,and his hand function, which was the greatest residualdeficit, was 65% of normal.

Case 11.-I. W., a 40-year-old man, dived into theDetroit River on August 8, 1955, and had to be pulledfrom the water because of total paralysis in all fourextremities. He was admitted to the City of DetroitReceiving Hospital at 7 p.m. He had a complete tetra-plegia with deep reflexes that were equal and active inthe upper extremities, but the right lower extremity wasareflexic. On catheterizing the bladder at 12 p.m.,800 ml. of urine was removed. Radiographs of thecervical spine revealed the C4 vertebral body dislocatedanteriorly on C5. Skeletal tong traction was applied anda 35-lb. weight added. Serial radiographs of the cervicalspine were taken of the facets. There was completereduction of the cervical fracture-dislocation and goodrealignment of the cervical spine so that the weight wasreduced to 10 lb. The patient had no proprioception, alevel of hypalgesia to the C3 dermatome bilaterally, andcomplete areflexia.On August 10, a lumbar puncture showed no evidence

of blockage of the subarachnoid space on the jugularcompression test. The spinal fluid was clear with only4 red blood cells per high-power field and a total proteinlevel of 102 mg. per 100 ml. At midnight of the sameday the patient had respiratory distress and difficulty inswallowing. It was decided that surgical interventionwas not indicated.On August 28, the patient had a slight return of motor

power and sensation in the lower extremities. By Sep-tember 4, these functions were markedly improved. Theskeletal tongs became disengaged on September 10, andit was thought advisable to discontinue their use. BySeptember 19, 1955, the patient had regained somedegree of motor power in both the upper and lowerextremities, exclusive of hand movement. The indwellingcatheter was removed.At the time he was transferred to Wayne County

General Hospital on September 22, 1955, he definitelyhad greater strength in the legs than in the upper arms,but the fingers and hands were still paralyzed. Pain andtouch sensations were normal, but he had no positionsense in the fingers of his right hand. The deep tendonreflexes were equal and active in the arms, but hyper-active in the legs. He showed bilateral Hoffmannresponses and extensor plantar reflexes. The patientrejected the cervical spinal fusion operation which wasrecommended, and was discharged in a Taylor backbrace with a Forester collar, on October 21, 1955.On March 6, 1956, examination showed that the

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patient had weakness in all four extremities, but therehad been progressive improvement in strength, and thatnow he could move his hands and fingers. Sensation wasnormal in all modalities. He had persistent pyramidaltract signs in all four limbs, with sustained left ankleclonus. Cervical spinal fusion was again advocated andthis operation was performed on March 13, 1956.

Case 12.-Mr. X, a 68-year-old man, stumbled andstruck his head and neck on the sidewalk on November25, 1955. He was admitted to his community hospitalwhere he complained of pain in the neck which radiatedinto both arms and hands. He also had paresis of theleft arm and leg. Radiographs of the cervical spinedemonstrated a fracture-dislocation of C5 vertebral bodyanteriorly on C,. Skeletal tong traction was appliedand a 20-lb. weight added.On the day after he was injured the patient required

catheterization. Three days after injury he began de-veloping mental disorientation, which was believed to becaused by cerebral anoxia secondary to decreased respira-tory function. On December 2, 1955, he complained ofsevere pains in his arms and legs. A nurse's note statedon December 6 that the patient had fairly good controlof his legs and often moved them but that he had lesspower in his arms. The right fingers and toes " werestiff ". He continued to cry out because of severe painin the extremities, and both physicians and nurses inter-preted this as a result of mental confusion. On Decem-ber 8, 1955, the patient had severe chest pain withassociated dyspnoea. By that time all motor power hadbeen lost in the lower extremities, but pain was stillpresent. An electrocardiogram two days later showed aright bundle branch block. He continued to have severediscomfort throughout the entire trunk and extre-mities.On New Year's Day, 1956, the skeletal tong traction

was removed, and six days later, the patient had pain inthe feet, legs, and arms and " he talked only of pain ".Flexor spasms occurred in both knees but he had somevoluntary movement in both, and marked improvementin feeling in both lower extremities. By January 10, 1956,the patient could move both lower extremities, had goodmotor power in the shoulders, poor elbow extension,fair motion in the forearm, but had no finger movementwhatever on the left side.The patient was transferred to Wayne County General

Hospital in January, 1956. The indwelling catheter wasremoved. There were muscle contractures in both elbows,hips, knees, and to a lesser extent, in both hands, makingevaluation difficult. Radiographs of the cervical spine,four months after trauma, demonstrated complete re-duction of the dislocation with calcification to thevertebral body both anteriorly and posteriorly.An examination on April 6, 1956, demonstrated that

the patient's strongest movements were in the lowerextremities in plantar and dorsiflexion of the feet. Theother muscle groups of the lower extremities were weak.He had slight weakness in both forearms with markedparesis in the hand grip bilaterally. Hypalgesia was notedbelow the T8 dermatome on the right. Touch was intact.Position sense was absent in the toes. Vibration sense

was present in the knees. He had normal biceps reflexes,no triceps reflexes, and symmetrically hyperactivepatellar and Achilles reflexes. Positive extensor plantarreflexes were demonstrated.

DiscussionMechanisms.-In recent years an increasing

amount of interest has been focused on the problemsof chronic anterior cervical cord compression byhypertrophic spurs (Bedford, Bosanquet, andRussell, 1952; Brain, Northfield, and Wilkinson,1952; Kahn, 1947; Spillane and Lloyd, 1952;Symonds, 1953), but too little attention has beendevoted to acute traumatic lesions of the cervicalspinal cord in such cases.Case reports 1 to 6 concern patients who had had

hypertrophic cervical arthritis and developed acutecentral cervical cord injury on the basis of hyper-extension injury to the cervical spine. In Cases 1,2, 3, and 6, the patients had suffered definite facialor forehead injuries, supporting the belief thathyperextension injury had occurred. The patient inCase 4 had been drinking; and in Case 5 the man hadbeen rendered unconscious, and therefore an accu-rate history concerning this specific point could notbe obtained.

All these case reports demonstrate how acutecentral cervical spinal cord injury may occur inhyperextension of the hypertrophic arthritic spinewithout compression fracture or fracture-dislocation,giving support to Taylor's (1951) thesis. They shouldalso serve as a warning against a too vigorous hyper-extension of the cervical spine in the intubation ofelderly patients for the administration of intra-tracheal anaesthesia. Reports have appeared in theliterature calling attention to contingent dangers,and one of the authors (R. C. S.) is presenting else-where a case in which such an anaesthetictechnique resulted in acute central cervical cordinjury, though the patient gradually recovered.The patient in Case 7 sustained a " crown -

shaped cervical compression fracture, and it couldnot be determined whether or not this injuryoccurred with hyperextension or flexion of thecervical spine.The syndrome probably resulted from acute

flexion injury to the cervical spine and spinal cordin Cases 8 to 12. The patient reported in Case 8had multiplemildcompression fractures and fracture-dislocations resulting in a " step " type of injurywith multiple points of simultaneous anterior andposterior compression of the cervical spinal cord.In Case 9, an acute flexion injury must have occurred,accompanied by a severe fracture-dislocation of thecervical spine, along with a momentary holding ofthe laminae of the more cephalad vertebra. This

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224 RICHARD C. SCHNEIDER, JOHN M. THOMPSON, AND JOSE BEBIN

squeezed the cord. An associated avulsion of thelaminae must also have been present, causing com-pression of the cord, with the result that it wasspared from complete transection. The fracture-dislocations in Cases 10 and 11 are the disruptionswhich are commonly found and result in a simplesqueeze of the cord rather than in transection.

In Case 12 the patient suffered initially a fracture-dislocation of a hypertrophic cervical spine withlittle immediate neurological deficit. After thefracture-dislocation was reduced, however, the cordwas probably drawn into some hyperextension overthe hypertrophic spur so that an acute centralcervical cord injury syndrome gradually developed.After skeletal traction was removed, the patientbegan to regain function following the characteristicrecovery pattern.Age.-A glance at the ages of these patients is

instructive. In Cases 1 to 6, the ages were 63, 55,61, 51, 52, and 72 years, respectively. As might beexpected, these were the individuals with hyper-trophic cervical spines who sustained acute centralcervical cord injuries in hyperextension, withoutfracture or fracture-dislocation. The ages in Cases 7to 11 were 36, 12, 52, 17, and 40 years, respectively,a much younger group as a whole. These individualsexhibited the syndrome in association with com-pression fracture or fracture-dislocation, more thanpossibly resulting from an acute flexion mechanism.The patient reported in Case 12 was 68 years oldbut his case was exceptional in that there was afracture-dislocation of a hypertrophic cervicalspine.Anatomy.-In the cervical spinal cord there is a

definite segmentation or pattern of fibres within thelateral corticospinal tract. The lumbar fibres, orthose which supply the lower extremities, lie laterallyin the cervical spinal cord. The thoracic or trunkfibres are in a medial position, while the cervical orupper extremity fibres assume a still more mediallocation with the finger fibres placed centrally. Whenthe cervical spinal cord is squeezed from an anteriorand a posterior position simultaneously, there maybe a central zone of cord destruction surroundedby a more peripheral one of spinal cord oedema.The degree of permanent disability which thesepatients incur will depend upon the extent of centralcervical cord damage, so that as the more peripheralzone of oedema recedes, the more peripherallylocated fibres in the lateral corticospinal tracts andadjacent tracts will regain function. As a result, thelegs will regain function first, then bladder functionreturns, the arms recover next, and finger movementsare regained last.

In order to study the various stresses which occur

when the spinal cord is subjected to anterior-posterior compression, a sponge rubber model wasconstructed by Pantek (Schneider et al., 1954).Upon this model had been painted a diagram of thecervical spinal cord and its various fibre tracts.About its periphery was a fine rim of firmer rubberwhich served to represent the pia mater and thepoints of attachment of the dentate ligaments. Themodel was then placed into a wooden vice so thatan anterior and posterior compressing force couldbe applied. By placing a grid over the model, it waspossible to measure types and degrees of distortion.The study revealed the presence of at least fourdefinite stresses, the predominant one being-as onemight expect-the anterior-posterior compressivestress (Schneider et al., 1954).*The use of this model obviously has its limitations,

for no observations can be made concerning theinfluence of stress on the vascular components ofthe cord, the comparative looseness of texture nearthe vicinity of the central canal versus the compact-ness of fibre bundles near the periphery, or the factthat many of the sensory fibre tracts lie near theperiphery of the cord so that they are affected merelyby oedema rather than undergoing complete des-truction. Ideally, the use of strain gauges in experi-mental animals would be an excellent method ofevaluating these stresses but at the present time eventhe smallest of these is too bulky to be used inexperiments with animals. The employment of thesponge rubber model and an analysis of the clinicalstudy which has been published elsewhere havegiven us only a small part of the information whichwe require.Pathology.-For many years physicians have

sought an explanation as to how the cervical cordcan be damaged with apparently no attendant injuryto the cervical spine. Holmes (1915) discussed thisproblem, stating that if the spinal cord were con-cussed, there might be either no gross evidence ofcord damage or a uniform swelling opposite thepoint of impact of the cord against the bone. Hesuggested that since the spinal cord lay in a water-jacket of cerebrospinal fluid, it might oscillate toand fro in the fluid when the trauma occurred.These movements might become asynchronous withthe motion of the cervical bony spine, and the spinalcord would then impinge upon the bone, causingconcussion or contusion, and thus produce physicaldisturbance " especially in the fluid axioplasm ofits fibres ". Holmes observed that the greatestpathological change was a pronounced oedema inthe affected segments, the most marked involvement

*The reader is referred to the original article for a complete discus-sion of this problem.


being found directly at the site of the blow. In hismicroscopic preparations of damaged cords, some

of the fibre tracts had been destroyed but in theremainder of the fibres the myelin sheaths and axiscylinders were swollen. In the grey matter there werefocal areas of softening, usually associated withhaemorrhages which had peripheral zones of neuro-

nal degeneration. These pathological findings couldaccount for the presence of neurological signs whichpartially or completely disappear as severe oedemasubsides. This is what occurs in the syndrome ofacute central cervical cord injury.Nerve fibres which have been compressed or

squeezed are more likely to recover function thanare those which have been acutely and severelyflexed so that the neurons are " fractured " andpermanent damage is sustained. A vascular impair-ment of the spinal cord is probable in patients thusaffected. In Case 6 not only the central elements ofthe spinal cord but also the posterior columns were

destroyed. Woodward and Freeman (1956) haveshown that when the peripheral nerve roots and theirassociated neuronal sheaths were ligated over a

zone of six segments (in dogs), central cavitationmight appear along with some loss of the posteriorcolumns. They attributed this loss to venous con-

gestion in these regions. The posterior surface ofthe cord is drained by paired posterior veins whichare not nearly as large and efficient in function as

the large anterior venous channels. Woodard andFreeman's work has not proved conclusively thatthe changes were caused only by venous congestion,for certainly some degree of the arterial supply as

well as the venous drainage must have been im-paired when six peripheral nerve roots and theirsheaths were ligated.

In Case 7, the delayed onset of the syndrome ofacute central cervical spinal cord injury couldscarcely have resulted from cervical cord oedemaso long after the injury, and one must thereforeconsider the possibility of a traumatic thrombosis inthe anterior spinal artery simulating the " lateapoplexy " seen in traumatic cerebral lesions. Theremay be another alternative. The patient in Case 7was psychotic; it is conceivable, therefore, that hecould have suffered one injury which was followedby another episode of unwitnessed trauma somehours later, which accounted for his neurologicalsigns.

TreatmentLumbar Puncture.-This procedure should prob-

ably be used in almost all cases of spinal cord injury,and yet it is surprising to note how infrequently itis performed. The usual reason given for omitting thetest is the fear of injuring the patient in manipulating

him into a proper position for inserting the needle.In our series of 12 patients, six had lumbar

punctures. In the three hyperextension injurieswhich showed hypertrophic arthritis and in whichspinal taps were made, there was no evidence of anyblock when the jugular vein compression test wasdone. This fits well with the data collected fromour original series of nine cases in which there werefour similar hypertrophic arthritis cases none ofwhich involved subarachnoid space block. In thepublication (Schneider et al., 1954) in which wereported these cases, it was suggested that there wereseveral points of compression or " squeeze" of thecervical cord, distributing the oedema of the cordover several segments rather than localizing it atany single given point. This meant that one of theimportant criteria for operation, namely, completesubarachnoid block, was lacking.

In the remaining six patients of the series pre-sented above, who may have sustained a cord injuryassociated with compression fracture or fracture-dislocation of the cervical spine, three lumbar punc-tures were made. In two of them there was no blockwhen the jugular vein compression test was carriedout. (The patient in Case 7 had sustained a " crowntype" compression fracture, and the individual inCase 8 had multiple compression fractures and" step " fracture-dislocations with multiple pointsof cord " squeeze ".) One patient in this group(Case 10) showed a straightforward fracture-disloca-tion of C5 vertebral body anteriorly on C6. Hehad a complete block on manometric testing. It isinteresting to note the examiner's observation:" Thirty minutes after the application of the cervicaltraction, there was complete return of sensation."One wonders whether repeated hourly taps wouldnot have demonstrated a release of pressure andoedema and a subsidence of the complete block.This may have occurred in Case 11, where thefracture-dislocation was reduced early. Since theoperative indication of complete block was presentin Case 10, no chances were taken and the patientwas treated by decompressive laminectomy. Hesubsequently made a fairly good recovery, but thequestion must be raised as to whether this wouldhave happened if operative intervention had notbeen employed.

Myelography.-This test was undertaken only inCase 1. It is mentioned again here only to emphasizethe danger of the procedure. Since it is alwaysnecessary to hyperextend the cervical spine in orderto prevent the flow of radio-opaque material intothe skull, there is a danger of increasing spinal corddamage, for it is in the hyperextended position thatthe original injury occurs.

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RICHARD C. SCHNEIDER, JOHN M. THOMPSON, AND JOSE BEBIN

Operation.-The usual criteria presented for earlyoperation upon patients with acute spinal cordinjuries are complete block (as shown by thejugular vein compression test), an increase in neuro-logical signs, or debridement of a compoundfracture. In the majority of cases, and particularlyin those where hypertrophic cervical spurring with-out fracture or dislocation of the cervical spine wasfound, these criteria were not present. In theseindividuals, anterior and posterior compression ofthe spinal cord existed simultaneously at severalsites, so that no single point of spinal cord oedemaor haematomyelia occurred and no subarachnoidblock was usually to be observed. Damage to thecervical cord was acute. There was no progressionof neurological signs but rather a regression, so thatanother of the customary indications for operationwas absent. In the first patient discussed in ouroriginal presentation of this syndrome (Schneideret al., 1954), surgical intervention actually created afurther compromise of the lateral cortico-spinaltracts which had already been damaged. Whenpressure was applied gently in order to retract thespinal cord, to section the dentate ligaments, and toexplore anterior to the cord, the lower extremitycomponents (which lie laterally in the pyramidaltracts) were pressed upon, and the lower limbs,which the patient had moved pre-operatively, wereparalyzed after operation. Conservative treatmentis the most satisfactory in patients with acute centralcervical cord injury. These people may be placed insome type of traction applied directly in the planeof the body until the spinal cord oedema has sub-sided. This usually requires about four weeks, atthe end of which time a collar may be substitutedfor the traction apparatus for a period of anothersix to eight weeks.A single point of " squeeze " of the cervical spinal

cord is frequently found in patients with an acutecentral cervical cord syndrome after flexion injurywith fracture-dislocation of the cervical spine. Acomplete block on the jugular vein compression testis more apt to be found in such patients than in thosewho incur the syndrome in hyperextension. Such asituation occurred in Case 10, where there was acomplete block, and immediate operation was there-fore indicated. No lumbar puncture was made inCase 9, because the patient's generally poor con-dition precluded operation even though a block hadbeen found. With the degree of fracture-dislocationshown radiologically, a complete block might cer-tainly have been present. Patients who demonstratethe acute central cervical cord injury syndrome withassociated fracture-dislocation need immediateoperation, therefore, only if a subarachnoid block isfound when the jugular vein compression test has

been made. Otherwise, cervical skeletal tractionshould be applied in an attempt to reduce thedeformity, and this should be followed by a spinalfusion some weeks later, after spinal cord oedemahas subsided.Myelotomy has been advocated in acute traumatic

haematomyelia by Elsberg (1941), Holmes (1915),Cohn (1931), and others. Allen (1911), in onepaper, and Freeman and Wright (1953), in another,have presented experimental evidence of sympto-matic improvement in animals with cord contusionswhen pial incision and dorsal myelotomy wasperformed.The present authors are inclined to agree with

Frazier (1918). He had observed that in traumatichaematomyelia there were numerous haemorrhagiczones in the spinal cord which were not necessarilyin continuity. Thus, myelotomy would damage anoedematous, but otherwise normal, spinal cord.McVeigh's (1923) observations, made on the basisof his experimental work on traumatic haemato-myelia, tend to support Frazier's thesis of multipleareas of haemorrhage and destruction in the spinalcord.

Prognosis.-In the patients who show the acutecentral cervical spinal cord injury syndrome, theprognosis is usually good. As the cord oedemasubsides, recovery follows the pattern describedabove. Power in the lower extremities returns first,bladder function in the upper extremities next,and finger movements last. If central destructionof the spinal cord is marked, only partial recoverymay result. Any residual neurological deficit ismost often present in the upper extremities withmost marked impairment in finger movement.The mere quiver of movement of a single muscle

or the presence of deep reflexes in the lower ex-tremity in spite of an otherwise complete motor andsensory loss has enabled the authors to give aguarded but reassuring prognosis to the family.They may be told that there is a fair chance ofrecovery of motor power in the lower extremities andperhaps even complete recovery of the entire bodyas well.

SummaryTwelve cases of the acute central cervical cord

injury syndrome have been presented in detail. Oneof these cases affords the first pathological con-firmation supporting the assumptions previouslymade relative to the syndrome. The importance ofaccurate diagnosis is stressed, with emphasis placedon the fact that operation is contraindicated, thatthe prognosis may be good, and that should recoveryoccur it will follow a definite pattern.Any paper of this type, which embraces compilation

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ACUTE CENTRAL CERVICAL CORD INJURY 227

of data from many sources, cannot be written without Bedford, P. D., Bosanquet, F. D., and Russell, W. R. (1952). Lancet,2, 55.the cooperation of many individuals and allied hospital Brain, W. R., Northfield, D., and Wilkinson, M. (1952). Brain,

services. In the present instance, these include ortho- 75, 187.Brooke, W. S. (1944). J. Amer. med. Ass., 125, 117.paedic and radiology services as well as the neurosurgical. Cohn, E. (1931). Arch. Psychiat. Nervenkr., 95, 439.The authors wish to express their appreciation to the Elsberg, C. A. (1941). Surgical Disease of the Spinal Cord, Mem-

branes, and Nerve Roots. Symptoms, Diagnosis and Treatment.several staffs of the hospitals which aided in this work. Hoeber, New York.In particular they are grateful to Dr. Will Glas, Depart- Frazier, C. H. (1918). Surgery of the Spine and Spinal Cord.ofSugeryWayeConty Gnera Hosital for Appleton, New York and London.ment of Surgery, Wayne County General Hospital, for Freeman, L. W., and Wright, T. W. (1953). Ann. Surg., 137, 433.

the opportunity of presenting cases from that institution. Holmes, G. (1915). Brit. med. J., 2, 769.The authors also wish to thank Drs. James Hall and KMahngh J.A.(1947).3) ArNeuosurg. 4(Ch,91), 7, 573Adam McClay, of Munson General Hospital, Traverse Schneider, R. C. (1951). J. Neurosurg., 8, 360.

(1955). Ibid., 12, 95.City, Michigan, who have graciously supplied them with ,(Cherry, G., and Pantek, H. (1954). Ibid., 11, 546.case material. and Crosby, E. C. To be published.

Spillane, J. D., and Lloyd, G. H. T. (1952). Brain, 75, 177.Symonds, C. (1953). Lancet, 1, 451.

REFERENCES Taylor, A. R. (1951). J. Bone Jt Surg., 33-B, 543.and Blackwood, W. (1948). Ibid., 30-B, 245.

Allen, A. R. (1911). J. Amer. med. Ass., 57, 878. Woodard, J. S., and Freeman, L. W. (1956). J. Neurosurg., 13, 63.

THE MAY (1958) ISSUE

The May (1958) issue contains the following papers:-

The Neuropathy of Multiple Myeloma. Maurice Victor, Betty Q. Banker, and Raymond D. Adams.

The Relapsing Course of Certain Meningiomas in Relation to Pregnancy and Menstruation. Edwin R. Bickerstaff,J. M. Small, and I. A. Guest.

A Case of Intramedullary Neurinoma. B. Ramamurthi, V. C. Anguli, and C. G. S. Iyer.

Recurrent Multiple Cranial Nerve Palsies. Sir Charles Symonds.

Finger Tremor in Tabetic Patients and its Bearing on the Mechanism Producing the Rhythm of Physiological Tremor.A. M. Halliday and J. W. T. Redfearn.

Sensory Nerve Action Potentials in Patients with Peripheral Nerve Lesions. R. W. Gilliatt and T. A. Sears.

The Psycho-galvanic Reflex: A Comparison of A.C. Skin Resistance and Skin Potential Changes. J. D. Montagu.

Clinical Aspects of Susceptibility to Menthylpentynol. Edward Marley and Allen A. Bartholomew.

An Investigation of the Rosenow Antibody Antigen Skin Reaction in Schizophrenia. W. P. Gurassa and H. H. Fleisch-hacker.

Multilocular Cystic Encephalopathy of Infants. L. Crome.

Book Reviews.

A number of copies are still available and may be obtained from the Publishing Manager, British MedicalAssociation, Tavistock Square, W.C.1, price 17s. 6d.

the syndrome of acute central cervical spinal

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