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PAIN AND ITS MANAGEMENT
D. C. MIKULECKY
PROFESSOR OF PHYSIOLOGY
SOMATOSENSORY
CORTEX
SOMATOTOPIC ORGANIZATION
MORE AREA TAKEN BY SENSITIVE
REGIONS (GREATER RECEPTOR DENSITYSMALLER RECEPTIVE FIELDS)
CELLS RESPONDING TO ONE TYPE OF
SENSATION IN VERTICLE COLUMNS(FOR
EXAMPLE..PACINIAN CORPUSCLES IN A
FINGERTIP)
THE ANTEROLATERAL PAIN AND
TEMPERATURE PATHWAY
SENSORY NEURONS SYNAPSE IN SUBSTANTIA
GELATINOSA
SECONDARY NEURONS CROSS MIDLINE AND
ASCEND IN ATEROLATERAL COLUMN
BRANCHES GO TO THE RETICULAR FORMATION
TERMINATE IN VENTROBASAL NUCLEUS OF
THALMUS
TERTIARY NEURONS GO TO SENSORY CORTEX
THE ANTEROLATERAL
PATHWAY
SUBSTANTIA
GELITANOSA
THE SENSATION OF PAIN
FAST PAIN
SLOW PAIN
MECHANICAL PAIN
CHEMICAL PAIN
THERMAL PAIN
PAIN NERVES:
TYPE DIAMETER CONDUCTI SENSORY
ON
INFORMATION
(m)
VELOCITY
(m/s)
III(A)
5
15
IV(C)
1
2
LIGHTLY
MYELINATED:
TOUCH,
PRESSURE, AND
PAIN
UNMYELINATED:
PAIN AND
TEMPERATURE
FAST PAIN
OCCURS IN ABOUT 0.1 SECONDS
SUBJECTIVE DESCRIPTION:SHARP, ACUTE, ELECTRIC
OR PRICKING
A FIBERS SYNAPSE ON CELLS IN LAMINA I (LAMINA
MARGINALIS) IN THE DORSAL HORNS
SECONDARY NEURONS CROSS AND TRAVEL THROUGH
THE ANTEROLATERAL PATHWAY TO THE VENTROBASAL
COMPLEX OF THE THALAMUS
TERTIARY NEURONS GO TO THE PRIMARY SENSORY
CORTEX
FAST PAIN PATHWAY
VENTROBASAL
NUCLEUS
LAMINA
MARGINALIS I
II
IV
III VI
V
VII
SUBSTANTIA
GELITANOSA
IX
VIII
ANTEROLATERAL
PATHWAY
SLOW PAIN
OCCURS AFTER A SECOND OR MORE
OFTEN ASSOCIATED WITH TISSUE
DESTRUCTION
SUBJECTIVELY DESCRIBED AS BURNING,
ACHING,THROBBING, NAUSEOUS, OR CHRONIC
C FIBERS WHICH SYNAPSE IN THE
SUBSTANTIA GELITANOSA
FINAL PROJECTION IS THE FRONTAL CORTEX
SLOW PAIN PATHWAY
VENTROBASAL
NUCLEUS
LAMINA
MARGINALIS I
II
IV
III VI
V
VII
SUBSTANTIA
GELITANOSA
IX
VIII
ANTEROLATERAL
PATHWAY
MECHANICAL, CHEMICAL
AND THERMAL PAIN
FAST PAIN IS GENERALLY MECHANICAL OR
THERMAL
SLOW PAIN CAN BE ALL THREE
CHEMICAL PAIN RECEPTORS: BRADYKININ,
SEROTONIN, HISTAMINE, POTASSIUM IONS,
ACIDS, ACETYL CHOLINE AND PROTEOLYTIC
ENZYMES
PROSTAGLANDINS ENHANCE PAIN SENSATION
BRAIN STRUCTURES AND PAIN
COMPLETE REMOVAL OF THE SENSORY
CORTEX DOES NOT DESTROY THE
ABILITY TO PERCIEVE PAIN
STIMULATION OF THE SENSORY CORTEX
EVOKES A SENSATION OF PAIN
PAIN CONTROL (ANALGESIA)
THE ANALGESIA SYSTEM
THE BRAIN’S OPIATE SYSTEM
INHIBITION OF PAIN BY TACTILE
STIMULATION
TREATMENT OF PAIN BY ELECTRICAL
STIMULATION
REFERED PAIN
THE ANALGESIA SYSTEM
PREAQUEDUCTAL GRAY
RAPHE MAGNUS NUCLEUS
PAIN INHIBITORY COMPLEX IN DORSAL
HORNS
PAIN INHIBITORY COMPLEX:
PRESYNAPTIC INHIBITION
BRAIN STEM.NEURON
ANTEROLATERAL
PATHWAY
INHIBITORY NEURON
PAIN
RECEPTOR
+
DORSAL HORN OF
SPINAL CORD
PAIN TRANSMISSION AND
INHIBITION
SUBSTANCE P IS THE
NEUROTRANSMITTER: BUILDS UP
SLOWLY IN THE JUNCTION AND IS
SLOWLY DESTROYED
PRESYNAPTIC INHIBITION BY
INHIBITORY NEURON BLOCKS THE
RELEASE OF SUBSTANCE P
(ENKEPHALIN)
THE BRAIN’S OPIATE
SYSTEM
OPIATE RECEPTORS EXIST IN MANY
CENTERS OF THE BRAIN, ESPECIALLY IN
THE ANALGESIA SYSTEM
AMONG THE NATURAL SUBSTANCES
WHICH ACTIVATE THESE RECEPTORS
ARE: ENDORPHINS, ENKEPHALINS, AND
MORPHINE
INHIBITION OF PAIN BY
TACTILE STIMULATION
STIMULATION OF LARGE SENSORY
FIBERS FOR TACTILE SENSATION
INHIBITS PAIN TRANSMISSION FOR
SAME REGION
RUBBING OFTEN EASES PAIN
LINAMENTS, OIL OF CLOVE, ETC.
POSSIBLE EXPLANATION FOR
ACUPUNCTURE?
ELECTRICAL
STIMULATION
STIMULATION OF LARGE SENSORY
NERVES
ELECTRODES IN SKIN OR SPINAL
IMPLANTS
INTRALAMINAR NUCLEUS OF THALAMUS
REFERED PAIN
VISCERAL PAIN FIBERS SYNAPSE ON
SAME SECONDARY NEURONS AS RECEIVE
PAIN FIBERS FROM SKIN
CLINICAL ASPECTS OF PAIN
HYPERALGESIA
THE THALAMIC SYNDROME
HERPES ZOSTER (SHINGLES)
TIC DOULOUREUX
THE BROWN-SEQUARD SYNDROME
HEADACHE
HYPERALGESIA
ENHANCED SENSITIVITY AROUND
DAMAGED TISSUE
SENSITIZATION OF NOCICEPTORS
BY SUBSTANCES RELEASED WHEN
TISSUE IS DAMAGED
THE THALAMIC
SYNDROME
LESION OF SOMATOSENSORY
THALMUS
USUALLY A DISTORTED AND
EXAGERATED SUBJECTIVE QUALITY
MAY CUT OFF PAIN TRASMISSION
FROM PERIPHERY
HERPES ZOSTER
(SHINGLES)
USUALLY AFFECTS THE DORSAL
ROOT
ONE DERMATOME AND ONE SIDE
TIC DOULOUREUX
CHRONIC NEURALGIA OF
TRIGEMINAL NERVE
SOMETIMES DUE TO INFLAMMATION
(NEURITIS)
SOMETIMES TREATED SURGICALLY,
BUT OFTEN RETURNS
THE BROWN-SEQUARD
SYNDROME
CHARACTERISTIC PATTERN OF
SENSORY LOSS DUE TO LOCALIZED
DAMAGE ON ONE SIDE OF SPINE
USUALLY ACCOMPANIED BY MOTOR
LOSS AS WELL
LESION ON RIGHT HALF
OF SPINAL CORD
LOSS OF PAIN SENSATION ON LEFT SIDE
BELOW LESION
LOSS OF TOUCH AND VIBRATION ON
RIGHT SIDE BELOW LESION
LOSS OF BOTH ON RIGHT SIDE AT SAME
LEVEL
NO LOSS ABOVE LESION
HEADACHE
SELDOM DUE TO BRAIN DAMAGE
NO SENSORY NERVES IN BRAIN LIKE THERE ARE
IN PERIPHERY
TENSION INDUCED MUSCLE TIGHTNESS
SWELLING OF THE MUCOUS MEMBRANES
EYE DISORDERS
DILATION OF CEREBRAL BLOOD VESSELS
INCREASED INTERCRANIAL PRESSURE
INFLAMMATION AND SWELLING