INTRODUCTION
NEUROPHYSIOLOGY
UNDERSTANDING HOW THE BRAIN CONTROLS BODY MOVEMENTS.
HOW NEUROMUSCULAR CONTROL CAN BECOME POTENTIAL PART OF TREATMENT IN PATIENTS.
THE NEUROPHYSIOLOGY OF MUSCULOSKELETAL PAIN: FROM TISSUE NOCICEPTION TO THE PAIN NEUROMATRIX
TISSUE
HOLD THE CAPACITY TO ALERT NERVOUS SYSTEM OF POTENTIAL DANGER, HENCE TO PRODUCE ACTION.
NOCICEPTORS
CONNECTED TO AN ION CHANNEL
TWO TYPES OF NERVES : A AND C FIBERS (PRIMARY SENSORY NERVE FIBERS)
A FIBERS
FAST PAIN TRANSMITTED FROM TISSUE TO CNS.
SMALL MYELINATED NERVE FIBERS
HIGH CONDUCTION SPEED
SHARP & LOCALIZED
C FIBERS
SLOW PAIN TRANSMITTED FROM TISSUE TO CNS.
DULLER AND MORE DIFFUSE
LASTS MUCH LONGER
SMALL UNMYELINATED NERVE FIBERS
LOW CONDUCTION SPEED.
ION CHANNEL
OPENS ONCE THE NOCICEPTOR IS ACTIVATED BY A STIMULUS.
SENSORY INFORMATION
ENTERS THE CENTRAL NERVOUS SYSTEM IN SPINAL CORD
PAIN MATRIX
WILL DECIDE WHETER OR NOT THE SIGNAL SHOULD BE INTERPRETED AS THREATENING TO THE BODY HOMEOSTASIS OR NOT.
TEMPORAL SUMMATION AND WIND UP
WIND UP
PROGRESSIVE INCREASE OF ELECTRICAL DISCHARGES FROM THE SECOND-ORDER NEURON IN THE SPINAL CORD IN RESPONSE TO REPETITIVE C-FIBRE STIMULATION.
CENTRAL SENSITIZATION.
BOX 2-1
The Nervous System as Source of Nociception and Pain: Neuropathic Pain Highlights for Clinicians
MUSCULOSKELETAL SYSTEM
CAN GENERATE NOCICEPTION.
NERVOUS SYSTEM
CAN BE A SOURCE OF NOCICEPTION
NEUROPATHIC PAIN
PAIN ARISING AS A DIRECT CONSEQUENCE OF A LESION OR DISEASE AFFECTING THE SOMATOSENSORY SYSTEM.
CAN BE: PERIPHERAL OR CENTRAL
LESION
AVAILABLE EVIDENCE FROM DIAGNOSTIC INVESTIGATIONS TO REVEAL ABNORMALITY OF THE NERVOUS SYSTEM.
MAY REFER TO POSTTRAUMATIC OR POSTSURGICAL DAMAGE TO THE NERVOUS SYSTEM.
DISEASE
UNDERLYING CAUSE OF THE LESION
SOMATOSENSORY
INFORMATION ABOUT THE BODY PER SE INCLUDING VISCERAL ORGANS, RATHER THAN INFORMATION ABOUT EXTERNAL WORLD.
PATIENT WITH NEUROPATHIC PAIN EXPERIENCE
BURNING
SHOOTING
PRICKING
SENSORY TESTING
PRIME IMPORTANCE FOR DIAGNOSIS OF NEUROPATHIC PAIN
INCLUDES TESTING OF THE FUNCTION OF SENSORY FIBERS.
TUNING FORK
VIBRATION
SOFT BRUSH
TOUCH
TEMPERATURE
COLD/WARM
SUGGESTIONS FOR NEUROPATHIC PAIN.
HYPERAESTHESIA
HYPOAESTHESIA
HYPERAGLESIA
HYPOALGESIA
ALLODYNIA
PARAESTHESIA
DYSAESTHESIA
AFTERSENSATIONS
DESCENDING NOCICEPTIVE FACILITATION
CATASTROPHIZING
AVOIDANCE BEHAVIOR
FACTORS TO PREVENT EFFECTIVE DESCENDING INHIBITION
ACTIVATE DESCENDING FACILITATION
BOX 2-2
Translating the Neurophysiology of Temporal Summation and Wind-Up to Clinical Practice
HANDS ON TECHNIQUES
MUSCULOSKELETAL THERAPISTS CAN APPLY
DELIVER IDENTICAL NOCICEPTIVE STIMULI TO THE SKIN
ONCE EVERY 3 SECONDS CAN ABLE TO TRIGGER PAIN AMPLIFICATION.
MYOFASCIAL TRIGGER POINTS
DIFFERS FROM NORMAL MUSCLE TISSUE BY ITS LOWER PH LEVELS
3 MONTHS
TISSUE INJURY HEALING
FOCAL PAIN RECOVERY
CHRONIC WIDESPREAD PAIN
INJURIES TO DEEP TISSUES WHICH DO NOT HEAL WITHIN SEVERAL MONTHS.
DESCENDING NOCICEPTIVE INHIBITION
DESCENDING INHIBITORY PATHWAYS
APPLY NEUROTRANSMITTERS
SUCH AS: SEROTONIN AND NORADRENALINE
FUNCTION IS TO FOCUS/TARGET THE EXCITATORY STATE OF DORSAL HORN NEURONS
SUPRESSING SURROUNDING NEURONAL ACTIVITY
EXERCISE-INDUCED ENDOGENOUS ANALGESIA
EXERCISE IS A PHYSICAL STRESSOR THAT ACTIVATES DESCENDING NOCICEPTIVE INHIBITION.
CHRONIC LOW BACK PAIN
HAVE NORMAL ENDOGENOUS ANALGESIC RESPONSE TO EXERCISE
MANUAL JOINT MOBILIZATION
HAVE BEEN SHOWN TO ACTIVATE DESCENDING NOCICEPTIVE INHIBITION.
PAIN NEUROMATRIX OR PAIN MATRIX
BRAIN CO-WORK OR COMMUNICATE WHEN THERE IS A PAIN.
THE PAIN NEUROMATRIX
BRAIN
CAN PRODUCE PAIN WITHOUT NOCICEPTION AND VICE VERSA.
CIRCUITRY
A NUMBER OF REGIONS THAT BECOME ACTIVE ALL TOGETHER WHEN A PERSON IS IN PAIN.
PRIMARY SOMATOSENSORY CORTEX
RESPONSIBLE FOR IDENTIFYING THE LOCATION OF PAIN IN THE BODY
THE MORE ATTENTION, MORE ACTIVITY OBSERVED
AMYGDALA
FEAR-MEMORY CENTRE OF THE BRAIN
KEY ROLE IN NEGATIVE EMOTIONS
PAIN RELATED MEMORIES
THALAMUS
SENDING INCOMING MESSAGES TO OTHER BRAIN REGIONS.
TARGET FOR DEEP BRAIN STIMULATION IN PATIENTS WITH NEUROPATHIC PAIN
BRAINSTEM
TOP-DOWN PAIN INHIBITION
KEY REGIONS FOR MAINTAINANCE OF CENTRAL SENSITIZATION PAIN IN HUMANS
BOX 2-3 Long-Term Pain Memories are often Apparent in Patients with Chronic Musculoskeletal Pain
KINESIOPHOBIA
FEAR OF MOVEMENT
EXTINCTION TRAINING
RESULTS INCREASED CONNECTIVITY BETWEEN PREFRONTAL CORTEX AND AMYGDALA
PREFRONTAL CORTEX
INHIBITS THE EXPRESSION OF PAIN MEMORIES
COMMUNICATES WITH AMYGDALA AND HIPPOCAMPUS
PAIN MEMORIES CIRCUITRY
PREFRONTAL CORTEX
AMYGDALA
HIPPOCAMPUS
ON-CELLS
PROMOTE NOCICEPTION
OFF-CELLS
SUPRESS NOCICEPTION
ANTERIOR CINGULATE CORTEX
IMPORTANT FOR AFFECTIVE-MOTIVATIONAL ASPECTS OF PAIN
EMPATHY AND SOCIAL EXCLUSION
INSULA
A BRAIN REGION THAT HAS A ROLE IN THE EMOTIONAL COMPONENT OF EVERY PAIN SENSATION.
CONTRIBUTES TO SENSORY DISCRIMINATIVE ASPECT OF PAIN
CENTRAL SENSITIZATION
AUGMENTATION OF RESPONSIVENESS OF CENTRAL PAIN SIGNALLING NEURONS TO INPUT FROM LOW THRESHOLD MECHANORECEPTORS.
PERIPHERAL SENSITIZATION
LOCAL PHENOMENON
IMPORTANT FOR PROTECTING DAMAGED TISSUE DURING THE EARLY PHASES POST INJURY.
GAMMA AMINOBUTYRIC ACID (GABA)
SECOND MECHANISM CONTRIBUTING TO THE OVERACTIVE PAIN NEUROMATRIX.
IMPORTANT INHIBITORY NEUROTRANSMITTER
LESS GABA MEANS LONG TERM STRESS
BOX 2-5 Recognition of Central Sensitization Pain in Musculoskeletal Pain Patients
CHRONIC MUSCULOSKELETAL PAIN
OSTEOARTHRITIS
LOW BACK PAIN
FIBROMYALGIA
RHEUMATOID ARTHRITIS
WHIPLASH
PELVIC PAIN
LATERAL EPICONDYLITIS
DOES THE AUTONOMIC NERVOUS SYSTEM INFLUENCE PAIN?
AUTONOMIC NERVOUS SYSTEM
HYPOTHALAMUS
PITUITARY
ADRENAL
STRESS RESPONSE SYSTEM
END OF LESSON 1(: