Pain

Views:
 
Category: Others/ Misc
     
 

Presentation Description

FOCUSSING ON THE NEUROPATHIC PAIN AND ITS MANAGEMENT.

Comments

Presentation Transcript

NEORO PATHIC Pain:

NEORO PATHIC Pain PAIN

Pain:

Pain An unpleasant sensory and emotional experience associated with the actual or potential tissue damage, or described in terms of such damage or both.

PowerPoint Presentation:

Injury Postoperative Flare ACUTE PAIN Neuropathic Mixed Nociceptive Visceral CHRONIC Cancer Pain Low Back Pain Diabetic Neuropathy PostHerpatic Neuralgia Radiculopathy Osteoarthritis Rheumatiod arthritis Fibromyaolgia IBS Pancreatitis Bladder Pain Noncariac chest pain Abdominal pain Syndrome Chronic pain exists beyond an expected time for healing. Acute pain is caused by injury, surgery, illness, trauma or painful medical procedures

Types:

Types Stimulation of a nociceptor, due to a chemical, thermal, or mechanical event that has the potential to damage body tissue, may cause nociceptive pain . Damage to the nervous system itself, due to disease or trauma, may cause neuropathic (or neurogenic) pain. Neuropathic pain may refer to: peripheral neuropathic pain, which is caused by damage to nerves central pain, which is caused by damage to the brain, brainstem, or spinal cord.

Nociceptive Pain:

Nociceptive Pain Nociceptive pain may be classified further in three types: Superficial somatic pain (or cutaneous pain) is caused by injury to the skin or superficial tissues (High receptors, Sharp Pain) Deep somatic pain originates from ligaments, tendons, bones, blood vessels, fasciae, and muscles (Low receptors, Dull Pain) Visceral pain originates from body's viscera, or organs.

Nociceptors:

Nociceptors Nociceptors are skin receptors that can detect mechanical, thermal or chemical changes above a certain threshold All nociceptors are free nerve endings of fast-conducting myelinated A delta fibers or slow-conducting unmyelinated C fibers , respectively responsible for fast, localized, sharp pain and slow, poorly-localized, dull pain, respectively

Transmission of Pain:

Transmission of Pain

Neuropathic Pain:

Neuropathic Pain Damage to the nervous system itself, due to disease or trauma, may cause neuropathic (or neurogenic) pain

Neuropathic Pain Symptoms:

Neuropathic Pain Symptoms Steady Pain (97%) -Burning -Aching -Stinging -Throbbing -Itching -Numbing -Pins & Needles -Pulling Brief Pain (87%) -Sharp -Jabbing -Shooting -Electric Evoked Pain (87%) -Mechanical -Thermal Watson and Babul. Neurology 1998;50:1837-41

Neuropathic Pain Signs:

Neuropathic Pain Signs Stimulus-Evoked Pain (Elicited by the Physician on Examination)

Neuropathic Pain:

Neuropathic Pain Pathophysiology

Neuropathic Pain Core Pathology:

Neuropathic Pain Core Pathology Nerve damage Metabolic factors High blood glucose Long duration of diabetes Low levels of insulin Abnormal blood fat levels Neurovascular factors Damaged vesa nervosum Autoimmune factors Inflammation in nerves

PowerPoint Presentation:

Woolf CJ, Mannion RJ. Neuropathic pain: aetiology, symptoms, mechanisms, and management. Lancet , 1999;353:1959-64. Syndrome Symptoms Pathophysiology Etiology Neuropathic pain Stimulus- independent pain Stimulus dependent pain Inc. Peripheral Excitability, Inc. Central Sensitization Metabolic Ischaemic Hereditary Compression Nerve damage Traumatic Toxic Infectious Immune-mediated Spontaneous Pain Evoked Pain

Mechanism Involved in Sustaining Neuropathic Pain:

Mechanism Involved in Sustaining Neuropathic Pain Peripheral Nerve Fibers Ectopic Discharge Mechanosensitivity Ephapatic Crosstalks Sympathetic Fibers Ephapatic Crosstalks Spinal Cord Brain Altered ”gating” Dorsal horn denervation hypersensitivity Gene expression exchange Receptive field change Altered ”gating” Dorsal horn denervation hypersensitivity Gene expression exchange Receptive field change Peripheral Sensitization Central Sensitization

Peripheral Sensitization:

Peripheral Sensitization SENSITIZING “SOUP” Hyderogen Ions Histamine Purine Leukotrines Noradrinaline Potassium ions Cytokines Nerve Groth Factors Bradykinin Prostaglandins 5-HT Neuropeptides Tissue Damage Inflammation Sympathetic terminalis Decreased Threshold for nociceptors Ectopic Discharges Abnormal accumulation of Na + Channels

Mechanism:

Mechanism

Neuropathic Pain Low intensity stimulus:

Neuropathic Pain Low intensity stimulus PNS CNS ` ` Low Threshold Mechanoreceptor A Beta Sensitized Nociceptor A Delta and C Wide Dynamic Range (WDR) neuron Hyperexcitable Dorsal horn neuron Pain

Neuronal Plasticity:

Neuronal Plasticity

Role of NMDA receptors:

Role of NMDA receptors Blocked by Mg ++ ions at resting membrane potential Depolarization by C and A δ -fiber input Mg++ ions displaced in voltage dependent Manner Glutamate binds to activated receptor Causes inward Ca++ ions flux Phosphoryaltion of NMDA receptor Causes decreased Mg++ ions blockade Central Sensitization

Diabetic Neuropathies:

Diabetic Neuropathies Diabetic neuropathies are neuropathic disorders that are associated with diabetes mellitus. These conditions are thought to result from diabetic microvascular injury involving small blood vessels that supply nerves (vasa nervorum).

Diabetic Neuropathies:

Diabetic Neuropathies Relatively common conditions which may be associated with diabetic neuropathy include: Third nerve palsy; Mononeuropathy; Mononeuropathy multiplex; Diabetic amyotrophy; A painful polyneuropathy; Autonomic neuropathy; Thoracoabdominal neuropathy.

Diabetic Neuropathies:

Diabetic Neuropathies

Diabetic Neuropathies Pathology:

Diabetic Neuropathies Pathology There are four factors thought to be involved in the development of diabetic neuropathy: Microvascular disease, Advanced Glycation Endproduct, Protein kinase C, and the Polyol pathway.

Microvascular disease:

Microvascular disease Blood vessels depend on normal nerve function, and nerves depend on adequate blood flow The first pathological change in the microvasculature is vasoconstriction. As the disease progresses, neuronal dysfunction correlates closely with the development of vascular abnormalities, such as capillary basement membrane thickening and endothelial hyperplasia, which contribute to diminished oxygen tension and hypoxia

Advanced Glycation Endproduct:

Advanced Glycation Endproduct Elevated intracellular levels of glucose cause a non-enzymatic covalent bonding with proteins, which alters their structure and destroys their function. Some of these glycosylated proteins have been implicated in the pathology of diabetic neuropathy and other long term complications of diabetes.

Protein kinase C (PKC) :

Protein kinase C (PKC) PKC is implicated in the pathology of diabetic neuropathy. Increased levels of glucose cause an increase in intracellular diacylglycerol, which activates PKC. PKC inhibitors in animal models will increase nerve conduction velocity by increasing neuronal blood flow.

Polyol pathway:

Polyol pathway Excessive activation of the Polyol pathway leads to increased levels of sorbitol and reactive oxygen molecules Also, decreased levels of nitric oxide and glutathione, as well as increased osmotic stresses on the cell membrane. Any one of these elements alone can promote cell damage, but here we have several acting together.

Symptoms:

Symptoms Numbness and tingling of extremities Dysesthesia (decreased or loss of sensation to a body part) Diarrhea Erectile dysfunction Urinary incontinence (loss of bladder control) Impotence Facial, mouth and eyelid drooping Vision changes Dizziness Muscle weakness Dysphagia (swallowing difficulty) Speech impairment Fasciculation (muscle contractions) Anorgasmia Burning (especially in evenings) Electric Stabbing Pains

Post Herpatic Neuralgia:

Post Herpatic Neuralgia

Postherpetic neuralgia:

Postherpetic neuralgia Postherpetic neuralgia (PHN) is a neuralgia caused by the varicella zoster virus. Typically, the neuralgia is confined to a dermatomic area of the skin and follows an outbreak of herpes zoster (HZ, commonly known as shingles ) in that same dermatomic area

Pathophysiology:

Pathophysiology Postherpetic neuralgia is thought to be nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months or even years.

Predisposing factors :

Predisposing factors Race: It may influence susceptibility to herpes zoster. African Americans are one fourth as likely as Caucasians to develop this condition.

Symptoms: :

Symptoms: With resolution of the HZ eruption, pain that continues for 3 months or more is defined as PHN. Pain is variable from discomfort to very severe and may be described as burning, stabbing, or gnawing.

Signs :

Signs Area of previous HZ may show evidence of cutaneous scarring. Sensation may be altered over involved areas, in the form of either hypersensitivity or decreased sensation. In rare cases, the patient might also experience muscle weakness, tremor or paralysis — if the nerves involved also control muscle movement.

Fibromyalgia:

Fibromyalgia

Fibromyalgia:

Fibromyalgia Fibromyalgia (FM) is a human disorder classified by the presence of chronic widespread pain and tactile allodynia. Recent studies suggest that people with fibromyalgia may be genetically predisposed. The disorder is not directly life-threatening. The degree of symptoms may vary greatly from day to day with periods of flares (severe worsening of symptoms) or remission

Initiating Factors:

Initiating Factors The following factors have been proposed to exacerbate symptoms of pain in patients: Increased psychosocial stress Excessive physical exertion (exercise seems to decrease the pain threshold of people with fibromyalgia but increase it in healthy individuals) Lack of slow-wave sleep Changes in humidity and barometric pressure

Cause:

Cause The cause of fibromyalgia is unknown However, Several hypothesis exist that might provide a clue for its development

Genetic Cause:

Genetic Cause Research has demonstrated that FM is associated with polymorphisms of genes in the serotoninergic, dopaminergic and catecholaminergic systems

Sleep Disturbance hypothesis:

Sleep Disturbance hypothesis According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder

Dopamine abnormality:

Dopamine abnormality Demonstrated a reduction in dopamine synthesis among fibromyalgia patients in several brain regions in which dopamine plays a role in inhibiting pain perception, including the mesencephalon, thalamus, insular cortex and anterior cingulate cortex leading to fibromyalgia pain

ACR Criteria for Diagnosis:

ACR Criteria for Diagnosis A history of widespread pain lasting more than three months—affecting all four quadrants of the body, i.e., both sides, and above and below the waist. Tender points—there are 18 designated possible tender or trigger points (although a person with the disorder may feel pain in other areas as well).

End…:

End… Module # 6

authorStream Live Help