Spinal Cord Compression

Postgraduate seminarNeurology UnitBy: Chidimma A Onwurah

Outline

Introduction Anatomy Aetiology Epidemiology Clinical features Investigations Management Conclusion

Spinal Cord Function

Transmits neural signals and contains neural circuits that control reflexes

Four major functions: Motor Sensory Reflex Autonomic function

Anatomy

Anatomy • Spinal cord terminates

at L1-L2• Covered by 3

connective tissue: Dura, Pia & Arachnoid

• Dural sac ends at S2

• Terminology– Conus medullaris: most

distal bulbous part– Filum termiale: tapering

part of conus medullaris (mostly fibrous tissue)

– Cauda equina: distal collection of nerve roots

3 layers of spinal coverings Pia mater

Arachnoid mater

Dura mater

Gray matter of spinal cord

Cell bodies of neurons which receive efferent information from the brain and send it to skeletal myocytes (somatic motor innervation)

Cell bodies of neurons which receive efferent information from the brain and send it to smooth myocytes, cardiac myocytes, and glands (autonomic motor innervation)

Cell bodies of neurons which receive afferent information from spinal nerves and send it toward the brain

White matter Carries afferent information into dorsal horn of gray matter

Carries efferent information away from ventral horn of gray matter

Corticospinal tract

Spinothalamic tract and dorsal column lemniscal pathway

Arterial supply to the spinal cord Intraspinal Arteries

Anterior spinal artery▪ Supply the ventral gray and white matter, except the dorsal

horns and dorsal white matter Posterior spinal arteries

▪ Supply the dorsal horns and dorsal white matter Extraspinal Arteries

Radicular arteries

Causes of Spinal Cord Compression

EXTRADURAL Vertebral: epidural abscess /Infection-

TB & bacterial; vertebral collapse, disc prolapse, spondylosis, spondylolisthesis, Paget’s dx, neoplasm (10 & 20)

Non- vertebral: Hodgkin’s leukemic infiltration or metastases, abscess, cyst

Contd INTRADURAL A] Extramedullary

▪ Neoplasm, nerve sheath tumours (schwannomas and neurofibromas ) meningioma; arachnoiditis; arachnoid cyst

B] Intramedullary ▪ Neoplasm, astrocytomas, ependymomas,

hemangioblastomas (primary spinal tumours); cyst/syringomyelia; haematomyelia [AVMalformation] and venous angiomas

Epidemiology

USA: spinal stenosis (54%), tumors (26%), ischemia (8%), infection (7%)

Gupta et al in India(2005-2008): spinal tumors (27%), TB spine (25%), transverse myelitis (22%)

Ogunniyi et al in Ibadan (1988-1993): spondylotic myelopathy (30%), TB spine (25%), neoplastic (12%)

History (SCCx) Onset Deficits

Motor Sensory

Progression Time to maximum disability Changes in deficits Sphincter dysfunction Autonomic changes Preceding illness Systemic complaints

Clinical findings UMN: preserved muscle bulk or atrophy of

disuse, no fibrillation/ fasciculation, hypertonia, brisk DTR, extensor plantar response, absent abdominal reflex

These occur late with intramedullary lesions but early with extramedullary lesion.

LMN: wasting, fibrillation/fasciculation, hypotonia, hyporeflexia, flexor plantar response

Inverted supinator jerk : C5/C6 lesion

Lasegue’s sign – lifting a straight lower limb causes pain.Shows a herniated disc

Shober’s sign- <5cm increase in distance between standing and bending to touch the toes when marks are placed 10cm above and 5 cm below the L5 vertebraPositive in ankylosing spondylosis

Syringomyelia

Fluid filled cavitation in the center of the cord

May be late sequelae of trauma Most common site is the cervical cord

Loss of pain and temperature Cape sensory loss Weakness of muscles in arms with atrophy and

hyporeflexia Later- leg weakness, spasticity with brisk

reflexes

Syringomyelia Can be associated with

Arnold Chiari malformation, spinal arachnoiditis, scoliosis, spinal vertebrae misalignment, spinal tumors, spina bifida, meningitis

Other central cord lesions: Hydromyelia, HematomyeliaIntramedullary tumors

Cervical spondylosis with myelopathy Most common form of myelopathy Degenerative disease of the spine

usually at mid and lower cervical spine vertebrae Narrowing of spinal canal and vertebral

foramina Progressive injury of the spinal cord and

spinal roots Prevalence of cervical degenerative

disease reaches 95 % at the age of 65 years

Pathology Fraying of annulus fibrosus Extension of disc material in the

spinal canal Bulging of annulus fibrosus Osteophytes Hypertrophied longitudinal ligaments

and ligamentum flavum Compression of posterior roots may

lead to degeneration in posterior columns

Compression of spinal cord may produce demyelination or focal necrosis

Pathogenesis

No clear explanation Compression High mobility of lower cervical vertebrae Diminished AP diameter of the spinal

canal Compression of spinal arteries and

ischemia Trauma from sudden extreme extension

Clinical features Radiculopathy Spondylotic Myelopathy Myeloradiculopathy Rotational vertebral artery occlusion,

Vertebro-basillar insufficiency Lhermitte’s Spurling’s- turning the patients head to the

affected side and flexing the neck leads to pain along the affected nerve/dermatome.

Intermittent neurogenic claudication

Bladder disturbance Fingers may feel swollen or clumsy Weakness of small muscles of the hand Clumsiness Weakness of the legs

Spasticity is more than weakness Quadriparesis

Muscle stretch reflexes Loss of biceps reflex, but exaggerated triceps

reflex Extensor plantar reflex

Sensory Changes Impaired vibration sense, joint position sense Romberg sign may be present Sensory gait ataxia in some subjects

Radiculopathy Symptoms usually begin on waking Symptoms worsen with Valsalva activities Motor and reflex changes

▪ C5/C6 disc herniation compresses C6 root▪ C6/C7 disc herniation compresses C7 root

Brown-sequard syndrome/lateral cord syndrome

Cord hemisection

Trauma or tumour De-myelination Burst fracture

Sign and symptoms Weakness on side of

lesion Dissociated sensory loss

▪ Contralateral loss of pain and temperature to lesion, 1 or 2 levels below;

▪ Ipsilateral propioceptive loss 1-2 segments below

Brown Sequard syndrome

Posterior cord syndrome Causes:

Cervical spondylosis, Multiple sclerosis Demyelination Spinal cord tumor Atlanto-axial subluxation Sub-acute combined degeneration

Signs Sensory ataxia (propioceptive loss) Urinary incontinence Lhermitte signs

Vascular disease of cord Arteriovascular malformation and

venous angiomas Occur primarily in the thoracic cord May present as acute, subacute or

chronic compressive lesion Can cause recurrent symptoms Associated with pain and bloody CSF if

they bleed.

Complete cord

Trauma- commonest cause Features:

Loss of sensory Loss of motor Loss of autonomic All below the level of lesion

Conus medullaris syndrome

•D12 burst fracturecompresses theconus.•All lumbar and sacralsegments canbe compressed

Conus medullaris syndrome

Early disturbance of bladder and bowel control, urine retention, constipation

Erectile impotence Symmetrical saddle anesthesia Pain is not common, but may occur

late

CAUDA EQUINA SYNDROME

•Acute central disc prolapse L4/5. •Medially placed sacral roots sustainmaximumcompression

Cauda equina syndrome

Early radicular pain in the distribution of lumbosacral roots, usually asymmetric

Pain May be unilateral Worse when lying down

Flaccid paresis - glutei, posterior thigh muscles, anterolateral leg muscles, and foot

Asymmetric saddle anesthesia Loss of ankle jerk Sphincter disturbance uncommon

Conus Medullaris vs. Cauda Equina lesionFindings CONUS

MEDULLACAUDA EQUINA

Motor Symmetric Asymmetric Sensory loss Saddle Saddle Pain Uncommon Common Reflexes Increased Decreased Bowel/bladder Common Uncommon

Spinal Tuberculosis Dorsolumbar region is the most frequently involved

with D.11 vertebra being most often affected Radiological features:

disc space narrowing only kissing lesions; half-moon wedge collapse of vertebra; vertebra plana; lesions localised in the vertebral body and/or its

appendages para-spinal abscesses; complete destruction of vertebral body.

Spinal tuberculosis

Other causes of spinal canal narrowing Ankylosing spondylitis Ossification of posterior longitudinal

ligament Paget disease Achondroplasia Platybasia and basilar invagination

Intra spinal tumors Most intraspinal tumours are benign Effects are usually due to compression

rather than infiltration Anatomical groups

Intramedullary▪ Primary▪ Metastasis

Extramedullary▪ Primary ▪ Metastasis

Primary neoplasms Intramedullary

▪ Astrocytomas, oligodendrogliomas, Ependymomas lipomas, teratomas

Extramedullary▪ Neurofibromas, more intradural than extradural ▪ Meningiomas, sarcomas, vascular tumours, chordomas

Secondary neoplasms Extramedullary

▪ Extradural▪ Carcinomas, lymphoma, myeloma

▪ Intradural▪ Usually lymphoma spreading to the meninges

Intramedullary▪ Bronchogenic carcinoma

Clinical features: tumors

Compression of spinal cord by tumor reduces the CSF space arround the cord

Loculation of CSF below the lesion Increase protein and xanthochromia

(Froin Syndrome

Intramedullary vs Extramedullary

Intramedullary Extramedullary

Poorly localized burning pain Prominent radicular pain

“sacral sparing” Early sacral sensory loss

Corticospinal tract signs appear later

Early spastic weakness in legs

Usually rapid progression (usually malignant lesion)

Usually slow progression (usually benign lesion)

Foramen magnum syndrome

Pain Suboccipital

Lhermitte symptoms Quadriparesis Neck stiffness Atrophy of the muscles of the hands and dorsal

neck muscles Lower cranial nerve palsies, IX – XII Horner’s syndrome Papilledema Downbeat nystagmus Cerebellar ataxia

Common Investigation

Spinal Xray- plain and contrast Spinal CT Spinal MRI Bone scan Tumor markers

Neurofibroma

Cervical astrocytoma

Lumbar spondylosis

Spinal meningioma

Cervical spondylosis

Treatment Goals: palliative, pain control,

preserve or restore ambulation & stability

Start definitive treatment ideally within 24 hours of Dx

Carefully plan surgery: consider fitness, prognosis, preferences

Urgent <24hours RT for definitive treatment if unsuitable for surgery

General management Bladder dysfunction – anticholinergics-

oxybutynin, α-adrenergic blockers-doxazocin, prazocin

Bowel dysfunction Decubitus ulcers Spasticity- baclofen, diazepam, dantrolene,

clonidine, tizanidine Deep vein thrombosis- antiembolism

stockings, pneumatic compression stocking, LMWH, IV heparin in acute DVT. INR 1.5-2.5, warfarin . Monitor PTTK,

Metastatic C management Analgesia: Conventional by WHO pain

relief ladder, ?specialist pain care Bisphosphonates: myeloma or breast Ca

and prostate if analgesia has failed; not for others

Corticosteroids: 16mg loading dexameth- 16mg/d, over 5-7/7 after RT or surgery- complications: sepsis, bowel perforation

Biopsy & stage (no., sites, extent)

Surgery

Vertebroplasty/kyphoplasty - consider if no malignant spinal cord compression or instability &:- mechanical pain resistant to analgesia- vertebral body collapse

Surgery: consider urgently if spinal instability, mechanical pain resistant to analgesia

External spinal support (halo, orthosis) if unsuitable for surgery

Radiotherapy Urgent (<24hrs) if definitive treatment or

unsuitable for surgery unless:- tetraplegia or paraplegia >24hrs and pain controlled; overall poor prognosis

Fractionated RT- definitive Tx if no neuro impairment, pain or instability

Post-operative RT offered when wound healed

TB: treatment/complications Treatment: AntiTB for 12 months,

Spinal support, decompression

Complications: Arachnoiditis, Froin syndrome, myelitis, Intraspinal granuloma, vasculitis with infarction,

Rehabilitation

Motorized wheel chair Pneumatic mattress Dedicated seats, toilets, walkways

Conclusion

Cord compression presents with a number of features attributable to the site of compression

The commonest cause is traumatic Non traumatic causes could be broadly

classified into extradural and intradural causes

Urgent diagnosis and treatment of acute SCCC is important to preserve neurologic function

Thank you