Compressive Myelopathy

48,371 views 38 slides Jan 22, 2010
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CME on Spinal cord Diseases Compressive Myelopathy By Prof .TITO`s Unit

Compressive Myelopathy Intra medullary Intradural Extradural Extramedullary

Extramedullary Intramedullary Motor a)UMN signs Common Late b)LMN signs 1or2segments at the site of root compression wide (Ant horn cell) Sensory a)Pain Root pain Funicular pain b)Dissociated sensory loss 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,rapid malignant Symmetrical,slow , progressive benign Vertebral No Pain and gibbus Pain and Gibbus

Extradural Intradural Intramedullary Spondylosis Disc prolapse Trauma Tumor- Metastasis,multiple myeloma CVJ anomalies Fluorosis TB spine Epidural abscess Epidural haematoma Tumor- NF,meningioma , lipoma,sarcoma metastasis Arachonoiditis Sarcoidosis Cervical menigitis AVM Leukemic infiltration Arachonoid cyst Syrinx Tumor – ependymoma astrocytoma Haemagioblastoma Haematomyelia COMPRESSIVE MYELOPATHY – CAUSES (mode compression based)

Spondylosis 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

Disc degeneration Annulus Fibrosis Dehydration of disc Loss shock absorbing capacity Articular Facet Hypertrophy Load ti Posterior elements of vertebra Prolapse of annulus Rupture of annulus Herniation of Nucleous pulposus Intraforaminal hermiations Posterolateral herniations Central disk herniations

narrow canal decreased disk height posterior osteophytes disk protrusions buckled posterior longitudinal ligamentand ligamentum flavum posterior subluxation

Clinical Aspects of Spondylosis : Cervical Spondylosis : common cause of progressive myelopathy commonly affects at cervical level;C5-C6 disc commonly involved >40yrs;M>F Neck pain,Root pain and LMN signs corresponding to compression UMN signs and Post colmn involvement below the compression level Axial compression test Spurling’s test Shoulder abduction relief sign Lhermitte's Sign (Barber Chair phenomenon) Finger Escape sign

Cervical Spine - AP, lateral, and oblique disk space height Facet status Osteophyte formation Spinal alignment MRI SPINE low signal intensity – degenerated disc focal extension of disc material – herniation Herniated disc may extend above and below Ligaments calcification and changing contour Occlude the canal Compress the spinal cord

Conservative: Nonsteroidal anti-inflammatory Tricyclic antidepressants for chronic case short courses of collar stretching (traction),dynamic, isometric, strengthening exercises, aerobic exercise Lifestyle modification- low high pillows SURGERY Indications : Moderate to severe myelopathy progressive motor/gait impairment Static deficits with significant pain Anterior Cervical Diskectomy With Fusion Multiple – Level Laminectomy MANAGEMENT:

LUMBAR DISC PROLAPSE Age 20-40 yrs; L4-L5 common site Acute or chronic Back ache Sciatic pain – S1comp Postero lateral calf and heel L5comanterolateral aspect of leg and ankle Femoral pain-L2-L3 to front of thigh SLR test Bragaard test lasegue test Most of the time it needs Surgery – Fenestration, Laminotomy,Hemilaminectomy,Laminectomy Manage ment similar to Cer spondylosis

LUMBAR CANAL STENOSIS Congenital narrowing of lumbar canal L4-L5 commonly affected Cauda equina lesion M>F;40-50 yrs Neurogenic claudication Stoop test positive Usually surgery needed- laminectomy

CRANIOVERTEBRAL JUNCTION ANOMALIES CONGENITAL MALFORMATIONS Malformations of occipital bone  Basilar invagination , Remnants around foramen magnum , Clivus segmentations) Malformations of atlas  Failure of atlas segmentation from occiput , Atlantoaxial fusion Malformations of axis Atlantoaxial segmentation failure Segmentation failure of C2-C3 Dens dysplasias – os odontoideum , odontoid hypoplasia / apla ossiculum terminale persistens

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 ( 1 / 2 0) - Klippel-feil anomaly - Occipitalisation of atlas - Atlanto -axial dislocation -Arnold Chiari malformation -Dandy Walker syndrome - Occipito cervical myelo meningiocoele -Posterior fossa cysts

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

CHAMBERLAIN’S LINE joins posterior tip of hard palate to posterior rim of foramen magnum dense 3.6mm below it Basillar invagination McRae’s LINE Joins 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 bone Tip of dens should not exceed 5 mm above this line FISHGOLD’S DIGASTRIC LINE – paramedian abnormality HEIGHT INDEX OF KLAUS – dense to tuberculam line < 30 basillar invagination

Spinolamellar line – atlas not intersected in ant fusion of atlas atlanto axial dislocation CLIVUS CANAL LINE – basillar invagination

KLIPPEL FEIL SYNDROME Congenital fusion of cervical vertebrae Failure of normal segmentation of the cervical vertebrae/ somite between 3 rd and 8 th 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 : Low posterior hair line(<L4) Short neck Limitation of head and neck movements / decreased range of motion in cervical spine

upper cervical spine  earlier age Rotational loss and lateral bending is usually more pronounced than loss of flexion and extension Scoliosis, Sprengel deformity/ high scapula pterygium colli - Webbing of soft tissues on each side of the neck ; Assocd torticollis Facial asymmetry Cardiovascular- VSD, PDA Urinary 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.

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

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 the fourth ventricle Type I – Cerbellar tonsilar herniation – adult onset,syrinx Type II -Part of Vermis , Medulla & 4 th Ventricle herniating upto mid cervical region – early ages;ass with mengiomyelocele Rx to do nothing Pregessive symptomatic  upper cervical laminectomy and enlargement of the foramen magnum 1) Increased ICT  headache , 2) progressive cerebellar ataxia, 3) progressive spastic quadriparesis , 4) downbeating nystagmus 5) cervical syringomyelia 6)lower cranial nerves palsies hydrocephalus,

Syringomyelia ( syrinx , “pipe” or “tube”) A chronic progressive degenerative or developmental disorder of the spinal cord, characterized by cavitation of the central part of Cervical Canal Associated with Vertebral and Base of Skull Anomalies 90% syrinx ass with Type-I chairy malformation 20-40yrs initial ;M=F Insidious onset ,irregular progressive over 5-10yrs Pt cant say when disease began Disease depends on 1.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 type Post column,spinothalamic tract involvement later Horner syndrome can occur Usually have tropic ulcers; vague pain may be presenting feature

BARNETT`s Classification Syringobulbia : affect the brainstem(medulla , pons ) 1. Vestibular nuclei  Vertigo & nystagmus 2. Nucleus ambiguus  dysphagia & hoarseness of voice 3. Spinal trigeminal nucleus  Analgesia & thermal anesthesia on ipsilateral face (Onion skin pattern ) 4. hypoglossal nucleus  Weakness of lingual muscles & dysarthria

Patho : Gardners hydrodyanamic theory Inves : MRI with contrast – slow filling cavity ; look other skeleatl manifestations CT Myelogram ; X ray of cervical spine and skull DD for Dissociated sensory loss: Pseudosyringomyelia -small fib polyneu ; DM,amyloia,heriditary sensory,fabrys ant Spinal arte thrombosis PICA Rx Type 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 syringotomy in Type I and some II Other types – surgery not useful

INFECTIVE EPIDURAL ABSCESS : Triad – Fever;Midline dorsal pain over spine;progressive limb weakness 2/3 – hematogenous spread 1/3 – extension of a local infection Lesion mainly – compress venous plexus direct compression Staph. Aureus is common Strepto,gram neg bacilli Inc ESR/CRP MRI; CSF analysis Bacterial culture pods <25% Rx: Decompressive laminectomy /drainage + long term parentral (6-8wk) antibiotic weakness several days – not improve with surgery Cauda equina – antibiotics is enough mostly Empiric Abx : Nafcillin plus metronidazole plus either cefotaxime or ceftazidime Vancomycin (1 g every 12 hours) can be substituted for nafcillin

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 years Lumbo -Sacral( cauda equina ) commonly involved Root pain one side next sidereflex changes motor weaknessspastic ataxia&sphincter disturbance CSF: moderate lymphocytosis,elev protein – acute stage sometimes normal due to complte block MRI:loss of normal ring of CSF,loculations CT myelogram : candle gutter appearance Management Steroids can be tried Surgery if cyst formed Pain relieving medications and surgeries ARACHNOIDITIS

POTT`S DISEASE skeletal TB  spinal is common Common in paediatric and adolscence group Dorsal 42%  >Lumbar> Dorsolumbar  , Cervical   Lesion could be Florid - 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

Pathophysiology : xtraspinal source of infection  osteomyelitis and arthritis (anterior aspect of the vertebral body adjacent to the subchondral plate) spread to adjacent intervertebral disks Child 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

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 loss Pain can be spinal or radicular Neurologic abnormalities - 50% spinal cord compression with paraplegia paresis, impaired sensation, nerve root pain, cauda equina syndrome Investigations Mantoux;IFN release assays; sputum AFB CXR;Xray Thracolumbar spine;CT spine MRI

X Ray appearances Lytic destruction of anterior portion of vertebral body anterior 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

Tb 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 Inflammatory Edema –vascular stasis,toxin Extradural Mass – Tuberculous ostetis,abscess Bony Disorder – Sequestra , Internal Gibbus Meningeal changes – ‘ dura as rule not involved’ Extradural granulation – contract  cicatrization  peridural fibrosis  paraplegia Infarction of spinal cord - Ant spinal artery Endarteritis, Periarteritis , Thrombosis Changes in Spinal cord- Myelomalacic,Syringomyelic change

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 pack and surgery

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 spasms 7.severe neuro deficcit Surgical techniques: 1 . Decompression -Failed response 2 . 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- T ransposition 6 . Laminectomy STS,secondary stenosis , posterior disease 7. Costotransversectomy – in tense paravertebral abscess

VASCULAR – Compressive myelopathy Epidural Haematoma : predisposing factors: Anticoagulation therapy,Trauma,Bleeding disorder,tumor Acute focal &/ radicular Pain Acute Spastic paraparesis or conus medularis syndrome Surgical decompression Haematomyelia : Haemorrhage into the substances of spinal cord  Trauma,parenchymal vascular malformations,vasculitis,tumors ACUTE PAINFUL TRANSVERSE MYELOPATHY – INTRAMEDULLARY subarachnoid hge can occur MRI; Spinal Angiography Conservative management only surgery if AVM is the cause

AV Malformation of cord: Reversible cause of paraparesis located posteriorly along the surface of the cord or within the dura at or below the midthoracic level Clinical features:  middle-aged man  progressive myelopathy that worsens slowly or intermittently with periodic remissions  incomplete sensory, motor, and bladder disturbances  mixture of upper and restricted lower motor neuron signs  Pain over the dorsal spine, dysesthesias , or radicular pain  symptoms 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 vessels surgical if ruptured

TUMORS AND COMPRESSIVE MYELOPATHY METASTASIS: Metastasis is common tumor(high marrow) Epidural type of compression is common Throacic is common; Lumbar&Sacral – Prostate and ovarian Breast>Lung>Prostate>Kidney>Lymphoma> Plasmacell dyscrasia old age pt Vertebral pain with acute onset of neurological deficit MRI – hypodense in T1;doesnot cross the adjacent disc space Bone 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 RT) Prognosis: Ambulatory pt – good response with RT Fixed motor deficit <12hr good response >12hr chance to improve >48hr no improvement

Intradural : Benign and slow growing ; progressive compression signs Meningioma,Neurofibroma,chordoma,lipoma dermoid,sarcoma MENINGIOMA: benign throcic cord level or near foramen magnum from  arachonoid cells forms Psommama bodies Radiation therapy-  Gammma Knife, proton beam treatment external beam NEUROFIBROMA: from schwwan cells arises near posterior root begins with radicular symptoms asymetric progressive spinal cord syndrome need surgical treatment INTRAMEDULLARY: uncommon cervical commonly central cord syndrome or hemicord syndrome Ependymoma,Haemangioblastoma,secondaries astrocytoma ( lowgrade ) Microsurgical debulking can be tried RT is not useful Primary tumors of spinal cord common in cervical

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