FUNCTIONAL NEUROANATOMY OF SPINAL CORD

DR. PIYUSH OJHADM RESIDENT

DEPARTMENT OF NEUROLOGYGOVT MEDICAL COLLEGE, KOTA

DEVELOPMENT

• Arises from the caudal portion of Neural tube

• Extends to

– lower end of Sacrum during early fetal development.

– L4-L5 level at 20 weeks gestational age.

– upper border of L3 vertbrae at birth.

– the adult level of L1-L2 by age of 2 months.

• Spinal cord lies in the vertebral canal.

• Extends from level of cranial border of Atlas (in continuation of Medulla) to lower border of L1 vertebrae or upper border of L2 in adults.

• Average length – 45 cm in adult male & 42-43 cm in adult female

• Weight = approx 30 gms

• Corresponding average length of spinal column is 70cm.

• Anchored to duramater by Dentate(Denticulate) ligament

• Cylindrical in shape and flattened dorso-ventrally.

• Has cervical (C5-T1) and lumbar (L3-S2) enlargements.

• Below lumbar enlargement, spinal cord narrows ending as Conus Medullaris.

• From Conus Medullaris, a fine pial thread (Filum Terminale, approx 20 cms long) passes down to dorsum of Coccyx.

• Although it is a continuous and non-segmental structure, 31 pair of originating nerves give it segmental appearance.

• 31 pair of spinal nerves:-– 8 Cervical

– 12 Thoracic

– 5 Lumbar

– 5 Sacral

– 1 Coccygeal

• The lower group of nerves congregate around Filum Terminale in spinal theca and known as Cauda Equina.

SPINAL CORD LEVELS RELATIVE TO THE VERTEBRAL BODIES

SPINAL CORD LEVEL CORRESPONDING VERTEBRAL BODY

Upper cervical Same as cord level

Lower cervical +1

Upper thoracic +2

Lower thoracic + 2 to 3 levels

Lumbar T 10 – T 12

Sacral T 12 – L1

CROSS-SECTIONAL ANATOMY

• Central placed gray matter (H-shaped) surrounded by white matter

• External surface marked by ventral median fissure and dorsal median sulcus dividing cord into 2 symmetric halves.

• Each lateral column has a dorsal horn and a ventral horn

• Additionally there is Intermediolateral Gray column– T1 to L2 - giving rise to preganglionic sympathetic

autonomic fibres.

– S 2,3,4 - Parasympathetic outflow

NUCLEI IN SPINAL GRAY MATTER

• Neurons of Ventral Gray column (Ventral horn cells) :

– A medial group subdivided into dorsomedial and ventromedial parts

– A lateral group consisiting of dorsolateral, ventrolateral and retrodorsolateral groups

– A central group represented by phrenic and accessory nuclei( in cervical region) and by lumbosacral nucleus (in lumbosacral region)

• Nuclei of Dorsal Grey column :-

– The substantia gelatinosa near the apex

– Nucleus Proprius( or dorsal funicular group)

– Dorsal nucleus (or thoracic nucleus or Clark’s column)

– Marginal zone or posteromarginal nucleus

• Recent studies have divided Gray matter into 10 laminae –

– Laminae 1 – corresponds to posteromarginal nucleus.

– Laminae 2 – substantia gelatinosa

– Laminae 3 & 4 – Nucleus Proprius

– Laminae 5 & 6 – to neck and base of dorsal column respectively.

– Laminae 7 - Intermediate zone ( contains predominantly interneurons)

– Laminae 8 and 9 - Ventral horn

– Laminae 10 – forms grey matter around central canal.

TRACTS OF SPINAL CORD

• A collection of nerve fibres within the central nervous system, that connects two masses of grey matter is called a Tract.

• A tract may also be defined as a collection of nerve fibres having the same origin,course and termination.

• Tracts may be ascending or descending.• Usually named after the masses of grey matter

connected by them.• Tracts are also sometimes referred as

Fasciculi(=bundles) or lemnisci(=ribbons)

PATHWAYS IN THE SPINAL CORD

Ascending (afferent) pathways Descending (efferent) pathways

MAJOR DESCENDING TRACTS

• Corticospinal tracts

• Rubrospinal tracts

• Tectospinal tracts

• Vestbulospinal tracts

• Olivospinal tracts

• Reticulospinal tracts

CORTICOSPINAL TRACTS

• Predominantly made up of axons of neurons lying in motor area of cerebral cortex (area 4)

• With some fibres from Premotor area (area 6) and somatosensory area (area 3,2,1)

• Pass through corona radiata – post limb of internal capsule – crus cerebri of mid brain –ventral part pons – pyramids in medulla

• Near lower end of medulla, 80% fibres cross to opposite side (decussation)

• Crossed fibres enter lateral funiculus of spinal cord and descend as Lateral corticospinal tracts.

• Most of the fibres terminate in laminae 4 to 8 (dorsal and ventral grey columns) – internuncialneurons carry impulse to ventral horn cells.

• The uncrossed fibres (20%) in medulla enter the anterior funiculus of spinal cord and continue as Anterior corticospinal tracts. On reaching appropriate levels, the fibres then cross midline to reach grey matter on opposite side of cord.

• So ultimately, corticospinal tracts (both ant and lateral) connect cerebral cortex of one side with ventral horn cells in opposite half of spinal cord.

• The cerebral cortex controls voluntary movements through corticospinal tracts.

• Interruption – leads to weakness of muscles concerned.

• Somatotropic arrangement - The longest fibres(sacral) lie most superficially, while shortest (cervical) lie most medially.

• They are facilitatory for flexors and inhibitory for extensors.

RUBROSPINAL TRACTS

• Made up of axons of neurons lying in Red Nucleus( lying in upper part of midbrain).

• Crossing occurs in lower part of tegmentum of midbrain.

• Crossing fibres are k/a Ventral Tegmental Decussation• After crossing – descends through pons and medulla –

lateral funiculus of spinal cord (just in front of lateral corticopsinal tract).

• End by synapsing with ventral horn cells in laminae 5 to 8.

• Facilitatory to flexors and inhibitory to extensors.

TECTOSPINAL TRACT• Arise from axons of neurons in superior colliculus

(midbrain).• Crossing at upper part of midbrain• Crossing fibres form Dorsal Tegmental

Decussation.• Descend through pons and medulla – anterior

funiculus of spinal cord.• End by synapsing with interneurons in laminae 6

to 8.• Involved in reflex postural movements in

response to visual stimuli.

VESTIBULOSPINAL TRACT

• 2 tracts – lateral and medial.

• Lateral vestibulospinal tract –

– Originate in lateral vestibular nucleus.

– Uncrossed and lies in anterior funiculus of cord.

– Ends in ventral grey column (laminae 7 & 8)

– Important efferent path for equillibrium

VESTIBULOSPINAL TRACT

• Medial vestibulospinal tract –

– Originate in medial vestibular nucleus.

– lies in anterior funiculus of cord.

– Partly crossed and partly uncrossed

– Ends in cervical segment of cord (laminae 7 & 8)

– Facilitatory to motor neurons supplying extensor muscles ( of the neck, back and limbs ) & is inhibitory to flexor muscles.

RETICULOSPINAL TRACT

• Reticular formation is connected to spinal grey matter through medial and lateral reticulospinaltracts.

• Medial Reticulospinal tracts – Fibres arise from medial part of reticular formation of

both pons and medulla– Descend in anterior funiculus– End directly or indirectly in spinal grey matter– Facilitatory to muscles of trunk and limbs– Concerned with postural adjustments of head, trunk

and limbs

RETICULOSPINAL TRACT

• Lateral Reticulospinal tracts

– Fibres arise from ventrolateral part of reticular formation of pons.

– Cross to opposite side in medulla

– Descend in lateral funiculus

– Apart from control of motor function, they may also influence transmission of pain through ascending tracts.

MAJOR ASCENDING TRACTS

• Posterior column (Medial Lemniscal pathway)

• Spinothalamic tracts

• Spinocerebellar tracts

• Convey afferent impulses arising in various parts of body to different parts of brain.

• Formed by axons of cells in spinal grey matter.

THE POSTERIOR COLUMN –MEDIAL LEMNSICAL PATHWAY

• Fasciculus Gracilis & Fasciculus Cuneatus :-– Occupy the posterior funiculus of spinal cord, hence

often referred as Posterior Column Tracts.– Formed predominantly by central processes of

neurons located in dorsal root ganglia– Fasciculus gracilis (located medially) composed of

fibres from coccygeal,sacral, lumbar and lower thotacic ganglia

– Fascilculus cuneatus (located laterally) consists of fibres from upper thoracic and cervical ganglia.

– Both the fasciculus terminate by synapsing with neurons in nucleus gracilis and nucleus cuneatus in lower medulla

• Medial Lemniscus:-– Neurons of gracile and cuneate nuclei are 2nd order

sensory neurons.

– Here the axons cross midline(Internal arcuate fibres).

– The crossing fibres of 2 sides form sensory decussation (Lemniscal decussation).

– After crossing midline, the fibres run upward in form of a prominent bundle k/a Medial Lemniscus.

– Medial lemniscus terminate in ventral posterolateralnucleus of thalamus.

– 3rd order sensory neurons from thalamus – >internal capsule -> corona radiata -> somatosensory area of cerebral cortex.

• Posterior column conveys :-

– Deep touch and pressure

– Tactile localisation

– Tactile dicrimination

– Stereognosis.

– Proprioceptive impulses

– Vibration sense

SPINOTHALAMIC PATHWAYS(ANTERIOR & LATERAL)

• 1st order neurons of these pathways are located in spinal ganglia.

• 2nd order neurons of this pathway are located in laminae 4,5,6 and 7. Axons of these neurons constitute anterior and lateral spinothalamictracts. They cross to opposite side.

• The fibres of lateral spinothalamic tracts cross within same segment of the cord, while those of anterior spinothalamic tract ascend to one or more segments before crossing to opposite side.

• The fibres of anterior ST tract enter Anterior funiculus while those of Lateral ST tract enter Lateral funiculus.

• Both tracts ascends as one continuous band.

• On reaching medulla, both tracts separate –– Ant ST tract – join medial lemniscus -> thalamus

– Lateral ST tract – travel as a separate bundle (SPINAL LEMNISCUS) to end in thalamus.

• All spinothalamic tracts end in Ventral posterolateral nucleus of thalamus.

• Anterior ST tract- carries sensation of crude touch and presure.

• Lateral ST tract – carries pain & temperature sense.

SPINOCEREBELLAR PATHWAYS

• Carry proprioceptive impulses arising in muscle spindles, golgi tendon organs, and other receptors to cerebellum.

• Constitute afferent component of reflex arc involving cerebellum, for control of posture.

• 1st order neurons of these pathways is located in dorsal nerve root ganglia with peripheral processes ending in golgi tendin organ, muscle spindles and other proprioceptive receptors.

• 2nd order neurons are arranged in various groups :-

– Neurons located in dorsal nucleus (C8 to L3) give origin to fibres of Dorsal (posterior) spinocerebellar tract. It is an uncrossed tract lying in lateral funiculus. Begins in lumbar segment and ascends to medulla to incorporate with Inferior cerebellar peduncle and reach vermis of cerebellum

– Neurons giving origin to Ventral (Anterior) Spinocerebellar tract are located in junction between ventral and dorsal grey columns in lumbar and sacral segments of cord. Predominantly crossed fibres. Ascend in lateral funiculus to enter into Superior Cerebellar peduncle and terminate in vermis of cerebellum.

– From functional point of view, both ventral and dorsal Spinocerebellar pathway are concerned mainly with lower limbs and trunk.

– Dorsal tract – fine co-ordination of muscles controlling posture & with movement of individual muscles.

– Ventral Tract – concerned with movement of limb as a whole.

BLOOD SUPPLY OF SPINAL CORD

• Main arterial supply is by Anterior spinal artery, paired Posterior spinal artery and the perimedullary plexus connecting them.

• Anterior spinal artery :-– Arise from vertebral artery

– Supply anterior ⅔ of spinal cord

• Posterior Spinal artery :-– Arise from vertebral artery or posterior inferior

cerebellar arteries (PICA)

– Supply posterior ⅓ of spinal cord

VENOUS DRAINAGE

• By six tortuous channels:-

– One along median fissure

– One along posterior median sulcus

– One pair, on each side, behind ventral nerve roots

– One pair, on each side, behind dorsal nerve roots

• Free communication

• Finally drain into inernal cerebral veins

LESIONS OF SPINAL CORD

COMPLETE SPINAL CORD TRANSECTION (TRANSVERSE MYELOPATHY)

• All ascending and descending tracts are interrupted.

• Thus all motor and sensory function below the level are disturbed.

• More often the damage is incomplete and irregular, and the findings reflect the extent of damage

• Acute onset causes :-– Trauma

– Tumour (metastatsis, lymphoma)

– MS

– Vascular disorders

– Epidural haematoma or abscess

– Paraneoplastic myelopathy

– Autoimmune disorders

– Parainfectious or postvaccineal syndromes

• All sensory modalities (touch, pressure, joint position, vibration, temperature) are impaired below the level of lesion.

• Clinically pinprick loss below a segmental level is most valuable in localizing the lesion.

• In complete lesion (particularly with extramedullary lesions), the sensory level may be many segments below the level of lesion. (Somatotropic distribution of fibres in lateral spinothalamictract with the lowest segments represented more superficially)

• Band like radicular pain or segmental paraesthesias are more helpful in localising if present.

• Localised vertebral pain, accentuated by palpation or vertebral percussion may also be localising value.

• Paraplegia or quadriplegia below the level of lesion occur due to interruption of descending corticospinal tracts.

• Initially there may be flaccid and areflexicparalysis because of spinal shock to be follwed by spastic, hyper-reflexic paralysis.

• LMN signs (paresis, atrophy, fasciculation and areflexia) in a segmental distribution at the level of lesion (due to damage to Ant horn cells or ventral roots ) may also help in localising level.

• Autonomic disturbances in the form of urinary and rectal sphincter dysfunction with incontinence may occur in transverse myelopathy.

• Urgency of micturition is the usual bladder symptom followed by urinary retention and incontinence seen in late stages.

• Constipation is the most common bowel symptom.

• Anhydrosis, trophic skin changes, impaired temperaturcontrol, vasomotor instability may be seen below the level of lesion.

• Sexual dysfunction (impotence) may be present.

HEMISECTION OF SPINAL CORD (BROWN-SEQUARD SYNDROME)

• Loss of pain and temperature sensation contralateral to the hemisection due to interruption of crossed spinothalamictracts. (sensory level is usually 1 or 2 segments below the level of lesion)

• Ipsilateral loss of proprioception due to disturbance of posterior column.

• Ipsilateral spastic weakness with hyper-reflexia and Babinski sign due to interruption of descending corticospinal tracts.

• Segmental LMN signs at the level of lesion due to damage to Ant horn cells and dorsal rootlets at the level.

• Ipsilateral loss of sweating caudal to the lesion due to interruption of descending autonomic fibres in the ventral funiculus.

CENTRAL SPINAL CORD SYNDROMES

• Initial symptoms include loss of pain and temperature sensation with preservation of joint position and vibration in a “vest-like” or “suspended” bilateral distribution (Dissociation of Sensory loss)

• With forward extension, anterior horn cell may be involved resulting in segmental neugenicatrophy, paresis and areflexia.

• Lateral extension may result in Horner syndrome, kyphoscoliosis, and eventually spastic paralysis below the level of lesion.

POSTERIOR COLUMN DISEASES

• Selectively damaged by Tabes Dorsalis.

• Inflammation and degeneration of dorsal roots cause secondary destruction of posterior columns of spinal cord.

• Usually 10-20 years after onset of infection.

• Impaired vibration and position sense and decrease tactile localization.

• Lower limbs affected more than upper limbs.

• c/o sensory ataxia more at night or in darkness.

• Positive Romberg sign due to proprioceptiveinterruption.

• Often patients fall forward immediately on closing eyes (wash basin sign or positive “sink” sign)

• Absent patellar and ankle reflexes.

ANTERIOR HORN CELL SYNDROMES

• Diffuse anterior horn cell damage results in diffuse weakness, atrophy and fasciculationsnoted in muscles of trunk and extremities.

• Muscle tone is usually reduced and stretch reflexes are usually depressed or absent.

• Sensory changes are absent as sensory tracts are unaffected.

VASCULAR DISORDERS OF SPINAL CORD

• Mostly in territory of Anterior Spinal Artery.• Mostly at watershed zones i.e. T1- T4 and L1 levels.• Lower thoracic segments and conus medullaris are

commonly involved.• Abrupt onset of neurological deficeits, often associated

with radicular or “girdle” pain.• Loss of motor function below the level occurs within

mins or hours due to damage to corticospinal tracts.• Impaired bowel and bladder control• Loss of pain and temperature sensation below d/t

damage to spinothalamic tracts.

• Position sense, light touch and vibration sense remain preserved due to preserved dorsal columns (supplied by posterior spinal arteries)

• Infarction in the territory of posterior spinal arteries is uncommon.

• Loss of proprioception and vibration sense below the level of lesion and loss of segmental reflexes.

• Preserved pain and temperature sense, except for involved segment of cord where global anaesthesia is present.

• Absence of motor deficits.

INTRAMEDULLARYVS EXTRAMEDULLARY CORD LESIONS

SYMPTOMS/SIGNS INTRAMEDULLARY EXTRAMEDULLARY

Radicular pain Unusual Common,may occur early

Vertebral pain Unusual Common

Funicular (central ) pain Common Less common

UMN signs Yes, late Yes, early

LMN signs Prominent & diffuse Unusual, if present segmental distribution

Paraesthesiasprogression

Descending progression Ascending

Sphincter abnormalities Early with caudal lesions Late

Trophic changes Common Unusual

• CAUDA EQUINNA LESIONS:-– Early asymmetric radicular pain in distribution of

lumbosacral roots.

– May cause Flaccid, hypotonic areflexic paralysis that affect glutei, posterior thigh muscles and anterolateral muscles of leg and foot.

– Asymmetric sensory loss in saddle region involving anal, perineal and genital regions extending to dorsal aspect of thigh, anterolateral aspect of leg and outer aspect of foot.

– Ankle reflex is absent.

– Sphincter disturbances occur late in the course of the disease.

• CONUS MEDULLARIS LESIONS:-

– Paralysis of pelvic floor muscles and early sphincter disturbances.

– Disruption of bladder reflex arc results in Autonomous neurogenic bladder (loss of voluntary initiation of micturition, increased residual urine and absent vesical sensations).

– Constipation, impaired erection and ejaculation are commonly present.

– Symmetric saddle anaesthesia.

THANK YOU

REFERENCES

• Gray’s textbook of anatomy 40th edition

• Textbook of Human Neuroanatomy by

Inderbir Singh 9th edition

• Anatomy of Central Nervous system by

S.Poddar, Ajay bhagat

• Localization in clinical neurology by Paul

W. Brazis 6th edition

• Bradley’s Neurolgy in clinical practice 6th

edition

LOCALIZATION OF SPINAL

CORD AT VARIOUS LEVELS

FORAMEN MAGNUM SYNDROME

AND LESIONS OF UPPER

CERVICAL CORD• Suboccipital pain in the distribution of greater

occipital nerve (C2) and neck stiffness occurs early.

• Lhermitte’s sign may be present.(indicating lesion of posterior columns)

• Numbness and tingling sensation of distal part of upper limbe are common.

• Spastic tetraparesis, sensory symptoms, bladder disturbances may be present.

• Lower cranial nerve palsies (9-12) may occur as extension of the pathologic process.

• An “ around the clock” type of UMN weakness may be seen(I/L UL–> I/L LL-> C/L LL -> C/L UL)

• Lesions at the foramen magnum may also present with downbeat nystagmus, papilloedema (secondary to CSF circulation obstruction) and cerebellar ataxia.

• Lesion at Medullo-cervical junction( where pyramidal tracts decussate) may cause HEMIPLEGIA CRUCIATA (contralateral UL and ipsilateral LL weakness)

FORAMEN MAGNUM SYNDROME

AND LESIONS OF UPPER

CERVICAL CORD

• Compression of UPPER cervical cord (C1-

C4)

– 11th cranial nerve may be affected

(sternocleidomastoid and trapezium

weakness)

– Diaphragm weakness (C3-5)

FORAMEN MAGNUM SYNDROME

AND LESIONS OF UPPER

CERVICAL CORD

• C5 – C6 Lesion :-– LMN signs at the corresponding segments and

UMN signs below the level.

– Specially affects supra and infraspinatus, biceps, deltoid, brachialis, brachioradialis, pectorals, triceps, latissimus dorsi and extensor carpiradialis.

– Associated with spastic paraparesis of lower limbs

– Biceps and brachioradialis (segments C5-6)

– Triceps (C7,8)

– Finger flexor reflex (C8-T1)

– Complete C5 lesion – sensory loss over entire body below neck and anterior shoulder

– Complete C6 lesions – same as C5 except lateral arm is spared

• C 7 lesion:-

– Normal diaphragmatic function

– Weakness of flexors and extensors of wrist &

fingers

– Biceps & Brachiradialis (C5-6) are preserved.

– Finger flexor reflex (C8-T1) exaggerated,

– Paradoxical Triceps reflex i.e. forearm flexion

on tappin olecranon process may be present.

– Sensory loss in 3rd and 4th digits and medial

border of arm and forearm.

• C8 and T1 lesion:-

– Weakness predominantly involves small hand

muscles

– Associated spastic paraparesis

– With C8 lesion, triceps (C7,8) and finger flexion

reflex (C8,T1) are decreased or absent.

– With T1 lesion, triceps reflex is preserved with

decreased finger flexion reflex.

– With C8-T1 lesion, there may be u/l or b/l horner

syndrome.

– Sensory loss- 5th digit and medial border of arm

and forearm.

• Thoracic segment lesion:-

– Paraplegia, sensory loss below a thoracic level, bowel bladder disturbances and sexual dysfuntion occurs.

– With lesions above T5, there may be impairment of vasomotor control (postural hypotension).

– Autonomic Dysreflexia may also be seen with lesions rostral to splanchnic sympathetic outflow (i.e. above T6 level) in which a stimulus such as bladder or rectum distension may result in sympathetic storm manifested by excessive sweating, extreme HTN, reflex bradycardia, pounding headaches, nasal blockage and cutaneous flushing.

• Lesions of first lumbar segment (L1):-

– All muscles of the lower extremities are weak.

– Area of sensory loss includes both lower

extremities upto the level of groin and back, to

a level above the buttocks.

– With chronic lesions, patellar (L2-4) and ankle

jerks (S1-2) are brisk.

• Lesions of Second lumbar segment (L2):-

– Spastic paraparesis

– Cremasteric reflex (L2) is weak

– Patellar reflex (L2-4) may be depressed.

– Ankle reflex (S1,2) are brisk.

– Normal sensation on upper anterior aspect of

thighs.

• Lesions of Third lumbar segment (L3):-

– Preservation of hip flexion (iliopsaos and

sartorius) and leg adduction (adductor longus,

pectineus and gracilis)

– Patellar jerks (L2-4) are diminshed or not

elicitable.

– Hyperactive ankle jerks.

• Lesions of Fouth lumbar segment (L4):-

– Better hip flexion and leg adduction than in

L1-3 lesions

– Knee flexion and leg extension is better and

the patient is able to stand by stabilizing the

knees.

– Patellar jerks are not elicitable

– Hyperactive ankle jerks.

– Normal sensation on upper anterior aspect of

thighs and superomedial aspects of knees.

• Lesions of Fifth lumbar segment (L5):-

– Normal hip flexion and adduction and leg

extension.

– Patellar jerks are present

– Ankle jerks are hyperactive.

– Sensory function is preserved on anterior

aspect of thighs and medial aspect of legs,

ankles and soles.

• Lesions of first & second sacral segments

(S1 & S2):-

– S1 segment lesion may cause weakness of

triceps surae, flexor digitorum longus, flexor

hallucis longus and small foot muscles. Ankle

reflex may be absent with preserved patellar

reflex. Complete sensory loss over sole, heel

and outer aspect of foot and ankle.

– S2 lesion cause weakness of flexor digitorum,

flexor hallucis longus and small muscles of

foot and diminshed ankle reflex with sensory

impairment also involving saddle area.