Showing posts with label MECHANISM. Show all posts
Showing posts with label MECHANISM. Show all posts

Tuesday, 17 January 2012

IPHREHAB : PAIN MODULATION AND MECHANISM

IPHREHAB
PAIN MODULATION
  • Variability of pain caused by similar injuries.
  • Psychological variability.
  • Even suggestions of pain relief helpful.
  • Existing brain circuits modulate pain transmission pathways.
  • One of these circuits has links with hypothalamus, midbrain, medulla oblongata.
  • This pathway selectively controls spinal pain transmission neurons through descending pathways.
  • Attention, suggestion and opiods work and modulate pain through this pathway.
  • Endogenous opiod peptides such as enkephalins and endorphins work through this pathway. 
  • Prolonged pain and fear are the most  reliable activating factors for endogenous opiod pathway.
  • Released during surgical procedures and even by placebo.
Pain modulating circuits can suppress and enhance pain.
  • Both pain-inhibiting  and pain-facilitating neurons in the medulla project to and control spinal pain transmission. Hence pain can be generated without any peripheral nocuous stimuli.
  • Increased activity of these circuits is seen during migraine.
  • Pain can also be induced by suggestions-psychological factors contribute to pain.
NEUROPATHIC PAIN:
  1. Lesions in central and peripheral pathways results in loss or impairment of pain sensation.
  2. Paradoxically the damage may also produce pain- diabetic neuropathy, herpes zoster.
  3. Also damage to spinothalamic tract or thalamus can also produce pain.
  4. Severe and notoriously intractable to standart treatment.
  5. Unusually burning, tingling or electric shock like quality.
  6. Examination-Sensory deficit in the area of pain.
  7. Hyperpathia/allodynia.
  8. Topical preprations (5% lidocaine) helpful.
Mechanisms
  • Sensitized primary afferent neurons.
  • Damaged primary afferent neurons.
  • Sensitized nociceptors.-generate impulses in absence of stimulus.
  • Increased concentration of sodium channels.
  • Sensitivity to norepinephrine.
Sympathetically Maintained Pain
  • Causalgia in peripheral nerve injury.
  • Pain often begins after a delay of hours to days or even weeks.
  • Pain accompanied by swelling of extremity, periarticular osteoporosis and arthritic changes in distal joints.
  • Pain relief by sympathetic blockages.
Similar events- reflex sympathetic dystrophy- without nerve damage including fractures, soft tissue injuries, MI, stroke.

Treatment :
  • History, Evaluate, examine.
  • Remove cause.
  • Analgesics NSAIDS, Opiods

IPHREHAB : PAIN cause and why?

IPHREHAB
PAIN
  • Unpleasant sensation.
  • Localised or not localised.
  • Described differently.
  • Associated anxiety and urge to escape or terminate the feeling.
  • Dualality.
  • Acute pain associated with behavioural arousal and stress response
  • Increased BP, pupil size, plasma cotisol
  • Local muscle contraction (limb flexion, abdominal wall rigidity)
PERIPHERAL MECHANISMS
  1. Primary Afferent Nociceptors
  2. Peripheral nerve containing three different types of axons-motor, sensory, sympathetic post ganglionic.
  3. Cell bodies in dorsal root ganglion.
  4. Two processes, peripheral and central.
  5. Primary afferent are Aδ & C (unmelinated) axons.
  6. Fibers present in skin and deep somatic and visceral structures.
  7. Most of these fibers respond maximally only to intense painful stimulus and produce subjective experience of pain when electrically stimulated
  8. This defines them as primary afferent nociceptors.
  9. Nociceptors respond to many different stimuli- heating, intense mechanical stimuli (pinch), irritating chemicals.
Sensitisation
  • Intense, repeated and prolonged stimuli to an inflamed tissue lowers the threshold for activating primary afferent nociceptors.
  • Frequency of firing is higher.
  • Mediators like bradykinin, PG’s, LT contribute. 
  • Even innocuous stimulus can produce pain
  • Clinically important as it contributes to tenderness, soreness, and hyperalgesia.
  • Sensitisation has importance in visceral tissue.
  • Normally viscera is insensitive but in presence of inflammatory mediators, the sensitivity increases especially to mechanical stimulus.
  • Such afferents are termed as silent nociceptors
Nociceptor induced inflammation
  • Neuroeffector function
  • Contan polypeptides in peripheral terminals - substance P.
  • Released from primary afferent nociceptors causing v/d, degranulation of mast cells, chemoattractant and increases production and release of inflammatory mediators.
  • Tissue protectors due to these mechanisms.


CENTRAL MECHANISMS
  • Spinal Cord and Referred Pain
  • Afferent Axons enter dorsal root→ dorsal horn → spinal neurons.
  • Each afferent neuron contacts many spinal neurons and each spinal neuron receives convergent input from many primary afferents.
  • Convergence takes place and this underlies the phenomenon of referred pain.
Ascending Pathways
Afferent neuron → Spinal neurons → contra lateral side → spinothalamic tract → thalamus (several regions) → cerebral cortex (several regions).
Spinothalamic tract is crucial as damage causes impairment in transmission of these sensations.

Saturday, 7 January 2012

IPHREHAB: OBESITY & LIFESTYLE HAZARDS AND CONTROL

IPHREHAB

OBESITY

*VERY COMMON NOW-A-DAYS
*USA IS OBESE COUNTRY OF WORLD
*CHILDHOOD OBESITY HAS BECOME NATIONAL PROBLEM
*18 YEARS OLD GIRL WEIGHING 320 POUNDS DIED IN CLEVELAND
*OBESITY REDUCES LIFE SPAN
*NOT A SINGLE CENTURION IS OBESE


*

*JAPAN  &  FRANCE ARE CALLED SLIM COUNTRIES
*RESPONSIBLE FOR MANY DISEASES- Osteoarthritis, Hypertension, Heart Attack
*FAST  FOODS  ARE   RESPONSIBLE  FOR THIS
*FIBRE IN DIET REDUCES WEIGHT
*ISAPHGOL (Grandmother’s Remedy) COMMONLY USED IN INDIA


WINE

WINE IF TAKEN PROPERLY GIVES PLEASANT INTOXICATION AND PRODUCES EXHILARATION, ENERGY, CONTENTMENT, COPULENCE, FREEDOM FROM DISORDERS, SEXUAL POTENCY AND STRENGTH
Charak Samhita 800 BC

ALCOHOL
In small amounts it is GOOD
In large amounts it is Dangerous
It increases HDL level
It reduces Cholesterol. & LDL
Two small  Pegs twice a week better with water than Soda.

STRESS
MAJOR CAUSE OF HIGH BLOOD PRESSURE
DIFFICULT TO DEFINE
IMPOSSIBLE TO MEASURE
ACUTE STRESS CAN BE FATAL
BUT IS ESSENTIAL FOR LIFE
 IT IS DRIVE FOR COMPETITION

PERFECTIONIST
HE  IS  NEVER  HEALTHY
HE HAS  PHYSICAL & MENTAL PROBLEMS
HE HAS EATING DISORDERS, DIFFICULT  RELATIONSHIPS & SUICIDAL  TENDENCIES
HE  IS  ANTISOCIAL
HE  SUFFERS FROM  HIGH BLOOD PRESSURE

WAYS TO RELAX
YOGA
   THEY ARE HINDU MEDITATIVE PRACTICES MAINLY CONTROL BREATHING & POSTURE
TRANSCENDENTAL MEDITATION (TM)
   USUALLY THINKING OF A WORD OR  SOUND

*PROGRESSIVE MUSCLE RELAXATION (PMR)
   ACHIEVE CONSCIOUS CONTROL OVER MUSCLES GROUP AND INDUCE DECREASE IN TONE
* BIO FEED MECHANISM
    REDUCES BLOOD PRESSURE DRAMATICALLY IN HYPERTENSIVE .