Powerstrips are helping people all over the world deal with body pains and aches. What is it?

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interventional pain management procedures based on probable etiologies,

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After tissue damage following any kind of injury there is release of membrane Phospholipids. By the action of enzyme PhospholipaseA2 this is converted to Arachidonic acid. It again is converted to Prostaglandins (PGs) by the action of Cyclooxygenase or COX. These PGs and other chemical mediators like bradykinin, subP serotonin, histamine, potassium and hydrogen ions sensitize A delta & C fibres (they are pain bearing nerves). So they are up regulated & impulse is easily generated and carried to the dorsal horn of spinal cord. There they synapse with cells of the spinothalamic tract, which carry the impulses up the spinal cord, through the brain stem to the thalamus. From the thalamus, impulses are delivered to various areas of the cerebral cortex that allow the perception of pain and reaction to pain.

In the dorsal horn of the spinal cord the afferent sensory nerves synapse with fibres of the ascending spinothalamic tract, either directly or via a complex system of connecting fibres or interneurons, employing a variety of neurotransmitters that include substance P and glutamate. The presynaptic terminal of the afferent sensory fibre contains opioid receptors which bind endogenous opioid substances (endorphins) or exogenous opioid medications. Such binding reduces or blocks the release of neurotransmitter by the afferent sensory fibre, reducing or relieving the sensation of pain. This is the prime site of action of exogenous opioid drugs. Similarly, activation of the inhibitory neurons in the dorsal horn, known to have endorphins as neurotransmitters, will reduce pain. The inhibitory neurons are stimulated by activity in the descending pathways from the brain or by activity in other sensory fibres in the same segment, explaining why massage, heat or electrical stimulation applied to a painful area may reduce pain. Other receptors in the dorsal horn may have an opposite effect. Activation of the N-methyl D-aspartate (NMDA) receptors sensitizes dorsal horn cells & will facilitate/perpetuate the sensation and may responsible for the reduced opioid sensitivity of neuropathic pain. The NMDA receptor antagonist, ketamine, can be effective in relieving pain in this situation.

Pain impulses transmitted to the thalamus are relayed to several areas of the cerebral cortex: the sensory areas of the parietal lobe that allow localization and interpretation of the pain; the limbic system, which is involved in both the affective and autonomic response to the pain; the temporal lobe, which is involved in pain memory; and the frontal lobe where cognitive function assesses the significance of the pain and the emotional response to it.

The major endogenous mechanism of pain inhibition is the suppression of pain impulses at the dorsal horn by pathways descending from the midbrain and brain stem. These centres receive input from the cortex, the thalamus and other midbrain centres and, by a variety of descending pathways, stimulate the inhibitory interneu�rons in the dorsal horn of the spinal cord, producing analgesia or reducing pain. The neurotransmitters involved with the descending inhibitory pathways are noradrena�line and serotonin. This is a possible explanation as to why drugs that block presynaptic re-uptake and augment the postsynaptic action of these substances, such as amitriptyline, may augment analgesia.

Neuropathic pain results from anatomical and/or physiological changes which may be due to damage to nerves or neural tissue rather than the stimulation of nociceptors by tissue injury or inflammation. Pain results from spontaneous electrical activity of the damaged nerves or to increased sensitivity to exogenous stimuli; the neural pathways involved are the same as for nociception. Damage to sensory afferent fibres results in a significant reduction in the number of opioid receptors in the presynaptic terminals of the affected fibres in the dorsal horn, possibly explaining the reduced opioid sensitivity of neuropathic pain. Damage to sympathetic nerve fibres may lead to sympathetic type pain in which neuropathic pain is accompanied by signs of autonomic dysfunction, including vasomotor instability and sudomotor (sweating) changes.

After tissue damage following any kind of injury there is release of membrane Phospholipids. By the action of enzyme PhospholipaseA2 this is converted to Arachidonic acid. It again is converted to Prostaglandins (PGs) by the action of Cyclooxygenase or COX. These PGs and other chemical mediators like bradykinin, subP serotonin, histamine, potassium and hydrogen ions sensitize A delta & C fibres (they are pain bearing nerves). So they are up regulated & impulse is easily generated and carried to the dorsal horn of spinal cord. There they synapse with cells of the spinothalamic tract, which carry the impulses up the spinal cord, through the brain stem to the thalamus. From the thalamus, impulses are delivered to various areas of the cerebral cortex that allow the perception of pain and reaction to pain.

In the dorsal horn of the spinal cord the afferent sensory nerves synapse with fibres of the ascending spinothalamic tract, either directly or via a complex system of connecting fibres or interneurons, employing a variety of neurotransmitters that include substance P and glutamate. The presynaptic terminal of the afferent sensory fibre contains opioid receptors which bind endogenous opioid substances (endorphins) or exogenous opioid medications. Such binding reduces or blocks the release of neurotransmitter by the afferent sensory fibre, reducing or relieving the sensation of pain. This is the prime site of action of exogenous opioid drugs. Similarly, activation of the inhibitory neurons in the dorsal horn, known to have endorphins as neurotransmitters, will reduce pain. The inhibitory neurons are stimulated by activity in the descending pathways from the brain or by activity in other sensory fibres in the same segment, explaining why massage, heat or electrical stimulation applied to a painful area may reduce pain. Other receptors in the dorsal horn may have an opposite effect. Activation of the N-methyl D-aspartate (NMDA) receptors sensitizes dorsal horn cells & will facilitate/perpetuate the sensation and may responsible for the reduced opioid sensitivity of neuropathic pain. The NMDA receptor antagonist, ketamine, can be effective in relieving pain in this situation.

Pain impulses transmitted to the thalamus are relayed to several areas of the cerebral cortex: the sensory areas of the parietal lobe that allow localization and interpretation of the pain; the limbic system, which is involved in both the affective and autonomic response to the pain; the temporal lobe, which is involved in pain memory; and the frontal lobe where cognitive function assesses the significance of the pain and the emotional response to it.

The major endogenous mechanism of pain inhibition is the suppression of pain impulses at the dorsal horn by pathways descending from the midbrain and brain stem. These centres receive input from the cortex, the thalamus and other midbrain centres and, by a variety of descending pathways, stimulate the inhibitory interneu�rons in the dorsal horn of the spinal cord, producing analgesia or reducing pain. The neurotransmitters involved with the descending inhibitory pathways are noradrena�line and serotonin. This is a possible explanation as to why drugs that block presynaptic re-uptake and augment the postsynaptic action of these substances, such as amitriptyline, may augment analgesia.

Neuropathic pain results from anatomical and/or physiological changes which may be due to damage to nerves or neural tissue rather than the stimulation of nociceptors by tissue injury or inflammation. Pain results from spontaneous electrical activity of the damaged nerves or to increased sensitivity to exogenous stimuli; the neural pathways involved are the same as for nociception. Damage to sensory afferent fibres results in a significant reduction in the number of opioid receptors in the presynaptic terminals of the affected fibres in the dorsal horn, possibly explaining the reduced opioid sensitivity of neuropathic pain. Damage to sympathetic nerve fibres may lead to sympathetic type pain in which neuropathic pain is accompanied by signs of autonomic dysfunction, including vasomotor instability and sudomotor (sweating) changes.

Chronic pain: a symptom or a disease?

Pain has been defined by International Society for Study of pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." Note the last few words, even in the absence of actual/potential tissue damage if a person describe unpleasant sensation in terms of actual/potential tissue damage it is called pain. Take the example of Phantom limb pain. Here patient feel painin the limb which is not there; so question of tissue damage does not arise. Till 1960s doctors thought it was due to psychological problem but now we know the exact pathophysiology of pain, which is a real painand not psychological. Similarly in lumbago, sciatica, CRPS, fibromyalgia etc. there are definite pathophysiological problem in the nervous system which can be reversed with interventional pain management. It is now definitely proved that with a few exception like Rheumatoid arthritis in all chronic pain there are problems in the nervous system and so Chronic pain can be called a disease itself.

painmay be broadly divided into two types:

Acute pain( may be called Physiological Pain)

? Nociceptive
? It is a symptom of a disease
? Treatment of diseases cures pain& it is self-limiting.
? It is proportional with tissue damage & correlates with clinical finding
? It is an alarm of a disease and is our friend.

Chronic pain(may be called Pathological Pain)

? Non-nociceptive, may be Neuropathic
? It is disease itself, a disease of nervous system.
? Difficult to treat & sustaining.
? It is disproportional with tissue damage & does not correlates with clinical finding
? It is a false alarm and is our enimy.

Definition of Chronic Pain:

Chronic pain has been defined in many ways. American chronic pain association defines it as pain that continues a month or more beyond the usual recovery period. Some has described chronic pain as pain persisting more than 3 months, some by 6 months. In other way all pain is acute pain till it becomes chronic pain. But sensitization is the constant feature in all types of chronic pain.

Sensitization is a phenomenon of inappropriate or disproportionate response to normal stimulus. Sensitization outside central nervous system (CNS) is called Peripheral sensitization and that in the CNS is called Central sensitization.

PERIPHRAL SENSITIZATION: Here there are following changes:

1. Sensitization of primary afferent terminals.

? Inflammatory soup containing PGs, bradykinin, Sub P, cytokines. � sensitization of afferent nerve terminals.
? Changes in nociceptors: Active nociceptors become sensitized and sleeping nociceptors awaken. Formation of new nociceptors.
? Results: Lower activation threshold, increased response to a given stimulus, spontaneous discharge.

2. Damaged axons changes.

? They sprout, forms collaterals.
? �Ephaptic cross talk� between axons (between A-delta & C fibers; Somatic & Sympathetic fibers)
? Increased density of abnormal Na-channel & Ca-channel leading to ectopic discharge.

3. Ectopic discharges along nerve axon, terminals & at Dorsal Root Ganglion (DRG).

4. Sympathetic Nerve fibers invade DRG.

5. Phenotypic switch in expression of neuropeptides like Sub P, CGRP.

CENTRAL NENSITIZATION : changes are following:

1. Central Reorganization. When these signals (for pain) are powerful & long continued they release some oncogenes in the dorsal horn. They are c-fos & c-jun. They in turn release neuropeptides in the spinal cord, which alters anatomy and physiology of nervous system. These changes are called central reorganization. They are as follows:

? A-beta fibres (carrying touch sensations and normally ends in the deeper lamina of spinal cord) develop connections in lamina 2 where pain-carrying fibres normally ends. This leads to Allodynia (touch causes pain sensation).
? Area of pain increases along other nerve distribution.
? Loss descending inhibitory pathways

2. Wind up (summation of signals): Repeated activation of dorsal horn cell by strong and /or sustained noxious stimulus leads to increased excitatory response of these cells.

3. Up-regulation of NMDA receptor

Acute pain ? AMPA receptors stimulated ? dislodges Mg from NMDA

receptors??activation of NMDA receptors. Activation of NMDA receptors leads to following changes:

? Increased signal transmission
? Release of NO, sub-P & PGs

4. Ectopic activity

5. Depression inhibitory synapses

6. Activation of Wide Dynamic Range cells.

All these leads to following clinical changes:

? Increased intensity of pain.
? Increased area of pain.
? Increased duration of pain.
? Decreased tolerability to pain.
? Development of psychological problems.
? pain become non-responsive to conventional analgesics.

Complications of untreated pain itself:
• Sympathetic stimulation & consequences like: flaring of diabetes, cardio-vascular effects like tachycardia, increased B.P. ischeamia and myocardial infarction.
• Adverse effect on our immune system, so more chance of getting infectious diseases.
• Pulmonary complications like atlectasis, infection and pneumonia.
• Gastrointestinal side effects like gastric stasis, ileus, nausea, vomiting.
• Urinary system complications like retention.
• Coagulation abnormality leading thrombotic diseases.
• Psychological disturbances like anxiety, depression, thought process abnormality & even suicides.
• Acute pain may become chronic pain which is difficult to treat.

Persistence of pain after spine surgery has been called bydifferent names such as failed back surgery syndrome, postlaminectomy syndromeor simply failed back syndrome. It does not represent failure of surgery; it representsa cluster of syndromes following spine surgery wherein the expectations of thepatient and surgeon are not met. Pain may persist, increase, may change itscharacter and may spread to a new area. Persistent pain following spine surgeryis common after discectomy, laminectomy, decompression, spinal fusions andminimally invasive surgical treatment. Reasons for this failure are: 1)Dural fibrosis, 2)Arachnoidal adhesions, 3)Muscle & fascial fibrosis, 4) Mechanical instability resulting from the partial removal of bony andligamentous structures required for surgical exposure and decompression, 5) presence of neuropathy, 6)Acquired stenosis, 7)Adjacent segment degeneration, 8)Internal disc disruption, 9)Recurrent disc herniation, 10)Retained disc fragment, 11)Facet joint pain, 12)Sacroiliac joint pain, 13)Discitis and 14)Arachnoiditis. In the animal models the following pathological changes are found in postlaminectomy syndrome: 1)Paraspinous muscle spasms, 2)Tail contractures, 3)Behavioral pain behaviors, 4)Tactile allodynia, 5)Epidural and perineural scarring, and 6)Nerve root adherence to the underlying disc and pedicle. Among these etiologies epidural fibrosis (20% to 36%), facet jointdysfunction (8% to 16%), sacroiliac joint dysfunction (upto 35% in spinalfusion surgeries), internal disc disruption, recurrent disc herniation, andspinal stenosis are very common and can be treated by interventional painmanagement procedures. Among the various interventional pain management procedures based on probableetiologies, the following are commonly done: 1) Epidural Adhesionolysisfor epidural fibrosis, 2) Facet joint block orRadio frequency medialbranch rhizotomy for facet joint dysfunction, 3) Sacroiliacjoint block or Radio frequency rhizotomy for sacroiliac joint dysfunction, 4) Nerve root block forpersistent radiculopathy5) Ozone nucleolysis forrecurrent or persistent herniation, spinal stenosis. But in many cases all these procedures may prove unsuccessful for long-termrelief and spinalcord stimulation may prove beneficial and cost effective in the longrun.

Slipped Disc or Disc Prolapse

The inter-vertebral discs are protective cushion-like shock-absorbing pads between the two bones of the spine called vertebrae. These discs are soft gel filled pads bounded by few layers of membrane called lamella. These discs do not actually "slip," they may split or rupture. Following this rupture the gel escape into the surrounding tissue. The leaking jellylike substance can produce pressure on the spinal cord or on a single nerve root and cause pain either around the damaged disc or anywhere along the area controlled by that nerve. This condition is also known as a herniated disc, ruptured disc, prolapsed disc, or, more commonly, slipped disc. The most frequently affected area is the low back, but any disc can rupture, including those in the neck. When the discs of low back are ruptured there will be pain in low back that will radiate to the legs. Similarly in case of neck there will be pain in neck that will be radiating to the hands. The nature of the pain is frequently electric shock-like pain or burning pain. This pain may be associated with some numbness, tingling sensations and sometime some muscle weakness. As there are so many discs in the spine, the exact area of pain depends on the nerve root involved and that again depends on the disc that is involved. Sciatica is a frequently used term both by doctors and by patients. It is a symptom and not a disease. Sciatica is defined as any pain that is starting in the low back and is going towards the legs. Sciatica is a non-specific term like fever. Like many diseases may produce fever, many diseases may be the cause of sciatica. Slipped disc is one of the most common cause of sciatica. Since disc prolapse was first diagnosed by Dandy and subsequently by Mixter and Barr it has been implicated as one of the important cause of low back & neck pain radiating to legs & hands. Apart from conservative therapy all other forms of treatment aim at decompressing the nerve roots. These can be done by taking the disc out by surgery or by decompressing the foramen and disc by different interventions. The various treatment options have confused clinicians due to significant failure rate associated with different kinds of surgeries as well as with different interventions. Outcome studies of lumber disc surgeries document a success rate between 49% to 95% and re-operation after lumber disc surgeries ranging from 4% to 15%. Reasons for this failure are: 1)dural fibrosis, 2)arachnoidal adhesions, 3)muscle & fascial fibrosis 4) mechanical instability resulting from the partial removal of bony and ligamentous structures required for surgical exposure and decompression 5) presence of neuropathy. There has been surge of interest in search of safer alternative nonoperative treatment of slipped disc to decompress the nerve roots maintaining the structural stability. Epidural steroid injection, transforaminal epidural decompressions has a high success rate (up to 85%) but chances of recurrences are there specially if these interventions are done at later stage. Chemonucleolysis using chymopapain has also high success rate (80%) with low recurrences but not popular owing to the chances of anaphylaxis following intradiscal chymopapain injection. Injection of ozone for slipped disc or discogenic radiculopathy (low back pain with radiation to legs) has developed as a nonoperative treatment of slipped disc which is an alternative to chemonucleolysis and disc surgery. Owing to its high success rate, less invasiveness, fewer chances of recurrences and remarkably fewer side effects, it is becoming popular day by day in the whole world. This is called ozone nucleolysis or ozone discectomy. Percutaneous discectomy is another less invasive nonoperative treatment of slipped disc where disc material is taken out with motorized probe that is introduced through a 17 G needle. Buy Online FGxpress Powerstrips or Solarstrips

Diagnosis of Migraine

Migraine is commonest type of headache that needs a visit to a doctor. It is also the commonest cause of severe headache. Migraine headaches are different from other types of headaches and can be diagnosed by its characteristics. Family history of migraines, age when the first attack occurred, and frequency and duration of headaches will also help to determine whether an individual is suffering from migraines or not.

Diagnosis of Migraine

The International Headache Society has laid down the guidelines to diagnose the two forms of migraine headaches:

1. Migraine without aura (common migraine)

2. Migraine with aura (classic migraine)

Migraine without aura/ Common Migraine

I. At least five attacks per year that last 4 to 72 hours
II. At least two of the following headache symptoms:

1. Pain on one side of the head
2. Pulsing/throbbing pain
3. Moderate-to-severe intensity that inhibits or prohibits one�s ability to work
4. Aggravation of pain by physical activity, such as climbing stairs etc.

III. At least one of the following associated symptoms:

1. Nausea and/or vomiting
2. Light/sound sensitivity (Intolerance to light and/or sound)

IV. No evidence of any other diseases that may cause these symptoms

Migraine with aura (classic migraine)

I. At least two attacks per year
II. At least three of the following symptoms:

1. One or more of the following aura symptoms that later subside.
Aura symptoms are:

a. Alterations in vision
b. Numbness or tingling in the face, arm, or hand on one side of the body
c. Muscular weakness or mild paralysis on one side of the body
d. Difficulty speaking or loss of speech.
2. Gradual development of at least one aura symptom over more than four minutes or two or more symptoms that occur at the same time
3. Aura symptoms that last no more than 60 minutes
4. Headache that occurs simultaneously with aura symptoms or follows aura within 60 minutes

III. No evidence of any other diseases that may cause these symptoms

Migraine Phases
Researchers believe that migraine attacks have four distinct phases. These phases are:
1. 1st phase or prodrome
It is experienced by 60% of migraineurs. It starts hours or days before a migraine attack. Many physical and psychological symptoms are seen in this phase. These symptoms vary between the individuals, but remain consistent for a particular individual. The symptoms include:

1. Stiff neck
2. Cold feeling
3. Sluggishness / Mental slowing / Fatigue
4. Hyperactivity / Restlessness
5. Dizziness / Drowsiness /Irritability
6. Increased thirst
7. Increased urination
8. Loss of appetite
9. Diarrhea / Constipation
10. Fluid retention
11. Food cravings
12. Sensitivity to light and/or sound
13. Depression
14. Euphoria

2. 2nd phase or aura

Aura is experienced by 20% of migraineurs suffering from classic migraine just before the migraine attack. It develops 5 to 20 minutes before a migraine attack and lasts less than an hour.
Aura symptoms include:

1. Scintillation scotomas, which are characterized by a bright rim of light around an area of visual loss and flashing lights or jagged lines that block the visual field.
2. Visual resizing or reshaping of objects.
3. Numbness or tingling of the face, arm, or hand on one side of the body.
4. Muscular weakness.
5. Mild paralysis on one side of the body.
6. Difficulty speaking or loss of speech.

3. 3rd phase or phase of migraine headache

Symptoms of migraine headache are different from other headaches.
Symptoms that distinguish migraines from other headaches:

1. Headache on one/both side of the head, behind /around the eyes, posterior or occipital area, or it may be generalized.
2. Intensity of pain is moderate to severe and worsened by physical activity
3. Loss of appetite /Nausea /Vomiting
4. Intolerant to light, sound, or odors
5. Blurry vision /Blocked nose /Pale face
6. Sensations of heat or coldness /Sweating
7. Tenderness of the scalp
8. Prominence of veins or arteries in the temple
9. Impaired concentration /Depression /Fatigue /Nervousness /Irritability

4. 4th phase or postdrome

Some individuals may experience the following symptoms after a migraine attack:
Fatigue /Irritability /Impaired concentration /Scalp tenderness /Mood changes.

There is no one in this earth who did not suffer from any type of headache in his lifetime. Fortunately most kinds of headache are of benign or harmless in nature. There are only a few kinds of headaches, which are serious. Thanks god, they are really very rare. Probably you are not suffering from such.
How to know which headaches are serious?
If you notice any of the following symptoms, it may be serious. Consult your doctor.
1. Sudden onset of severe headache.
2. It is a new type headache that you have never felt before.
3. Your headache is taking bad shape quickly.
4. Headache is associated with other symptoms like projectile vomiting, visual problems, weakness of one or both sides of face/body, fever etc.
5. Your headache is increasing with forward bending.
6. New kind of headache starting at older age.

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