CNS PHYSIOLOGY

BYAtifa Ambreen (Lab technologist )

Spinocerebellar tract• Functions of spino-cerebellar

tract:– Subconscious kinesthetic

sensations.– Impulses from proprioceptors cerebellum coordination of movements & posture maintenance.

– Information to cerebellum about motor impulses, which have reached the ventral horn motor neurons along the cortico-spinal & rubro-spinal tracts.

Miscellaneous ascending tracts:Spino-tectal tract:

1st order neurons:• Enter spinal cord through

posterior nerve root synapse with neurons in the grey matter of spinal cord.

2nd order neurons:• Arise from here cross over

to opposite side antero-lateral white column tract ascends medulla joins spinal leminiscus terminate into superior colliculus in tectum of midbrain.

Function:– Afferent pathway for spino-

visual reflexes control movement of head & eyes towards source of stimulation.

Miscellaneous ascending tracts:Spino-reticular tract:

1st order neurons:• Enter spinal cord through posterior nerve root

synapse with neurons in lateral grey horn of spinal cord.

2nd order neurons:• Arise from here lateral white column on same side

(mainly no crossing over) ascends as spino-reticular tract terminates in reticular formation of medulla, pons & midbrain.

Function:• Important in control of level of consciousness /

alertness, awareness.

Miscellaneous ascending tracts:Spino-olivary tract:

1st order neurons:• Enter the spinal cord through posterior nerve root

synapse with neurons in grey matter of spinal cord.2nd order neurons:• Arise from here no crossing over lateral white

column ascends medulla synapse with neurons in inferior olivary nucleus.

3rd order neurons:• Arise here cross to opposite side inferior

peduncle terminate in cerebellum.Function:• Carries proprioceptive impulses.

Descending motor pathways / tracts:

1) PYRAMIDAL / CORTICO-SPINAL.2) EXTRA-PYRAMIDAL / EXTRA CORTICO-

SPINAL. (All the descending motor pathways, other than pyramidal are called extrapyramidal).

PYRAMIDAL TRACTS:• Consist of 1 million fibers.

• Mostly myelinated fibers, but slow conducting.

• Tract originates from cerebral cortex.

• 30% of fibers originate from primary motor area.

• Another 30% from pre-motor area & supplementary motor area.

• 40% from somatic sensory area of cerebral cortex.

• All these fibers converge through corona-radiata towards internal capsule.

• In internal capsule, the tract occupies the genu (the bent portion) & anterior 2/3 of posterior limb.

• When tract passes through the internal capsule, fibers for cervical parts of body are in genu & fibers for lower parts of body are in posterior limb of internal capsule.

• Then tract passes into midbrain, where it occupies middle 3/5 of cerebral peduncle / crus cerebri.

• In cerebral peduncle, fibers for cervical parts of body are medial & fibers for lower parts are lateral.

• From midbrain, tract enters the pons, where tract is broken into small bundles by transverse ponto-cerebellar fibers.

• When these bundles enter medulla, these gather / unite along the anterior border of medulla to form the pyramid (a swelling).

• The tract is named pyramidal because of pyramid formation along anterior border of medulla.

• In lower part of medulla, 80% of fibers cross over to opposite side, to form MOTOR DECUSSATION.

• After motor decussation, crossed fibers enter lateral white columns of spinal cord to form lateral cortico-spinal tract.

• Fibers of tract which remain uncrossed, enter anterior white column of spinal cord to form anterior cortico-spinal tract.

• Fibers of anterior cortico-spinal tract terminate in ventral horn of cervical & upper thoracic segments of spinal cord.

• These fibers terminate onto motor neurons ( aplha & gamma).

• It is thought that these fibers are from supplementary motor area, for control of attitudinal or positional movements,e-g, in climbing posture.

• Fibers of lateral cortico-spinal tract terminate onto the motor neurons in ventral horn of spinal cord at various levels.

• From cortico-spinal tract as a whole,

• 45% fibers terminate in cervical segments,

• 35% in lumbar • 20% in thoracic segments

of spinal cord.

• Most of cortico-spinal fibers for their termination first synapse with inter-neurons which in turn synapse with motor neurons (alpha & gamma).

• Only fibers which arise from Betz cells (Giant pyramidal cells), which form only 3% fibers, terminate directly into motor neurons.

• Certain branches of cortico-spinal tract go to different brain parts:

– To caudate & lentiform nuclei.

– To red nucleus.

– To olivary nuclei & reticular formation.

– There are also cortico-bulbar fibers which come along cortico-spinal tract. In the brain stem these fibers cross over to opposite side to terminate with motor neurons in nuclei of cranial nerves.

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.

RUBRO-SPINAL TRACT (Cont..)

• Red nucleus receives fibers from:– Cerebral cortex &– Cerebellum.

• FUNCTION:– 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.

• Function: 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 RETICULO-SPINAL 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.

• Function: 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.

• Function: It is inhibitory for extensors (like rubro-spinal).

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 pre-gang parasymp. neurons in segments S2 – S4.

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.

VESTIBULO-SPINAL TRACT:• 2 components of the tract:• Major component Lateral V.S

Tract– lat. Vest. Nuclei. Lat. V.S Tract

• Minor component Medial V.S Tract.– med Vest. Nuclei. Med. V.S Tract

• Function: Vest-spinal tract is excitatory for extensors (unlike rubro-spinal).

• cerebellar fibers Vestibular nuclei

• internal ear fibers (vestibular apparatus Vestibular nuclei.

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.• Function: This tract controls activity of motor

neurons in spinal cord.• Inferior olivary nucleus receives fibers from cerebral

cortex, corpus striatum, reticular formation & spinal cord.

MOTOR SYSTEM CONSISTS OF 2 TYPES OF NEURONS:

• UMN: upper motor neurons

• LMN: lower motor neurons

LMN:

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

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 of LMN:

• 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 EXTRA-CORTICO-SPINAL OR EXTRA-PYRAMIDAL TRACT.

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. ReflexD) 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.

• ABNORMAL PLANTAR REFLEX (Babinski’s sign):– When we scratch dorsiflexion of big toe &

fanning out of other 4 toes.– In addition, also physiologically seen in:

• 1) Infants (due to incomplete myelination of cortico-spinal tract).

• 2) during sleep.• 3) alcohol intoxication.

• LOSS OF SUPERFICIAL ABDOMINAL REFLEX:– Due to loss of excitatory effect of cortico-spinal

tract on inter-neurons in reflex arc. This reflex is polysynaptic because inter-neurons are also involved.

– Root value = T7 – T11.• LOSS OF CREMASTERIC REFLEX:– Also due to loss of facilitation of inter-neurons by

cortico-spinal tract. This reflex is also polysynaptic.– Root value is L1.

LESIONS OF EXTRA-CORTICO-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.

LESIONS OF EXTRA-CORTICO-SPINAL TRACT:

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 don’t 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.

LMN LESION:

• LEVEL OF LESION: – Level is alpha motor neuron

in ventral horn.

• 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 (Pyramidal & Extra-pyramidal)

• LEVEL OF LESION: – Level is above alpha motor

neuron in cerebral cortex, basal ganglia & brain stem.

• 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.

• CONTRACTURE:– Present.

• FASCICULATION / FIBRILLATION:– Present (slow degeneration of

LMNs).• HEMIPLEGIA:

– Not a common feature.• SUPERFICIAL REFLEXES:

– Lost.

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.

• CONTRACTURE:– Absent.

• FASCICULATION / FIBRILLATION:– Absent . – There is loss of skilled

movements of peripheral limbs.• HEMIPLEGIA:

– Common • SUPERFICIAL REFLEXES:

– Lost. (abdominal, cremasteric).

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Brown-Sequard Syndrome

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