EXTRA-PYRAMIDAL TRACTS:

All descending tracts other than cortico-spinal / pyramidal are included in it.

1) RUBRO-SPINAL TRACT:
ORIGIN: Red nucleus (midbrain). Fibers cross over to opposite side & descend through pons & medulla lat white column of spinal cord. Fibers terminate on inter-neurons. Inter-neurons synapse with alpha & gamma motor neurons.

FIBERS FROM CEREBRAL CORTEX

RED NUCLEUS

MID BRAIN FIBERS FROM CEREBELLUM

DEEP CEREBELLAR NUCLEI

LATERAL WHITE COLUMN RUBRO-SPINAL TRACT

Red nucleus receives fibers from: Cerebral cortex & Cerebellum. Rubro-spinal tract is an alternate pathway, through which cerebral cortex & cerebellum control activity of motor neurons in spinal cord.

 This tract is excitatory for flexors & inhibitory for extensors (anti-gravity muscles).

2) TECTO-SPINAL TRACT:
ORIGIN: superior colliculus located in tectum of midbrain. Tract fibers descend without crossing. Fibers terminate onto motor neurons in ventral horn of upper cervical segments of spinal cord, through inter-neurons.

 This tract controls reflex movements of head & neck, in response to visual stimuli, e.g, something shines behind reflex turning of head & neck back to the shining object.

RETICULO-SPINAL TRACT:
ORIGIN: Tract arises from reticular formation (groups of scattered neurons along with nerve fibers present in midbrain, pons & medulla). * Superiorly reticular formation is connected to cerebral cortex & inferiorly to spinal cord.

 Reticulo-spinal tract has 2 components: A) PONTINE component B) MEDULLARY component

PONTINE RETICULOSPINAL TRACT:

ORIGIN: Nuclei of reticular formation of pons. Fibers remain uncrossed & descend to enter anterior white columns of spinal cord. Tract terminate on motor neurons in ventral horn of spinal cord, through inter-neurons & finally motor neurons. excitatory for extensors & Inhibitory for flexors (unlike rubro-spinal).

MEDULLARY RETICULAR FORMATION:

ORIGIN: Nuclei of reticular formation in medulla. Fibers cross to opposite side. Tract descends to enter lateral white column of spinal cord. Terminate onto the motor neurons in ventral horn. It is inhibitory for extensors (like rubro-spinal).

VESTIBULO-SPINAL TRACT:
ORIGIN: Vestibular nuclei in lower pons & medulla. Mostly fibers remain uncrossed. Then enter Ant. White column of spinal cord. Terminate on alpha & gamma motor neurons, through interneurons.

2 components of the tract: Major component Lat. V.S Tract Minor component Med. V.S Tract. Lat. V.S Tract lat. Vest. Nuclei. Med. V.S Tract med Vest. Nuclei.

 Vest-spinal tract is excitatory for extensors (unlike rubro-spinal). Vestibular nuclei cerebellar fibers Vestibular nuclei internal ear fibers (vestibular apparatus).

OLIVO-SPINAL TRACT:
ORIGIN: Inferior olivary nucleus in medulla. Fibers cross over to opposite side & descend into lat. White column of spinal cord. Fibers terminate onto motor neurons in ventral horn through interneurons.

 This tract controls activity of motor neurons in spinal cord. Inferior olivary nucleus receives fibers from cerebral cortex, corpus striatum, reticular formation & spinal cord.

DESCENDING AUTONOMIC PATHWAY:

ORIGIN: Cerebral cortex, hypothalamus, amygdala & reticular formation. This pathway accompanies reticulo-spinal tract. These fibers enter lat. white column of spinal cord & terminate onto pre-gang. Sympathetic neurons in segments T1 L2 & also onto pregang parasymp neurons in segments S2 S4.

MOTOR SYSTEM CONSISTS OF 2 TYPES OF NEURONS:

UMN LMN

LMN:
Motor neurons which innervate the skeletal muscles. These form the final common pathways to skeletal muscles. If any motor impulse has to pass to skeletal muscle, it has to pass to LMN.

 These neurons include: Alpha motor neuron in ventral horn of spinal cord & also motor neurons in nuclei of cranial nerves in brain stem.

UMN:
These are present above the level of LMN. These control motor activity through separate pathways. These neurons may be located in cerebral cortex, basal ganglia & also in brain stem.

FEATURES OF LMN LESION:

May involve LMN in ventral horn of spinal cord or motor nuclei of cranial nerves or their nerve fibers. CAUSES OF LESION: Traumatic Infective (poliomyelitis) Inflammatory Degenerative Neoplastic Vascular (lesion)

FEATURES:
Only a few muscles are involved in LMN lesion. Flaccid paralysis in LMN lesion, i-e, loss of voluntary movements with hypotonia or atonia. Loss of superficial reflexes. Loss of deep reflexes / tendon jerks. Muscle atrophy (*main cause is loss of trophic actions of motor nerves, supplying skeletal muscles). Disuse is minor cause.

 There are fasiculations (when bundles of muscle fibers contract) & fibrillations (individual muscle fibers contract) seen when there is slow degeneration of LMNs. Shortening of paralyzed muscles contractures. Reaction of degeneration: response to faradic stimulation & galvanic stimulation.

 In LMN lesion, muscles respond to faradic stimulation upto 7 days & to galvanic stimulation upto 10 days.
After 10 days, no response (faradic = interrupted current stimulation & galvanic = direct current stimulation). Babinski sign is not present.

FEATURES OF UMN LESION:

1) FEATURES OF LESION OF PYRAMIDAL OR CORTICO-SPINAL TRACT: 2) FEATURES OF LESION OF EXTRACORTICO-SPINAL OR EXTRAPYRAMIDAL TRACT.

1) FEATURES OF LESION OF PYRAMIDAL OR CORTICO-SPINAL TRACT:

FUNCTION: Control of fine skilled voluntary movements specially of distal parts of limbs. Incase of UMN lesion of pyramidal tract: A) LOSS OF FINE SKILLED VOLUNTARY MOVEMENTS, SPECIALLY OF DISTAL PARTS OF LIMBS. B) + BABINSKI SIGN / ABNORMAL PLANTAR REFLEX. C) LOSS OF SUPERFICIAL ABDOM. REFLEX

D) LOSS OF CREMASTERIC REFLEX.

NORMAL PLANTAR REFLEX:

When we scratch along lateral border of sole of foot plantar flexion of all the toes. Segment value of normal plantar reflex is S1. In addition, also + in: 1) Infants (due to incomplete myelination of cortico-spinal tract). 2) during sleep. 3) alcohol intoxication.

ABNORMAL PLANTAR REFLEX:

When we scratch dorsi-flexion of big toe & fanning out of other 4 toes.

LOSS OF SUPERFICIAL ABDOMINAL REFLEX:

Due to loss of excitatory effect of corticospinal tract on inter-neurons in reflex arc. This reflex is polysynaptic because interneurons are also involved. Root value = T7 T11.

LOSS OF CREMASTERIC REFLEX:

Also due to loss of facilitation of interneurons by cortico-spinal tract. This reflex is also polysynaptic. Root value is L1.

LESIONS OF EXTRACORTICO-SPINAL TRACT:

FEATURES: A) SPASTIC PARALYSIS. B) INCREASED MUSCLE TONE. C) SLIGHT MUSCLE ATROPHY. D) TENDON JERKS. E) ANKLE OR KNEE CLONUS. F) CLASP KNIFE RIGIDITY.

A) SPASTIC PARALYSIS:
Loss of voluntary movements with increased muscle tone. In this lesion large no. of muscles are involved. It may be hemiplegia.

B) INCREASED MUSCLE TONE:

This is due to facilitation of stretch reflex or myotatic reflex becomes hyperactive.

C) SLIGHT MUSCLE ATROPHY:

This is due to disuse slight atrophy.

D) TENDON JERKS:
They become brisk or exaggerated due to facilitation of stretch reflex.

E) ANKLE OR KNEE CLONUS:

This is present when we apply a sudden maintained stretch to musles rhythmic, repeated muscle contraction.

F) CLASP KNIFE RIGIDITY:

In the patient, if we try to flex arm at elbow there is initial resistance to flexion, but when we continue flexion there is rapid flexion. Mechanism: Initially: stretch reflex is initiated, which is hyperactive in these patients. Triceps contracts extension at elbow. Later on: muscle tension increases. There is activation of inverse stretch reflex due to excitation of golgi tendon organs muscle relaxes rapid flexion.

CLINICAL PICTURE OF UMN LESION:

We dont get patients with lesion of one type of tract. The lesions involve both pyramidal & extra-pyramidal tracts. So we get mixed type of clinical features in clinical practice.

DIFFERENCES BETWEEN:
LMN LESION: UMN LESION (Pyramidal & Extrapyramidal) LEVEL OF LESION: Level is above alpha motor neuron in cerebral cortex, basal ganglia & brain stem.

LEVEL OF LESION: Level is alpha motor neuron in ventral horn.

 LMN LESION: TONE: Loss of voluntary movements with hypotonia / atonia. No. OF MUSCLES INVOLVED: Small no. of muscles are involved. TYPE OF PARALYSIS: Flaccid paralysis.

UMN LESION:
TONE: Loss of voluntary movements with hypertonia. No. OF MUSCLES INVOLVED: Large no. of muscles involved. TYPE OF PARALYSIS: Spastic paralysis (clasp knife rigidity).

 LMN LESION: CAUSE OF ATROPHY: Due to loss of trophic action of nerves mainly. REFLEXES: Loss of deep reflexes. No ankle / knee clonus. Negative babinski sign.

UMN LESION:
CAUSE OF ATROPHY: Due to disuse & only slight atrophy. REFLEXES: Reflexes become exaggerated due to facilitation of stretch reflex. ankle / knee clonus. Positive babinski sign.

 LMN LESION:
CONTRACTURE: Present. FASCICULATION / FIBRILLATION: Present (slow degeneration of LMNs).

UMN LESION:
CONTRACTURE: Absent. FASCICULATION / FIBRILLATION: Absent . There is loss of skilled movements of peripheral limbs.

 LMN LESION:
HEMIPLEGIA: Not a common feature. SUPERFICIAL REFLEXES: Lost. CONTROL OF MOTOR ACTIVITY: Final common pathway to skeletal muscles.

UMN LESION:
HEMIPLEGIA: Common SUPERFICIAL REFLEXES: Lost. (abdominal, cremasteric). CONTROL OF MOTOR ACTIVITY: Controls motor activity through separate pathways.