Descednig teacts

1. By Dr. Ramita Sharma
Guided by Dr. A.K. JAIN sir

2. Descending tracts implies to nerve fibers descending
from brain through spinal cord to control motor
activity of different parts of body.

6. PYRAMIDAL
EXTRA PYRAMIDAL TRACTS
EXTRAPYRAMIDAL

8. CORTICOBULBAR TRACTS
CORTICO PONTO CEREBELLAR TRACTS
CORTICO RUBRAL TRACTS
CORTICO OLIVARY TRACTS
CORTICO RETICULAR TRACTS

9. LATERAL MEDIAL

12. ORIGIN
COURSE
DECUSSION
DESTINATION
FUNCTION
CLINICAL IMPLICATION

13. AKA PYRAMIDAL TRACTS

14. 30% from PRIMARY
MOTOR CORTEX
=AREA 4
30% from
SECONDARY MOTOR
CORTEX=AREA 6,i.e
from the Pre motor=
and Supplementary
motor area
40% from PRIMARY
SENSORY CORTEX
=AREA 1,2,3

16. MOTOR HOMUNCULUS

17. COURSE
•Descending fibres
converge in corona
radiata
•Posterior limb of
internal
capsule(closest to
genu cervical fibres
most posteriorly lower
extremities)
•Midbrain at middle
1/3 of crus cerebri.
•Pons at basilar part.
•Medulla oblongata –
anterior swelling
pyramids

21. DECUSSATION
Most decussate
at lower medulla-
pyramids and
called as
corticospinal tract
Some continue
as
corticospinal
tracts crosses at
the level of
destination (neck
and upper
thorasic region)

22. DESTINATION
Terminate by
synapsing with
the internuncial
neuron in the
spinal cord or
directly with
alpha and
gamma motor
neuron of the
anterior horn cell

24. FUNCTION
Rapid skilled voluntary movements .
Especially of the distal ends of limbs.
Opposite side of the body w.r.t the site of origin of the
tracts in cerebral cortex.
Anterior corticospinal tract controls the bilateral axial
muscles hence the postural movement of the body.

25. SALIENT FEATURES
Fibres are unmyelinated
at birth
Myelination begins in
2nd post natal week and
completed by 2 years
Babinski reflex till 2
years of life
80% small and 20%large
fibres
Large fibres disappears
at old age causing
automatic shaking or
shivering movements.

26. CLINICAL IMPLICATIONS
UMN LMN
All descending pathways of
brain and spinal cord
involved in voluntary control
of muscle.
It includes cerebral cortex,
corticospinal and other tracts
with all the subcortical region
like midbrain, pons, medulla.
Inhibition of muscle stretch
reflex.
Motor neuron of spinal cord
which directly innervates
skeletal muscle.
It includes anterior motor
neuron and spinal nerve
following the neuron.
Forms the motor component
of muscle stretch reflex.

29. LESIONS
UMN lesion LMN lesion
Spastic paralysis.
Disuse atrophy.
Hypertonia
Fasciculations absent.
Babinski reflex present.
DTR exagerrated.
Decreased speed of voluntary
movement.
Unchanged conduction velocity
in peripheral nerve.
Area involved – regional.
Flaccid paralysis.
Wasting atrophy.
Hypotonia .
Fasciculation present.
Planter mute .
DTR descreased to lost.
Complete loss of movement.
Conduction velocity of nerve
decreased to absent.
Area involved – segmental.

30. CAUSES OF LESIONS
UMN LMN
INFARCTION
POSTERIOR LIMB of
INTERNAL CAPSULE.
PRIMARY MOTOR CORTEX
and PRE MOTOR CORTEX.
POLIOMYELITIS
NERVE LESION.

31. BABINSKI SIGN
On scratching skin along
lateral aspect of sole of
foot
Great toe becomes
dorsally flexed with other
toes fanning outward.
Normal response-planter
flexion of all the toes.
Reason:CS tract planter
flex which becomes non
functional leading to
influence of other
descending tracts
becomes apparent.

32. BABINSKI LIKE REFLEXES
1. BINGE SIGN- mutiple pin pricks on dorsum of foot
2. CORNELL SIGN- scratching along inner side of extensur
hallucis longus tendon.
3. Chaddock sign- stroking the lateral malleolus.
4. Doug sign- through nerve conduction study.
5. Gonda sign- flexing and suddenly releasing forth toe.
6. Gordon sign- squeezing the calf muscle.
7. Moniz sign- forcefully passive planter flexion of ankle.
8. Oppenheim sign- applying pressure to medial side of
tibia.
9. Schaeffer sign- squeezing the achilles tendon.
10. Starnsky sign- vigoursly abducting and suddenly
relealing little toe.

34. HOFFMANN’S REFLEX
Hoffmann’ s reflex is
upper limb equivalent of
babinski sign.
Monosynaptic reflex
involving flexor
digitorum profundus.

35. WEBER SYNDROME
Loss of 3rd nerve.
I/L ptosis(LPS lost)
I/L divergent squint(MR
lost)
I/L down and out eyeball(
loss of SR,MR.IO and
unopposed SO,LR)
Cortico pontine tract.
UMN paralysis of C/L
lower half of face.
Pyramidal tract loss.
C/L hemiplegia of UMN
type.
OCCLUSION OF PERFORATING BRANCHES OF
PCA

36. MILLARD GUBLER
SYNDROME
Loss of 6th nerve
I/L convergent squint.
Loss of 7th nerve
I/L facial paralysis of
LMN type.
Loss of pyramidal tract
C/L hemiplegia of UMN
type.

37. MEDIAL MEDULLARY
SYNDROME
Loss of 12th nerve.
I/L tongue paralysis
Loss of medial
laminiscus.
C/L loss of
proprioception.
Loss of pyramidal tract
C/L hemiplegia.

38. CORTICONUCLEAR
TRACTS

39. ORIGIN
30% from PRIMARY
MOTOR CORTEX
=AREA 4
30% from
SECONDARY
MOTOR
CORTEX=AREA 6,i.e
from the Pre motor=
and Supplementary
motor area
40% from PRIMARY
SENSORY CORTEX

40. COURSE and
DECUSSATIO
N
•Descends through corona
radiataand genu of internal
capsule with few fibres in
posterior linm also.
•Passes from cortex down
to midbrain to cerebral
peduncles – crus cerebri.
•Middle third of crus cerebri
contain corticobulbar and
cortico spinal tracts.
•Only 50% of corticobulbar
tract decussate.

41. DESTINATIO
N
•Corticobulbar tract exit at
appropriate level of brain
stem to synapse with
lower motor neuron of
cranial nerve.
•Innervates cranial motor
nuclei bilaterally except
the lower facial
nuclei(below the eyes)
and genioglossus muscle.
•Directly innervates the
5,7,9,10,11and 12 cranial
nerve nuclei.

42. FUNCTION
• Slightly stronger connection contralaterally then
ipsilateral is observed.
• Muscles of head, neck and face is controlled by
corticobulbar system.

43. PSEUDOBULBAR PALSY
AKA supra nuclear bulbar palsy.
UMN lesion involving cortico bulbar pathway.
Pattern of involvement.
1. Unilateral: transient weakness of many muscles
supplied by cranial nerve.
2. Bilateral: persistant weakness of many muscles
supplied by brainstem nuclei.
3. Causes : CVA,e.g, B/L internal capsule infarcts, Brain
stem tumor, Demyelinating illness like MS,Head
injury.

44. PRESENTATION
TONGUE: paralysis with no wasting or fasciculations.
Palatal movements absent.
Nasal regurgitations present.
Persistant dribbing of saliva.
Facial muscle paralysis can be present.
DTR exagerrated. {jaw jerk}.
Facial paralysis.
Dysphonia .
Dysphagia.
Emotional lability can also be present.

46. From RED
nucleus
(magnocellular
part)
Present at the
tegmentum area
of midbrain at the
level of superior
colliculus
Input from
cerebral cortex
and deep

47. COURSE and
DECUSSATION
•Just after arising
from red nucleus
crosses the
midline at the
level of nucleus
only.
•Descends in the
lateral white
column of spinal
cord just anterior
to lateral
corticospinal
tract

48. DESTINATION
Terminate by
synapsing with
internuncial
neuron in
anterior grey
matter of the
spinal cord

49. FUNCTION
Facilitates flexor activity
Inhibit extensors or anti gravity
muscles

50. CLINICAL IMPLICATIONS
CORTICORUBROSPINAL SYSTEM
RED nucleus gets input from cerebral cortex and deep
cerebellar nuclei
If corticospinal tract is destroyed and CRS pathway is
intact – discrete moevement can occur but fine
movement of hand and fingers are lost.

51. RETICULOSPINAL TRACT

52. In midbrain,
pons and
medulla
oblongata –
group of
scattered nerve
cells and fibres
called reticular
formation
PONTINE RETICULOSPINAL
TRACT
Input from deep cerebellar
nuclei and vestibullar nucleus
MEDULLARY
RETICULOSPINAL TRACT
Input from corticospinal and
rubrospinal tracts

53. COURSE and
DECUSSATI
ON
•Pontine
reticulospinal tracts
are mostly
uncrossed and
descends in the
anterior white
column of spinal
cord.
•Medullary
reticulospinal tract
are both crossed
and uncrossed and
descends in the
lateral white column
of spinal cord.

54. DESTINATION
Both medullary
and pontine
reticulospinal
tract relay in the
anterior grey
column of spinal
cord and
synapses with the
alpha and gamma
motor neuron
present in anterior
motor neuron

55. FUNCTION
• PONTINE RETICULOSPINAL tract facilitate alpha and gamma motor
neurons of anti gravity muscles especially of vertebral column ,i.e,
allow a person to stand.
• MEDULLARY RETICULOSPINAL tract inhibit anti gravity muscles
• Hypothalamus control AUTONOMIC outflow through these fibres.

56. CLINICAL IMPLICATIONS

57. DECEREBRATE RIGIDITY
Trans-section of brainstem at the level
of midbrain(above vestibular and
below red nucleus).
Clinically due to damage to upper brain
stem.
MEDULLARYRS tract loosetheir input
and there is unopposed action of
PONTINE RS tracts.
It leads to extensor posturing in both
upper and lower limbs
Arms abducted and extended.
Wrist pronated and fingers flexed.
Legs are stiff and extended.
Planter flexion of feet.

58. DECORTICATE
RIGIDITY
•Trans – section of
midbrain abovesuperior
colliculus.
•Clinically due to damage to
cortico spinal tract of one
or both side-strokeor
tumor.
•Some inhibitory control
through MEDULLARYRS
tract is present as red
nucleus is intact.
•Arms are adducted and
flexed with wrist and finger
flexed on chest.
•Legs are stiff and extended
and internally rotated with
planter flexion of feet.

59. TECTOSPINAL TRACT

60. ORIGIN
Midbrain at
the
superior
colliculus.

61. COURSE and
DECUSSATIO
N
•Crosses mid
line just after
their origin
•Descend
close to MLF
in anterior
white column
close to
anterior
median
fissure

62. DESTINATION and FUNCTION
• Relay with the internuncial neuron present
in the anterior gray column of upper cervical
segments of spinal cord
• Reflex postural movement in response to
visual stimulus.
• Co – ordinate head, neck and eye
movements

63. VESTIBULOSPINAL TRACT

64. ORIGIN
•Vestibular
nucleus
situated at the
floor of 4th
ventricle .
•Vestibular
nucleus
receives its
input from
vestibular
nerve and deep
cerebellar
nuclei.

65. COURSE and
DECUSSATIO
N
Descends
uncrossed in
the anterior
white
column of
spinal cord

66. DESTINATION and FUNCTION
• Synapse with internuncial neuron of anterior gray
column of spinal cord.
• Facilitates extensors and inhibit flexors of mainly
axial muscles thus maintaining balance of the
body.

67. SOME CEREBELLAR
CONNECTIONS

71. THANK YOU