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SPINAL CORD & ITS COMPRESSIVE DISORDERS

SHRUTHI.S.JAYARAJ 53rd, Calicut Medical College

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• Basics of spinal cord•Determining the level of lesion• Special pattern of spinal cord diseases• Compressive disorders of spinal cord

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SPINAL CORD• Most important content of the vertebral

canal• Extension : medulla,upper border of C1 till

lower border of L1 /upper border of L2 (termination is variable)

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• Normal spine has a cervical and lumbar lordosis and thoracic kyphosis

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• Cervical enlargement : C3 to T2

• Lumbar enlargement : L1 to S3

• Lowest conical part : conus medullaris

( S3,S4,S5)• Conus continuous as a

fibrous cord- filum terminale - extend to coccyx

• Lower end of central canal expand to form terminal ventricle- conus

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Concept of spinal segments• Length of spinal cord giving

origin to rootlets of one spinal nerve

• 31 spinal segments• C - 8 • T - 12• L - 5• S - 5• C - 1

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• During embryological dvpt, growth of the cord lags behind that of vertebral column

• Lower spinal nerves have to taka an increasingly downward course to enter the corresponding intervertebral foramina-bundle of nerves- cauda equina

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• Important for localising lesions causing spinal cord compression• For eg, sensory loss below umbilicus – T10 – involvement of cord

adjacent to 7th or 8th thoracic vertebral body

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• MENINGES• Dura,Arachnoid –

second sacral vertebra

• Ligamentum denticulatum- to the inner aspect of dura

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Determining the level of lesion

1. The presence of a horizontal level below which sensory ,motor and autonomic function is impaired is a hallmark of spinal cord disease.

2. Sensory loss below a particular level is due to damage to spinothalamic tract on the opposite side one or two segments higher in case of a unilateral lesion.

SENSORY !

MOTOR !SPHINCT

ER !

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• 2nd order neurons ascend for for one or two levels as they cross anterior to the central canal to join the opposite STT

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• Sensory symptoms include numbness, tingling ,pins and needles, dermal hypersensitivity, burning sensation, altered temperature sensation and tight band like sensation.

• A complete cord syndrome- loss of all sensory modalities below the level of lesion.

• Partial syndromes produce variable findings

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• Posterior column – loss of joint sense,vibration,tactile discrimination,with positive romberg’s and ataxic gait (sensory ataxia)

• STT – Contralateral loss of pain & temperature sensation

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SENSORY LEVEL• Zone of hyperaesthesia (dorsal

column) :level of lesion is just below it

• Girdle like sensation exaggerated by cough and sneezing- dorsal column

• Involvement of specific dermatomes

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3. At the level of lesion – LMN signs – focal muscle wasting,

fasciculations, hypo- or areflexia due to involvement of AHCs

Radicular pain or dermatomal sensory loss d/t involvement of sensory roots

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4. Interruption of motor tracts (pyramidal /extrapyramidal)

UMN signs below the level of lesion if corticospinal tract – pyramidal pattern

of weakness – greater in the antigravity muscles – paraplegia in extension

if extrapyramidal tracts - progravity

muscles are affected more – paraplegia in flexion – may be associated with ‘mass reflex’

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Mass reflex

• Spontaneous urination, defaecation, sweating on scratching skin on the medial aspect of thigh

• a/w reflex ejaculation and erection on squeezing glans penis

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5.The lesions that transect the motor tracts cause paraplegia or quadriplegia with heightened DTRs ,babinski sign and eventual spasticity ( Upper motor neuron syndrome)

6. If Acute compressive lesion (traumatic/vascular/inflammatory) : stage of neuronal shock prior to the stage of spasticity

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7. Transverse damage to the cord produces

autonomic disturbances -absent sweating below the implicated cord level and bowel, bladder, sexual dysfunction

8. Most common sphincter disturbances resulting from spinal cord diseases are urgency,frequency, urge incontinence. retention

a /c transverse lesions –retention is the rule

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Localising the uppermost level of a spinal cord lesion

‘segmental signs’• Band of altered sensation

(hyperalgesia/hyperpathia) at the upper end of sensory disturbance

• Fasciculations or muscle atrophy in muscles supplied by that sement

• Absent DTR at this level

How to differenciate from focal root or peripheral nerve disorder?

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Uppercervical cord lesion:Quadriplegia Weakness of

diaphragm(above C4)

Arnold chiari - downbeating nystagmus &

cerebellar ataxia

Lower cervical cord lesions

Atrophy and weakness of

corresponding muscles

Spastic paralysis of trunk and lower limbAbsent biceps,radial

jerkHorner’s syndrome

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Lumbar cord lesionsL2-L4:weakness of Flexion and

adduction of thighLoss of knee jerkSpastic paralysis

below,exaggerated ankle jerkExtensor plantar

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Cauda equina and conus medullaris lesions

CONUS MEDULLARIS CAUDA EQUINAB/L saddle anaesthesia asymmetric leg weakness and

sensory loss

Prominent bowel,bladder symptoms,impotence

Relative sparing of bowel-bladder function

Bulbocavernous ( S2-s4) and anal reflexes (s4-s5) are absent

Variable areflexia in lower extremities

Muscle strength largely preserved Low back and radicular pain

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SPECIAL PATTERNS OF SPINAL CORD DISEASES

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BROWN SEQUARD SYNDROME

• HEMICORD SYNDROME• I/L corticospinal,dorsal

column,spinothalamic tract

• I/L – weakness,loss of joint and vibration sense

• C/L – loss of pain,temp

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Central cord syndrome

• Selective damage to grey matter and crossing spinothalamic tracts

• Syringomyelia,intrinsic tumors of spinal cord,trauma

• Dissociated anaesthesia

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Shoulders,lower neck,upper trunk –cape distribution

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Anterior spinal artery syndrome

• Infarction d/tanterior spinal artery occlusion

• B/L tissue destruction which spares posterior column

• All spinal cord functions –motor,sensory and autonomic – are lost below the lesion

• Striking exception of retained vibration and position sense

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FORAMEN MAGNUM SYNDROME• Lesions in this area

interrupt decussating pyramidal fibres destined for the legs,which cross caudal to those of the arms resulting in weakness of the legs :CRURAL PARESIS

• Around the clock pattern of weakness

• Suboccipital pain spreading to neck and shoulders

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COMPRESSIVE DISORDERS OF SPINAL CORD

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Compressive myelopathies

• Acute compressive Myelopathy / Chronic Myelopathy

• Extramedullary / intramedullary

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Compressive Myelopathy

Intra medullary

Intradural

Extradural

Extramedullary

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• Cord compression

Extramedullary (95 %) Intramedullary(5%)

Intradural Extradural (15%) (80%)

MENINGIOMANEUROFIBROMAPATCHY ARACHNOIDITISAV MALFORMATIONS

NEOPLASMSPOTT’S SPINEIVDPEPIDURAL ABSCESSTRAUMA

SYRINGOMYELIAGLIOMA,EPENDYMOMA OF CORD

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Extramedullary lesions

• Long duration of history• Root pain (+)• Vertebral body tenderness (+)• Motor involvement usually

asymmetrical • Sensory level, all sensations diminished

below this level• Early loss of sensation in the saddle

area ( S3,S4,S5)• Autonomic involvement late

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Intramedullary lesions

• Short duration,painless onset• early bladder involvement• Motor – usually symmetrical• Jacket sensory loss• Dissociative sensory loss • Sacral sparing

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EXTRADURAL EXTRAMEDULLARY CAUSES

• 1. DICS PROLAPSE : Cervical disc prolapse :most common if centrally located, can cause acute or

subacute cord compression Thoracic disc protrusions : sub a/c or

chronic cord compression.Can cause paraparesis / brown sequard syndrome due to asymmetrical compression

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• Clear cut sensory level is usual• Neurological symptoms may

fluctuate over time• MRI demonstrate the cord

compression due to disc prolapse.

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• Treatment : • immobilising in a cervical collar• If highly symptomatic – surgical

decompression• Complication of cervical disc surgery

– irreversible paraplegia due to cord infarction

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2. Spinal epidural abscess clinical triad : Midline dorsal pain

(Over spine / Radicular) Fever

(WBC,ESR,CRP elevation) Progressive limb

weakness

Prompt recognition to prevent permanent sequelae

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• Abscess expand – venous congestion and thrombosis – further cord damage

• Rapid progression once the features of myelopathy develops

• a/w impaired immune status, IV drug abuse,skin and tissue infections

(furunculosis,pharyngeal/dental abscess/bacterial endocarditis,pott’s spine,)

local causes :epidural anaesthesia, LP ,decubitus ulcer ,vertebral osteotomies

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• S.aureus, Streptococcus, anaerobes, gram neg bacilli, fungi

• MRI ,sometimes LP• Treatment : Surgical evacuation, decompressive

laminectomy , long term antibiotics

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TUMORS AND COMPRESSIVE MYELOPATHY

Metastasis - epiduralThracic is common; Lumbar & Sacral – Prostate and ovarianBreast > Lung > Prostate > Kidney > Lymphoma old age pt :Vertebral pain with a/c onset of neurological deficit

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MRI – hypointense lesion in T1; does not cross the adjacent disc spaceBone scan may be useful to detect the all other metastasis

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PAIN !! Recent onset,particularly

thoracic

(aching,localised,sharp,radiating quality)

Typically worsens with movement, coughing, sneezing and

Characteristically awakens the patient at night

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Management:-Glucocorticoid – upto 40mg/d Dexamethasone-RT – 3000cGy in 15 daily fractions

Newer : IMRT (INTENSITY MODUALTED RT)-Surgery- laminectomy or vertebral resection (IF neuro signs worsen even with RT)

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Prognosis:• Ambulatory pt – good response

with RT• Fixed motor deficit once

established <12hr good response

>12hr chance to improve

>48hr no improvement

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POTT`S DISEASE

Common in paediatric and adolescent groupIncidence Reduced with pasteurisation – bovine bacillusTHORACIC cord – most commonInfective process begins in the vertebral body and spreads to adjacent bodies leading to their collapse and angulation of spine Conservative treatment with anti tuberculous chemotherapy if severe- surgical decompression

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NEUROFIBROMA: • arises near posterior root• May or may not be a/w generalised NF• Can occur at any level of spinal cord• Equally in both sexesMENINGIOMA: • Benign -thoracic cord level more common in females

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REFERENCE

• Brain’s book of neurology• Harrison’s Principles of internal medicine, 18th

E• Neuroanatomy,inderbir singh,8th edition

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