Pain Reflex Action YouTube Lecture Handouts

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PAIN

  • Word is from Greek word POENA meaning penalty or punishment

  • Sherrington defined Pain as:

“The psychical (pertaining to mind) adjunct (joined to) of an imperative (urgent) protective reflex”

  • It is unpleasant sensory experience usually associated with emotional disturbances. It also indicates actual or potential tissue damage

  • Though unpleasant but has great survival value

Purpose of pain

  • Informs not only about quality of stimulus but

  • Has protective function

  • Informs that harmful agent is close to body

  • The part of body or stimulus should be removed

Types of Pain

  • FAST pain eg. Skin is cut with a sharp knife. Usually not in deeper tissues

  • Acute pain

  • Appear with in 0.1 ms. After the application of stimulus

  • Sharp, well localized pricking sensation

  • Carried by Aδ Myelinated fibers

  • Fibers have topographic representation in cerebral cortex

  • It elicits withdrawal reflex

  • Sym. Response seen—

    • Tachycardia

    • Increase in B.P.

  • Chemical transmitter --Glutamate

Slow pain

  • Appears after a second or more

  • Poorly localized, dull, throbbing or burning sensation

  • Carried by Type C unmyelinated fibers

  • Produces, nausea, vomiting, lowering of BP

  • Feeling of Intense unpleasantness

  • Chemical Trans.--- substance P

Pain perception

  • Occurs at sub cortical level at Thalamus

  • Somatosensory cortex help in exact localization and meaningful interpretation of degree & quality of pain

Visceral Pain

  • Characteristics

    • Poorly Localized (receptors are few)

    • Unpleasant often associated with nausea, vomiting & other Autonomic disturbances

    • Usually Radiates

Causes

  • Distension of hollow viscera

  • Intestinal obstruction

  • Inflammation

  • Ischemia

  • Traction on mesentry

  • Spasm of hollow structures eg. Gall bladder, ureter etc.

Viscera insensitive to pain

  • Parenchyma of liver

  • Alveoli of lungs

Neural Pathway

  • Afferents reach the Spinal cord via Autonomic nerves

  • Cell bodies are in Dorsal Roots

  • In CNS path is same as that of somatic sensation

  • Visceral pain results in Guarding (contraction of abdominal muscles) which protects underlying viscera

Referred Pain

  • Visceral or deep somatic pain is frequently felt not in the viscus but in the somatic structure considerably away from it.

  • Radiation of Pain: visceral Pain is both local and Referred

eg.

  • Cardiac Pain radiating to the inner aspect of the Lt. Arm

  • Irritation of diaphragm causes pain in the tip of shoulder

  • Pain of gall bladder stone, tip of rt. shoulder

Organs from heart to ureter

Organs

Organs from heart to ureter

Mechanisms

  • Dermatomal Rule

  • Pain is usually reffered to the structure that has developed from the same embryonic segment or dermatome eg. Heart and Arm have same segmental origin

Role of convergence

Nerves from viscera & somatic structure converge on the same Spin thalamic N.

Since somatic Pain is more common, Brain has learned that activity in a given pathway is caused by pain in a particular somatic structure. Now even if the activity is in viscera, it is projected to somatic area

Visceral and skin fibres

Visceral and Skin Fibres

Visceral and skin fibres

Facilitation Effect

  • Activity in Visceral afferents produce subliminal fringe effect & lowers the excitability threshold of Spin thalamic neurons

  • Now any activity in somatic area (which normally dies out) is facilitated and reaches conscious level

Role of past experience

  • It also plays imp. Role

  • The main cause is Plasticity in the CNS and Convergence of somatic & visceral fibers on the second order neurons

  • Imp. Visceral Pain initiates reflex spasm of abdominal muscles & make them rigid. It is called guarding & is protective

Pain Suppression System

Observations:

  • Reaction to pain varies from person to person

  • Rubbing or massaging reduces pain

  • Soldiers feels less pain in battle field

  • Counter irritants reduce pain

  • Acupuncture reduces pain

  • (TENS) Trans cutaneous electric Nerve Stimulation

Analgesic Systems

I Analgesia produced by stimulation of nerves. It is at two levels

  • Spinal &

  • Supraspinal

II Release of Endogenous Opioid Peptides

Spinal System

Gate control theory (Melzack & Wall)

  • A hypothetical Gate is in Dorsal Horn

  • Interaction is between large diameter proprioceptive fibers & peripheral fibers carrying pain sensation

  • Pain signals entering in Lateral Spin thalamic Tract are modified here

Image of Gate Control System

Image of Gate Control System

Image of Gate Control System

  • Stimulation of large fibers ‘Close the Gate’

  • Stimulation of small fibers ‘Open the Gate’

Supraspinal System

  • Mesencephalic Pain Inhibitory System: Fibers arise from Mid Brain and descend down to the Dorsal Horn of Spinal Cord

  • Following structures are invol

    • Periaqueductal grey & Periventricular area

    • Nucleus Raphe Magnus in Medulla

    • Dorsal horn of spinal cord

Image of Third Ventricle

Image of Third Ventricle

Image of Third Ventricle

Neurotransmitters

  • Periaqueduct neurons---Enkephalin

  • Raphae Magnus Nu. -----Serotonin

  • Dorsal horn neuron------Enkephalin

  • This neuron in dorsal horn causes Pre & Post Synaptic Inhibition of incoming type C & A δ fibers

Pain signals are blocked at initial entering point

Morphine & Opiate receptors

It was long known that injection of morphine into periventricular & periaqueductal areas cause exteeme degree of analgesia.

Endogenous Opioids

  • Morphine and Opioid Peptides produce analgesia by binding to Opiate receptors

  • Three types of receptors

    • µ -- β- Endorphin

    • ĸ -- Enkephalins

    • δ -- Dynorphins

Physiological Significance

  • Morphine acts by two mechanisms

  • Spinal level---decreases release of substance ‘P’

  • Supraspinal level--activates descending pathways

Hyperalgesia

Is decrease in pain threshold

  • Two types

    • Primary &

    • Secondary

Motor activity of body

Two motor sy.

  • Medial motor system: Phylogenetically old. Includes:

    • Axial & girdle Muscles

    • Action involves the Axis & Proximal limbs

    • Determine Posture & Equilibrium

Tracts involved

  • Ant. Cortico spinal

  • Some fibers of Corticobulbar

  • Lat. Vestibulospinal

  • Medial “

  • Retoculospinal

  • tectospinal

Lateral Motor system: phylogenetically new

  • Muscles of digits & distal segment of limb

  • Regulates skill voluntary movements

Tracts are

  • Corticobulbar

  • Lateral Corticospinal &

  • Rubrospinal

Descending/ Motor Tracts

  • Pyramidal &

  • Extrapyramidal: all other tracts

    • Reticulo spinal

    • Rubro “

    • Vestibulo “

    • Tecto “

    • Olivo “

Pyramidal tract

Salient features:

  • Longest tract

  • Fib. Unmyelinated at birth, myelination begins in II postnatal week & is completed by 2 years

  • 80% fib. Are small diameter 1 to 4 µm 20% are large 11 to 22 µm

  • Large fib. Arise from cells of Betz present in primary motor cortex

  • Large fib. Have a tendency to disappear at old age causing automatic shaking movement

  • Phylogenetically ant. Pathway is old

Pathway

  • Corticonuclear: begins in cerebral cortex & ends in brain stem (motor cranial nuclei)

  • Corticospinal: from cerebral cortex to Spinal ventral horn cells

Origin

  • Motor cortex, area 4 ----------30%

  • Premotor cortex, area 6------ 30%

  • Somatosensory area I & II--- 40% and adjacent parietal lobe association cortex

Path

  • Fibs. Form Corona radiata to reach I.C.

  • In Internal Capsule tract lies in the Genu, and ant. 2/3 of posterior limb

  • Fibs. Are arranged in sequential order

  • Mid brain, fibs. Lie ventral to the substantia nigra occupying middle 3/5 of this reg.

  • Pons, here the tract is broken up into scattered bundles by the nuclei pontis & the fibs. Of middle cerebellar peduncle

  • Medulla, fibs. Reunite before entering medulla. They in ventral part producing a bulge the Pyramids (tract named)

    • 80% cross– Lateral Corticospinal

    • 20% uncrossed—Ant. Corticospinal

Image of Motor Cortex

Image of Motor Cortex

Image of Motor Cortex

Functions

  • Controlls, voluntary, fine, precise skilful movements of the limbs

  • Fibers are closely packed in Internal capsule & Brainstem small lesion here can cause widespread paralysis

Extrapyramidal Tracts

  • Rubrospinal

  • Reticulospinal

    • Medial & lateral

  • Vestibulospinal

  • Tectospinal

  • Medial longitudinal fasciculus

  • Olivospinal

Rubrospinal tract

  • Origin: Red nucleus (magnocellularis)

  • Course: crossed, does not extend below thoracic region

  • Termination: on interneurons in dorsal horn

  • Functions: facilitatory to flexor mus.

Inhibit extensors / antigravity mus.

Reticulospinal

Medial (pontine) Reticulospinal

  • Origin: Medial pontine reticular format.

  • Course: mostly crossed

  • Termination: interneurons terminating on alpha & gamma neurons

Lateral (medullary) reticulospinal

  • Origin: Gigantocellular component of medullary reticular formation

  • Course: mostly uncrossed

  • Termination: interneurons

Functions of RS

  • Two tracts are mostly antagonistic

  • Antigravity Mus.

    • Pontine ----Ex.

    • Medullary----Inhi.

  • Mus. Tone, act through gamma mn.

    • Pontine----Facilitatory

    • Medullary ---Inhi.

  • Can control ANS.

Vestibulospinal

  • Origin: lateral vestibular nucleus of cerebellum (Deiters Nu.)

  • Course: uncrossed, runs entire length of spinal cord

  • Termination: some directly on alpha mn. (alpha rigidity)

Functions

  • Facilitatory to extensors

  • Inhib. To flexors

  • MAINTENANCE OF POSTURE

Tectospinal

  • Origin: Sup. Colliculi

  • Course: crossed, cervical rg.

  • Termination: inter neurons

  • Functions: Spino Visual Reflex

  • Turning of head & moving the arms in response to visual, hearing, & other exteroceptive stimuli

Medial Longitudinal Fasciculus

Origin: from

  • Vestibular nu.

  • Reticular formation

  • Sup. Colliculi

  • Interstitial Nu. Of Cajal

  • Course: uncrossed, well defined in upper cervical seg.

Functions

  • Ocular move. In response to vestibular & auditory stimuli.

  • Integration of eye & neck movement.

Olivospinal tract

  • Presence is doubtful

  • Functions: exact is not known probably involved in reflex movement.

Applied Aspects

Important points

  • 1 Common Motor path

    All motor activities are finally controlled by α motor neuron

  • 2 Total separation of Pyramidal & E.P. is not possible, usually both are affected simultaneously

Common terms:

  • Monoplegia: paralysis of one limb. Injury to area 4 (fibs. Are scattered)

  • Hemiplegia: paralysis of one side of body. Injury at Internal capsule.

  • Paraplegia: paralysis of both the lower limbs. Injury of Spinal cord in lower part

  • Quadriplegia: paralysis of all 4 limbs. Injury of Spinal cord in upper Cervical rg.

Lesions of the pyramidal Tracts

  • Findings are on the opposite side

  • Acute stage / stage of shock

    • Hypotonia

    • Flaccid paralysis (no reflex movement)

    • Vol. muscles are more affected eg. Mus. of face, leg, arm, hand etc.

    • Mov. Of respiration, head, trunk & abdominal wall retained

    • If corticobulbar fibs. Escape, eyeball mov. Persist

    • Emotional mov. Persist & are strong

    • All reflexes super. & deep are lost

  • Stage of recovery

  • The affected mus. Become spastic

  • Body assumes characteristic position

  • Associated mov. Can be aroused

  • All superficial reflexes lost

  • Deep reflexes hyperactive

  • Babinski sign ‘positive’

  • Patient may walk with slight limp

  • Power returns in arm & face

  • Gait. Spastic hemiplegic gait

Effects of upper motor neuron lesion and lower motor neuron lesion

Image of Clinical Confirmation And Clinical Observation
Image of Clinical Confirmation And Clinical Observation

Effects

Upper motor neuron lesion

Lower motor neuron lesion

Clinical Observation

1. Muscle tone

Hypotonia

Hypotonia

2. Paralysis

Spastic type of paralysis

Flaccid type of paralysis

3. Wastage of Muscle

No Wastage of Muscle

Wastage of Muscle occurs

4. Superficial reflexes

Lost

Lost

5. Plantar reflex

Abnormal plantar reflex-—Babinski’s sign

Plantar reflex—absent

6. Deep reflexes

Exaggerated

Lost

7. Clonus

Present

Lost

Clinical Confirmation

8. Electrical activity

Normal

Absent

9. Muscles affected

Groups of Muscles are affected

Individual muscles are affected

10. Fascicular twitch in EMG

Absent

Present

Image of Normal Toe Flexion And Positive Babinski's Reflex

Image of Normal Toe Flexion and Positive Babinski's Reflex

Image of Normal Toe Flexion And Positive Babinski's Reflex

Lesions of Spinal Cord

  • Complete transection: Causes

    • Gunshot injury

    • Dislocation of spine

    • Occlusion of blood vessels

  • Incomplete Trans. Here some fibers escape

  • Hemisection: one lateral half affected

Complete Transection

Clinical stages:

  • Stage of Spinal Shock

  • Stage of Recovery / Reflex Activity

  • Stage of Reflex Failure

Stage of Spinal shock

  • Immediately after injury -- there is cessation of all activities

    • Cervical trans. - Fatal, because of respiratory paralysis

    • Transection at Lower level– Patient feels as if he is cut in two parts

  • Upper part unaffected

  • Lower part deprived of all sensory & motor activities

Changes in lower part

  • All sensations lost

  • Muscle Tone is lost

  • All Reflexes superficial & deep lost

  • Change in BP depends on level of transection

    • If at T1 marked fall in BP.

    • Below L2 no significant effect

  • Urinary bladder & rectum are paralysed

  • The penis is flaccid & erection is impossible

Cause of Spinal shock: sudden stoppage of excitatory impulses from higher centers

  • Duration & severity depends on degree of encephalization (evolution of animal) higher the animal longer the period

  • Frog--------------few minutes

  • Cats & dogs-----few hours

  • Monkeys---------few days

  • Humans ---------about 3 weeks

Stage of recovery/stage of reflex activity

  • Smooth muscles are First to recover

    • Sphincter of UB gets tone very soon

    • Retention of urine

    • Reflex evacuation of bladder & Ref. defecation

  • Next tone of blood vessels regained

    • BP becomes normal

    • Skin becomes normal

    • Bed sores if any heals rapidly

  • Skeletal mus. Tone recovers after ~3 weeks

  • Tone returns first in flexors, paraplegia of flexion

  • Limbs cannot support body weight

  • No wasting of muscles

  • Reflex activity returns few weeks after return of muscle tone

  • First reflex to return is Babinski positive

  • Extensor reflex appears after some time

  • Mass reflex established

Stage of Reflex Failure

  • Due to malnutrition, infection, toxaemia

  • Gen. Condition deteriorates

  • Threshold of stimulus increases

  • Reflexes more difficult to elicit

  • Mass reflex abolished

  • Muscles become flaccid

  • Wasting present

Incomplete Transection of SC

  • There is partial lesion involving both the sides of spinal cord

  • SC. is gravely injured, but does not suffer from complete division

  • Effect occurs in three stages

  • Stage I & III are similar to complete Transection

  • Stage II differs remarkably

Table of Complete Transection And Incomplete Transection
Table of Complete Transection And Incomplete Transection

SN

Complete Transection

Incomplete Transection

1

TONE returns in Flexor muscles First

In Extensor muscles first because some descending fib. may escape injury (Vestibul ospinal & Ret. Spinal)

2

Paraplegia in Flexion

(higher tone in flexor muscles)

Paraplegia in Extension (higher tone in extensor mus)

3

Flexor Reflexes return first eg. Withdrawal Reflex

Extensor Reflexes return first eg. Stretch Reflex.

  • In incomplete transection range of reflex activity is greater & movement of locomotion can be carried out to some extent. Stepping movements can be seen (Phillip sons Reflex)

Brown Squared syndrome Hemisection of S.C

Lateral half of S.C. is involved

  • Immediate effect– Spinal shock

  • Late effects-

    • Changes below the level

    • Changes at the level

    • Change above the level

Below the level

  • Same side

    • Sensory: Loss of fine touch, tactile localization, tactile discrimination, vibration sense, kinaesthetic sense & Stereognosis.

    • Motor

  • UMN paralysis

    • Vasomotor

Temporary loss of tone, leads to fall in BP.

  • Opposite side

    • Sensory: Total loss of Crude touch, temp. & pain sensation

  • Motor

Not much, UMN paralysis of few muscle fibs. May be because of damage to direct pyramidal fibers

In nutshell

  • Same side: extensive motor loss little sensory loss.

  • Opposite side: extensive sensory loss little motor loss.

At the level

Same side:

  • Sensory ---- all sensations lost

  • Motor--------LMN paralysis

    • Flaccid paralysis

    • all reflexes lost

    • no muscle power

    • Wasting & degen. Seen

  • Vasomotor system --- complete & permanent failure

Opposite side:

  • Sensory

    • Some loss of pain & temp. (Horizontal fibs.)

    • Tracts of Gall & Burdach not affected

  • Motor

    • Usually no change

Above the lesion

  • Same side

    • Sensory, a band of hypaesthesia can be seen because of irritation of damaged ends of nerve fibers

    • Motor, twitching of muscles can be present due to irritation of nerves

  • Opposite side

    • Not much changes

Image of Lemniscal System

Image of Lemniscal System

Image of Lemniscal System

Image of Site of Lesion

Image of Site of Lesion

Image of Site of Lesion

Tabes Dorsalis

Causes: Usually caused by Syphilis, bilateral degeneration of post. Nerve roots & post. Funiculi. (Sp. Fas. Gracilis) Characteristic features

  • Lightning pain due to stimulation of pain fib. in DNR with pain free intervals

  • Pain sensitivity decreases, resulting in trophic changes

    • Perforated ulcers of skin at pressure points

    • Charcot joints deformation due to repeated trauma caused by loss of pain sensation

  • Loss of sensation: on same side at and below the lesion. Position sense, vibration, Stereognosis, discriminative touch lost

  • Reflexes: tendon reflexes lost

  • Sensory ataxia due to lack of co-ordination of muscles Romberg’s Sign positive

Syringomyelia

Causes: Excessive over growth of glial tissue along with cavitation in grey matter around central canal of spinal cord. Cervical enlargement is more frequent site effected

Characteristic features:

  • Sensory: dissociated anaesthesia. Loss of pain & temp. With retention of touch

  • Symptoms are bilateral usually hands & arms affected due to predilection for cervical region

  • Motor: occurs with further spread of gliosis & cavitation

  • Flaccid paralysis LMN type

  • Progressive spastic paralysis, if diseases progresses to involve Pyramidal & Extrapyramidal tracts

Sub-acute Combined degeneration

  • Cause: usually associated with Pernicious Anaemia, lack of Intrinsic Factor essential for Vit. B12 absorption

  • Bilateral degeneration of white fibs. Of the dorsal & lateral column of S.C. lumbo sacral region is especially involved

  • Manifestation: loss of position & vibration sense of lower extremities

  • UMN type paralysis, Babinski positive

Disseminated (Multiple) Sclerosis

  • Widespread demyelination in CNS.

  • Nerve cells are replaced by Glial cells.

  • Crippling disease

  • Both sensory & motor symptoms may be present

  • Sign & symptoms depend on Asc. or Des. Tracts involved