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Spinal cord Diseases Compressive Myelopathy Prof Nabil Khalil Suez canal university Ismailia EGYPT

Compressive spine disease

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Page 1: Compressive spine disease

Spinal cord Diseases Compressive Myelopathy

Prof Nabil KhalilSuez canal university

Ismailia EGYPT

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Compressive Myelopathy

Intra medullary

Intradural extramedullary

Extradural exrtamedullary

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Extramedullary Intramedullary

Motor

a)UMNL signs Common Late

b)LMNL signs

1or2segments at the site of root compression

wide (Ant horn cell)

Sensory

a) Pain Root pain dythesia pain

b) Dissociated sensory loss(loss of pain& temperature but preseved touch)

Absent present

c) Sacral sensation Lost Preserved

d) Joint sensation Lost Late involvement

e) Lhermitte`s sign present absent

Autonamic involvement – Bowel and Bladder

Late Early

Intradural Extradural

Mode of onset Asymmetrical , acute,rapidmalignant

Symmetrical,slow, progressiveBenign

Vertebral No Pain and gibbus Pain and Gibbus

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Extradural Intradural Intramedullary

SpondylosisDisc prolapseTraumaTumor-Metastasis,multiple myelomaC V J anomaliesTB spineEpidural abscessEpidural haematoma

Tumor-NF,meningoma, lipoma,sarcoma metastasisArachonoiditisSarcoidosisCervical menigitisAVMLeukemic infiltrationArachonoid cyst

SyrinxTumor – ependymoma astrocytoma HaemagioblastomaHaematomyelia

COMPRESSIVE MYELOPATHY – CAUSES (mode compression based)Degenerative,CONGENITAL,trauma,tumours,vuscular,infections

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COMPRESSIVE MYELOPATHY – CAUSES

1-Degenerative2-CONGENITAL3-infections4-vuscular5-Tumours6-trauma

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Spondylosis 1-Degenerative

• spondylosis is a general term encompassing a number of degenerative conditions– Degenerative disc disease (DDD)– Spinal stenosis– With or without degenerative facet joints– With or without the formation of osteophytes– With or without a herniated disc

• One single component as a diagnosis is rare,

Usually multiple signs.

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DISC DISEASE

Disc degeneration Annulus Fibrosis

Dehydration of discLoss shock absorbing capacity

Articular Facet Hypertrophy

Load to Posterior elements of vertebra

Prolapse of annulusRupture of annulus

Herniation of Nucleous pulposus

Intraforaminal hermiations Posterolateral herniations Central disk herniations

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Advaced cervical spondylosisnarrow canaldecreased disk heightposterior osteophytesdisk protrusionsbuckled posterior longitudinal ligamentand ligamentum flavumposterior subluxation

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Clinical Aspects of Spondylosis:Cervical Spondylosis:

common cause of progressive myelopathycommonly affects at cervical level;C5-C6 disc commonly involved >40yrs; M>FNeck pain,Root pain and LMN signs corresponding to compressed rootUMN signs and Post colmn involvement below the compression level

Axial compression test Neck movement test Shoulder abduction relief sign

Lhermitte's Sign(Barber Chair phenomenon) Finger Escape sign

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Cervical Spine - AP, lateral, and oblique disk space height Facet statusOsteophyte formation Spinal alignment

MRI SPINElow signal intensity – degenerated discfocal extension of disc material – herniationHerniated disc may extend above and belowLigaments calcification and changing contourOcclude the canalCompress the spinal cordMid cervical region -common

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Conservative:Nonsteroidal anti-inflammatory Tricyclic antidepressants for chronic caseshort courses of collarstretching (traction),dynamic, isometric, strengthening exercises, aerobic exerciseLifestyle modification- low high pillows

SURGERY Indications: Moderate to severe myelopathy

progressive motor/gait impairment Static deficits with significant pain

Anterior Cervical Diskectomy With Fusion or notPosterior Multiple – Level Laminectomy

MANAGEMENT:

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LUMBAR DISC PROLAPSEAge 20-40 yrs; L4-L5 common siteAcute or chronic Back acheSciatic pain – S1 root compPostero lateral calf and heel

L5 root companterolateral aspect of leg and ankleFemoral pain-L2-L3 rootsRadiate to front of thigh

SLR test

Foot dorsiflexion test

lasegue test

Most of the time it may need Surgery : – Fenestration,Laminotomy,Hemilaminectomy,Laminectomy

Medical Management similar to Cervical spondylosis

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LUMBAR CANAL STENOSIS

Congenital narrowing of lumbar canalL4-L5 commonly affectedCauda equina lesionM>F;40-50 yrsNeurogenic claudicationClaudicating distance positive

Usually surgery needed- laminectomy

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CRANIOVERTEBRAL JUNCTION ANOMALIES

Malformations of occipital boneBasilar invagination, Remnants around foramen magnum,Clivus segmentations)

Malformations of atlasFailure of atlas segmentation from occiput, Atlantoaxial fusion

Malformations of axisAtlantoaxial segmentation failureSegmentation failure of C2-C3Dens dysplasias – os odontoideum, odontoid hypoplasia/apla

ossiculum terminale persistens

2-CONGENITAL MALFORMATIONS

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2. DEVELOPMENTAL AND ACQUIRED ABNORMALITIES

Foramen magnum abnormalities

ATLANTOAXIAL INSTABILITY

SKELETAL ANOMALIES

NEURAXIAL ANOMALIES

-Foraminal stenosis (eg.achondroplasia ,MPS )

-Secondary basilar

invagination eg.

Paget’disease, osteomalacia, hyperparathyroidism

-Traumatic atlantoaxial / occipitoatlantal dislocation-Degenerative (ligamentous disruption at CV junction)-Inflammatory (RA, ankylosing spondylitis)-Tumours ( chordoma, syringomyelia, NF )-Down’s syndrome

-Platybasia-Basilar invagination ( 10 / 20)

-Klippel-feil anomaly-Occipitalisation of atlas-Atlanto-axial dislocation

-Arnold Chiari malformation-Dandy Walker syndrome-Occipito cervical myelomeningiocoele-Posterior fossa cysts

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CV junction malformation Vs Neurological symptoms

Mechanisms:– Bone and soft tissues compress directly on medulla or

upper cervical cord– Associated CNS developmental anomalies – Raised ICT due to impaired CSF flow

Around 20-25 yrs; both sexes Painful or restricted cervical movements Pyramidal signs with varying motor disabilities in

one or mostly all limbs. Muscle wasting in UL;progressive over 5yrs

Cerebellar signs usually;sensory symptoms(lat and Pos)

Neuro vascular symptoms rare. transient reversible weakness may present

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CHAMBERLAIN’S LINE -joins posterior tip of hard palate to posterior rim of foramen magnum dense 3.6mm below it-Basillar invagination

McRae’s LINEJoins anterior and posterior edges of foramen magnum: sagittal diameter of foramen magnum. (Avg – 35mm);dense below the line

foramen stenosis

MCGREGOR’S LINE (Basal line)-Joins hard palate to lowest point of occipital boneTip of dens should not exceed 5 mm above this line

FISHGOLD’S DIGASTRIC LINE – paramedian abnormality

HEIGHT INDEX OF KLAUS – dense to tuberculam line < 30basillar invagination

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KLIPPEL FEIL SYNDROME• Congenital fusion of cervical vertebrae• Failure of normal segmentation of the cervical vertebrae/somite

between 3rd and 8th weeks of fetal development (rather than a secondary fusion)

• Incidence – 1 in 42,000 births ;more in females• Autosomal dominant inheritance – C2-C3 fusion. Autosomal recessive –

C5- C6 fusion

FEIL’S TRIAD :1. Low posterior hair line(<L4)2. Short neck3. Limitation of head and neck movements / decreased range of motion in cervical spine

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KLIPPEL FEIL SYNDROME cont.upper cervical spine earlier ageRotational loss and lateral bending is usually more pronounced than loss of flexion and extensionScoliosis, Sprengel deformity/ high scapulapterygium colli - Webbing of soft tissues on each side of the neck ; Assocd torticollis Facial asymmetryCardiovascular- VSD, PDAUrinary tract abnormalities – agenesis of kidney, horseshoe kidney, hydronephrosis,Deafness (absence of auditory canal and microtia)Neurologic deficit- facial nerve Palsy, rectus muscle palsy, ptosis of eye, cleft palate, etc

Cervical spine routine x-ray followed by flexion/extension lateral X-rays. - flattening and widening of vertebrae, hemivertebrae or block vertebrae, instability. MRI with head flexed and extended - subluxation and cord compression

cord anomalies.

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Occipitalization of Atlas Atlando Axial Dislocation

Diagnosis- Atlas-Dens interval of more than 5 mm in children and more than 3 mm in adults is diagnostic

Platybasia >135

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Arnold-Chiari Malformation

1) Extension of a tongue of cerebellar tissue, posterior to the medulla and spinal cord, into the cervical canal 2) displacement of the medulla into the cervical canal, along with the inferior part of thefourth ventricle

Type I – Cerbellar tonsilar herniation – adult onset,syrinxType II-Part of Vermis, Medulla & 4th Ventricle herniating upto mid cervical region – early ages;ass with mengiomyeloceleTreatmentto do nothingProgessive symptomaticupper cervical laminectomy andenlargement of the foramen magnum

1) Increased ICTheadache,2) progressive cerebellar ataxia, 3) progressive spastic quadriparesis,4) downbeating nystagmus5) cervical syringomyelia6)lower cranial nerves palsieshydrocephalus,

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Syringomyelia (syrinx, “pipe” or “tube”)

A chronic progressive degenerative or developmental disorder ofthe spinal cord, characterized by cavitation of the central part of Cervical Canal

Associated with Vertebral and Base of Skull Anomalies90% syrinx ass with Type-I chairy malformation20-40yrs initial ;M=FInsidious onset ,irregular progressive over 5-10yrsPt cant say when disease beganDisease depends on1.cross sectional extent 2.longitu extent.

Classic elements: a) segmental weakness and atrophy of the hands and arms b) loss of some or all tendon reflexes in the arms

c)segmental anesthesia of a dissociated type (loss of pain and thermal preservation of touch)over the neck,shoulders,and arms(cape sensation)

Pyramidal tract: UL : Reflexes preserved or brisk amyotrophy of shoulders and hands spastic

LL: Spastic typePost column,spinothalamic tract involvement laterHorner syndrome can occurUsually have tropic ulcers; vague pain may be presenting feature

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BARNETT`s Classification

Syringobulbia : affect the brainstem(medulla ,pons)1. Vestibular nuclei Vertigo & nystagmus2. Nucleus ambiguus dysphagia & hoarseness of voice3. Spinal trigeminal nucleus Analgesia & thermal anesthesia on ipsilateral face (Onion skin pattern )4. hypoglossal nucleus Weakness of lingual muscles & dysarthria

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Investigations: MRI with contrast – slow filling cavity ; look other skeleatl manifestationsCT Myelogram; X ray of cervical spine and skull

DD for Dissociated sensory loss:Pseudosyringomyelia-; DM,,ant Spinal artery thrombosisPICA ischaemia

TreatmentType I-surgical decompression of foramen

magnum and upper cervical canal(relieve headache, pain,mildy improve motor sym;ataxia&nystagmus persist

Syringostomy or Shunting by T tube by syringotomyin Type I and some II

Other types – surgery not useful

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3-INFECTIVE EPIDURAL ABSCESS :

Triad – Fever;Midline dorsal pain over spine;progressive limb weakness

2/3 – hematogenous spread 1/3 – extension of a local infectionLesion mainly – compress venous plexus leads to oedema

or direct compression of neural tissue

Staph. Aureus is commonStrepto,gram neg bacilli

Inc ESR/CRPMRI; CSF analysisBacterial culture positive <25%

Rx: Decompressive laminectomy /drainage + long term parentral(6-8wk) antibioticweakness several days – not improve with surgery immediately

In Cauda equina – antibiotics is may be enough mostlyEmpiric Abx:Nafcillin plus metronidazole plus either cefotaxime or ceftazidimeVancomycin (1 g every 12 hours) can be substituted for nafcillin

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Syndrome of painful root and spinal cord symptoms;patchy motor symptoms

adhesions between the arachnoid and dura

Causes;TB,syphilis,viral & bacterial meningitis,anesthesia,LP

acute or delayed for weeks, months, or even yearsLumbo-Sacral(cauda equina) commonly involvedRoot pain one side next sidereflex changes

motor weaknessspastic ataxia&sphincter disturbance

CSF: moderate lymphocytosis,elev protein – acute stagesometimes normal due to complte block

MRI:loss of normal ring of CSF,loculationsCT myelogram: candle gutter appearance

ManagementSteroids can be triedSurgery if cyst formedPain relieving medications and surgeries

ARACHNOIDITIS

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POTT`S DISEASE T B

skeletal TB spinal is commonCommon in paediatric and adolscence groupDorsal 42% >Lumbar>Dorsolumbar , Cervical

Lesion could beFlorid - invasive and destructive lesion Non destructive - lesion suspected clinically but identifiable by investigations Carries sicca Hypertrophied Periosteal lesion.

Anatomically the lesion could be :Paradiscal - destruction of adjacent end plates Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process Central - Cystic or lytic, concertina collapse Anterior –longitudinal lig Synovitis in post facet

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Pathophysiology:xtraspinal source of infection osteomyelitis and arthritis

(anterior aspect of the vertebral body adjacent to the subchondral plate)

spread to adjacent intervertebral disksChild may de direct invasion

bone destruction

vertebral collapse and kyphosis(throcic>lumbar>cervical)

abscesses, granulation tissue, or direct dural invasion

spinal cord compression and neurologic deficits

Kyphotic deformity

Healing by fibrous tissue

bony ankylosis vertebrae.

Paravertebral abscess anterior longitudinal lig

Groin abscess Thoracic abscess

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Clinical Features:Back pain is the earliest and most common symptom Duration of symptoms at the time of diagnosis is 3-4 months fever and weight lossPain can be spinal or radicular Neurologic abnormalities - 50%

spinal cord compression with paraplegiaparesis, impaired sensation, nerve root pain, cauda equina syndrome

InvestigationsTubercline Test -Mantoux;IFN PCR, sputum ,AFBXR;Xray Thracolumbar spine; CT spineMRI

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X Ray appearancesLytic destruction of anterior portion of vertebral bodyanterior wedging Collapse of vertebral body Reactive sclerosis Intervertebral disks shrunk or destroyed Vertebral bodies may show destruction Enlarged psoas shadow with or without calcification Fusiform paravertebral shadows

MRI

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T B spine with PARAPLEGIA

INCIDENCE 10-30% Dorsal spine (MC) Motor functions affected before /greater than sensory Sense of position & vibration last to disappear

Patho of Tuberculoses Paraplegia

1. Inflammatory Edema –vascular stasis,toxin 2. Extradural Mass – Tuberculous ostetis,abscess 3. Bony Disorder – Sequestra, Internal Gibbus 4. Meningeal changes – ‘dura as rule not involved’ Extradural granulation

–contractcicatrizationperidural fibrosis paraplegia 5. Infarction of spinal cord - Ant spinal artery Endarteritis, Periarteritis,

Thrombosis6. Changes in Spinal cord- Myelomalacic,Syringomyelic change

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Seddon’s Classification: GROUP A_-Early onset - in active stage of the disease within first 2 years(active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus, stenosis and deformity can cause compression) GROUP B -Late onset- Usually after 2 years of onset of the disease(Healed disease - Usually internal gibbus and acute kyphotic deformity)

Kumar’s classification(paraplegia) 1 Negligible :Unaware of neural deficit, Plantar extensor/ Ankle clonus 2 Mild :Walk with support 3 Moderate :Nonambulatory, Paralysis in extention,sensory loss <50% 4 Severe :3+ paralysis in flexion/sensory loss>50%/ Sphinters involved

MANAGEMENT:ATT – prolonged R and surgery may be

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Surgical indications:1. No sign of Neurological recovery after trial of 3-4 weeks therapy 2. Neurological complication during treatment 3. Neuro deficit becoming worse 4. Recurrence of neuro complication 5. Prevertebral cervical abscesses,neurological signs 6. Advanced cases- Sphincter involvement, flaccid paralysis, Severe flexor spasms7.severe neuro deficcit

Surgical techniques: 1. Decompression -Failed response2 .Debridement+/- Failed response after 3-6 fusion months,3 .Debridement +/- Recrudescence of disease DECOMP+/- fusion 4 Debridement+/- Prevent severe Kyphosis fusion 5 .Anterior Severe Kyphosis +neural deficit- Transposition 6 .Laminectomy STS,secondary stenosis, posterior disease

7.screws fixation and bone graft7. Costotransversectomy– in tense paravertebral abscess

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4-VASCULAR – Compressive myelopathy

Epidural Haematoma:predisposing factors:

Anticoagulation therapy,Trauma,Bleeding disorder,tumorAcute focal &/ radicular Pain Acute Spastic paraparesis or conus medularis syndromeSurgical decompression

Haematomyelia: Haemorrhage into the substances of spinal cord

Trauma,parenchymal vascular malformations,vasculitis,tumorsACUTE PAINFUL TRANSVERSE MYELOPATHY – INTRAMEDULLARYsubarachnoid hge can occur MRI; Spinal AngiographyConservative management only

surgery if AVM is the cause

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AV Malformation of cord:

Reversible cause of paraparesislocated posteriorly along the surface of the cord or within the duraat or below the midthoracic level

Clinical features:middle-aged manprogressive myelopathy that worsens slowly or intermittently with

periodic remissionsincomplete sensory, motor, and bladder disturbancesmixture of upper and restricted lower motor neuron signsPain over the dorsal spine, dysesthesias, or radicular painsymptoms that change with posture, exertion such as singing, menses

Foix-Alajouanine syndrome - progressive thoracic myelopathy with paraparesis

Investigation:MRI contrast;CT myelogram;Selective spinal angiography

Management: Endovascular embolization of feeding vesselssurgical if ruptured

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5-TUMORS AND COMPRESSIVE MYELOPATHY

METASTASIS:Metastasis is common tumor(high marrow)Epidural type of compression is commonThroacic is common; Lumbar&Sacral – Prostate and ovarianBreast>Lung>Prostate>Kidney>Lymphoma>Plasmacell dyscrasiaold age pt Vertebral pain with acute onset of neurological deficit

MRI – hypodense in T1;doesnot cross the adjacent disc spaceBone scan may be useful to detect the all other metastasis

Management:-Glucocorticoid – upto 40mg/d Dexamethasone-RT – 3000cGy in 15 daily fractions-Surgery- laminectomy or vertebral resection(neuro signs worsen even with Radiotherapy)

Prognosis:Ambulatory pt – good response with RTFixed motor deficit-time of surgery

<12hr good response>12hr chance to improve >48hr no improvement

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Intradural : Benign and slow growing ; progressive compression signsMeningioma,Neurofibroma,chordoma,lipomadermoid,sarcoma

MENINGIOMA: benignthrocic cord level or near foramen magnumfrom arachonoid cells forms Psommama bodies Radiation therapy- Gammma Knife, proton beam treatment

external beamNEUROFIBROMA: from schwwan cells

arises near posterior rootbegins with radicular symptomsasymetric progressive spinal cord syndromeneed surgical treatment

INTRAMEDULLARY: uncommoncervical commonlycentral cord syndrome or hemicord syndromeEpendymoma,Haemangioblastoma,secondaries

astrocytoma(lowgrade)Microsurgical debulking can be triedRT is not useful

Primary tumors of spinal cord common in cervical

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6-Spinal Cord Injuries; and spine Fractures

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CAUSES OF SCI

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SYMPTOMS

The vertical location of the injury

• In general, injuries that are higher in our spinal cord produce more paralysis.

The severity of the injury.(T S section)

• Spinal cord injuries are classified as partial or complete, depending on how much of the cord width is damaged.

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Classification of Injuries Simple Compression (1-2 column injury) Stable burst (2-3 column injury) Unstable burst (3 column injury) Flexion distraction (2 nonconjoined columns) Chance (3 column failure all in tension) Fracture dislocation (3 column injury) Pure Dislocation (rare) (3 column injury) Pathological (any and all) Insufficiency (any and all) Multiple contiguous fractures (nly 1-2 columns)

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Unstable Burst 3 column involvement Possible neuro

involvement Severe communition Significant pedicle

widening Look for laminar

fracture (asso. with root entrapment)

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Treatment of Neurologic Injury

• Methylprednisolone protocol (30 mg/kg loading and 5.4 mg/kg x 24 (or 48) hours

• Only for central injuries- not peripheral nerve injuries (conus is central injury)

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Time to healing

• Most non-surgical fractures heal within 12 weeks• Back support with braces(types)on

whenever .patient upright• When healed- 4 weeks of PT for deconditioning• Residuals of barometric sensitive discomfort and

occasionally problems with lifting• 10 % may need to go on to surgery from

instability,NEUROLOGIC DEFICITS,Pain.• Surgery is reduction and fixation by pedicle screws or

any suitable device

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Thank You