2. At the end of the class, Student should be able to:
• Classify descending tracts.
a) Pyramidal tract
b) extrapyramidal tract
• Describe origin, course termination of the descending
tracts.
• Functions of the descending tracts.
• Differences between pyramidal & extrapyramidal tract
• Differences between lower & upper neuron lesion
3.
4.
5.
6.
7.
8.
9. Functions of pyramidal tracts
Tracts : Lateral corticospinal tracts
Function: Controlling the voluntary movements- fine,
precise movements of the fingers and hands to carry
out skilled work.
Tracts : Anterior corticospinal tracts
Function: Control of muscles of trunk & proximal
portions of the limbs to carry postrual adjustments
and gross movements
10. • They form a part of the pathways for superficial
reflexes such as cremasteric, abdominal and plantar
reflexes.
• Some corticospinal fibers end at excitatory synapses on
α and γ-motor neurons, whereas other end on
interneurons that may excite or inhibit the α-motor
neurons. Thus the effect of the corticospinal pathway
on the α-motor neurons may be excitatory or
inhibitory.
• Some fibers transmit information from the brain to
‘afferent’ neurons and so can effect afferent system,
they do this by ending either:
(a) Presynaptically on the axon terminals of afferent
neurons as these fibers enter the CNS; or
11. • Corticospinal fibers arising from the somatic sensory
area (I and II) and parietal lobe association cortex are
concerned with sensory-motor coordination. For
example, aiming the hands towards it, hand-eye
coordination etc. lesion of these areas causes defects
in motor performance that are characterized inability
to execute learned sequences f movements such as
eating with a knife and fork.
12. Functions of corticobulbar (corticonuclear)
tracts
• These are responsible for voluntary control of
muscles of larynx, pharynx, palate, upper and
lower face, jaw, eye etc. Pseudobulbar Palsy is a
condition resulting in paralysis or weakness of
the muscles which control swallowing, talking,
tongue and lip movements due to bilateral
lesion of these tracts.
13. EXTRAPYRAMIDAL TRACTS
• Extrapyramidal system is made up of those
areas the CNS (other than the pyramidal and
cerebellar system) that are concerned with
muscular movements and posture. Its fibers
have many synapses in their descending path
with cells of the nuclear masses on the way
which include: nuclei of the cerebral cortex,
basal ganglia, hupothalamus and nuclei of the
reticular formation in the brain stem. In the
spinal cord the fibers form separate groups
according to their site of origin.
14. FUNCTIONS OF EXTRAPYRAMIDAL TRACTS
• Corticobulbar (corticonuclear) fibers control the movements
of the eye balls.
• They are responsible for control of tone, posture and
equilibrium (rubrospinal- for tone and posture; tectospinal-
for visuospinal reflex; vestibulospinal -for the equilibrium).
• They control complex movements of the body and limb such
as coordinated movements of arms and legs during walking.
• They exert tonic inhibitory control over the lower centres.
Their damage increases rigidity of the muscles, called release
phenomenon.
• If the pyramidal tracts are damaged, they can carry out
voluntary movement to some extent.
15. Descending pathways that contribute to the
extrapyramidal system
TRACTS DESCRIPTION(ORIGIN AND COURSE) Main function
1. Rubrospinal It originates from the Red nucleus Facilitatory influence
tract (nucleus Magnocellularis i.e. large over flexor muscle tone.
nucleus ) located in the mid brain;
crosses immediately to the
opposite side, some fibers end in
the cerebellum. The tract does
not extend below the thoracic
region.
2. Tectospinal It originates from the superior Mediate reflex postural
and tectobulbar colliculus (which is an optic movements in response
tract centre); crosses at once to the to visual and auditory
opposite side. The tract descends stimuli.
upto the lower cervical region.
16. 3. Reticulospinal Origin from neurons of the (i) Facilitate or inhibit
tract reticular formation in pons and voluntary
medulla. movements, mainly
(ii)Medial division i.e. fibers influence γ–motor
from the pontine reticular neurons.
formation are mainly crossed (ii) Alteration in muscle
(iii)Lateral division i.e. tone, respiration
medullary reticular fibers and blood pressure
descend uncrossed.
4. Vestibulospinal Origin: from lateral vestibular Facilitatory influence
tract nucleus located at the junction upon reflex activity in the
of pons and medulla. It receives spinal cord and upon the
fibers from the vestibular mechanism which
division of VIII nerve. control muscle tone
Both lateral and medial division (mainly extensor group
descend uncrossed throughout i.e. antigravity group of
the entire length of the spinal muscles).
cord
17. 5. Medial Origin: from the medial Coordinator of reflex
longitudinal vestibular nucleus, reticular ocular movements and
fasiculus formation, superior colliculus integration of eye and
(orbundle) and interstitial nucleus of Cajal; neck movements.
the tract descend uncrossed
upto upper cervical region
18. Major differences between pyramidal
exrapyramidal tracts
Pyramidal tracts Extrapyramidal tracts
1. Origin Origin
2. Its axons pass without relay to the They have many synapses in their
spinal segmental levels where they form descending path with cells of nuclei of
synapses with either interneurons in the the striatum (caudate and putamen), the
dorsal horn or directly with the motor globus pallidus, the hypothalamus and
neurons themselves. the nuclei of the reticular formation.
3. They have grater influence over motor They are more involved with coordination
neurons that control muscles involved in of the large muscle groups used in the
the fine movements, particularly those of maintenance of upright posture, in
the fingers and hand. locomotion, and in head and body
movements when turning towards a
specific stimulus.
4. Lesion of this tract produces ‘spasticity’ Its lesion produces ’rigidity’ of the
in the muscles involved. involved muscles.
19. Differences between lower and upper
motor neuron lesion
Lower motor neuron lesion(LMNL) Upper motor neuron lesion(UMNL)
1. It is due to lesion of the lower It is due to lesion of the upper motor
neurons (LMNs) i.e. the spinal and neurons (UMNs) i.e. the neurons in the
cranial motor neurons that directly brain and spinal cord that can influence
innervate the muscles the activity of LMNs; major cause being
lesion of pyramidal tracts.
2. Here usually single or individual It involves a group of muscles.
muscle is affected.
3. Muscle becomes completely Affected muscles due to pyramidal tract
paralysed (flaccid paralysis). This is due lesion become hypertonic (spastic
to complete loss of muscle tone which paralysis). This is due to:
depends on integrity of the reflex arc.` (ii)Release phenomenon i.e. loss of
higher inhibitory control; and
(iii)Denervation hypersensitivity of
centres below the transection.
20. 4. Disuse atrophy of the muscle occurs i.e. The Muscle atrophy is not severe (if
shrinkage of muscle fiber which is finally present, very mild) because muscles
replaced by fibrous tissue(fibrous muscle). though not used in the voluntary
movements are continuously in action to
maintain posture by ‘reflexes’.
5. All reflexes (superficial or deep) are (i) Deep reflexes are hyperactive
absent (lost) as the motor pathway is (accentuated) because of increased γ-
damaged motor discharge; and
ii) Superficial reflexes; only abdominal,
cremastric and anal reflexes are lost.
6. Babinski plantar response: Babinski sign Babinski sign: positive (abnormal). In
not elicited. UMNL, stroking outer edge the sole of the
foot with firm tactile stimulus produces first
an upward movements (dorsiflexion) of the
great toe and fanning out (abduction) of
the small toes. This is due to contraction of
extensor hallucis longus (Anatomists
misleadingly call it an ‘extensor response’),
physiologically a ‘flexor’ (withdrawal
response. (note: All the muscles which
contract during a flexor response are called
physiological flexors.)
