By Dr Piyush Ojha , DM Resident, GMC Kota under guidance of Prof. Dr Vijay Sardana (HOD,Neurology)

1. FUNCTIONAL NEUROANATOMY
OF SPINAL CORD
DR. PIYUSH OJHA
DM RESIDENT
DEPARTMENT OF NEUROLOGY
GOVT MEDICAL COLLEGE, KOTA

3. 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.

5. • 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

6. • 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.

7. • 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.

8. 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

9. 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

12. 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)

13. • 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

14. • 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.

17. TRACTS OF SPINAL CORD

18. • 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)

19. PATHWAYS IN THE SPINAL CORD
Ascending (afferent) pathways Descending (efferent) pathways

20. MAJOR DESCENDING TRACTS
• Corticospinal tracts
• Rubrospinal tracts
• Tectospinal tracts
• Vestbulospinal tracts
• Olivospinal tracts
• Reticulospinal tracts

21. 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)

22. • 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) – internuncial
neurons 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.

23. • 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.

25. 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.

26. 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.

27. 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

28. 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.

29. RETICULOSPINAL TRACT
• Reticular formation is connected to spinal grey
matter through medial and lateral reticulospinal
tracts.
• 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

30. 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.

31. 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.

32. 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

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

35. • Posterior column conveys :-
– Deep touch and pressure
– Tactile localisation
– Tactile dicrimination
– Stereognosis.
– Proprioceptive impulses
– Vibration sense

36. 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 spinothalamic
tracts. 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.

37. • 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.

39. • Anterior ST tract- carries sensation of crude
touch and presure.
• Lateral ST tract – carries pain & temperature
sense.

40. 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.

41. • 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

42. – 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.

43. 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

44. 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

45. LESIONS OF SPINAL CORD

46. 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

47. • Acute onset causes :-
– Trauma
– Tumour (metastatsis, lymphoma)
– MS
– Vascular disorders
– Epidural haematoma or abscess
– Paraneoplastic myelopathy
– Autoimmune disorders
– Parainfectious or postvaccineal syndromes

48. • 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 spinothalamic
tract with the lowest segments represented more
superficially)
• Band like radicular pain or segmental
paraesthesias are more helpful in localising if
present.

49. • 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 areflexic
paralysis 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.

50. • 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 temperatur
control, vasomotor instability may be seen below the
level of lesion.
• Sexual dysfunction (impotence) may be present.

51. HEMISECTION OF SPINAL CORD
(BROWN-SEQUARD SYNDROME)
• Loss of pain and temperature sensation contralateral to the
hemisection due to interruption of crossed spinothalamic
tracts. (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.

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

54. 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.

55. • c/o sensory ataxia more at night or in
darkness.
• Positive Romberg sign due to proprioceptive
interruption.
• Often patients fall forward immediately on
closing eyes (wash basin sign or positive “sink”
sign)
• Absent patellar and ankle reflexes.

56. ANTERIOR HORN CELL SYNDROMES
• Diffuse anterior horn cell damage results in
diffuse weakness, atrophy and fasciculations
noted 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.

57. 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.

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

59. • 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.

60. INTRAMEDULLARY
VS 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
Paraesthesias
progression
Descending progression Ascending
Sphincter abnormalities Early with caudal lesions Late
Trophic changes Common Unusual

61. • 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.

62. • 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.

63. THANK YOU

64. 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

65. LOCALIZATION OF SPINAL
CORD AT VARIOUS LEVELS

66. 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.

67. • 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

68. • 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

69. • 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 carpi
radialis.
– 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

70. • 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.

71. • 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.

72. • 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.

73. • 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.

74. • 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.

75. • 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.

76. • 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.

77. • 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.

78. • 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.