This document summarizes neuropathic pain and the agents used to treat it. It discusses how neuropathic pain is initiated by damage or dysfunction in the nervous system and often presents as burning pain. It then describes various neuropathic pain conditions and classes of agents used to treat neuropathic pain, including antidepressants, anticonvulsants, and local anesthetics. It provides details on the mechanisms and indications for tricyclic antidepressants, SSRIs, SNRIs, and various anticonvulsants in treating different types of neuropathic pain.
This document summarizes information about neuropathic pain, including its classification, mechanisms, signs and symptoms, types, and current treatment options. It begins with definitions of neuropathic pain and its classification by the International Association for the Study of Pain. It then discusses the mechanisms, development, and pathophysiology of neuropathic pain. Following sections provide details on the signs and symptoms, types (peripheral vs central neuropathy), most common conditions, and current treatment options including tricyclic antidepressants, anticonvulsants, opioids, gabapentin, and pregabalin. It highlights the mechanisms, pharmacokinetics, dosing, and clinically proven efficacy of pregabalin for treating neuropathic pain conditions like diabetic peripheral neuropathy and fibromyalgia.
The document discusses neuropathic pain, including its pathophysiology, symptoms, causes, assessment, and treatment approaches. It provides details on pharmacological and non-pharmacological treatment options for peripheral and central neuropathic pain, including guidelines on first-line therapies such as antidepressants, anticonvulsants, and topical lidocaine. Emerging treatments currently under investigation are also mentioned.
This document discusses neuropathic pain, its causes, symptoms, and treatment options. It begins by defining neuropathic pain as pain resulting from damage or disease affecting the somatosensory nervous system, such as diabetic neuropathy or postherpetic neuralgia. Symptoms include abnormal sensations like tingling, burning, and pain from stimuli that are normally non-painful. Treatment options discussed include tricyclic antidepressants, gabapentin, pregabalin, serotonin-norepinephrine reuptake inhibitors, topical lidocaine, opioids, and emerging treatments like botulinum toxin, cannabinoids, spinal cord stimulation, and intrathecal drug delivery.
This document discusses neuropathic pain, its definition, symptoms, pathophysiology, assessment, and management. Some key points:
- Neuropathic pain is caused by damage or disease affecting the somatosensory nervous system. It is characterized by spontaneous ongoing pain, abnormal sensations, and hypersensitivity.
- Common causes include diabetic neuropathy, postherpetic neuralgia, spinal cord injury. Assessment involves history, exam, and tools like LANSS and DN4.
- Management includes non-pharmacological options like TENS, physical therapy, as well as drugs like gabapentin, pregabalin, tricyclic antidepressants.
- For severe cases, neurosurgical options like cord
Current concept for management of neuropathic painNeurologyKota
The document discusses pain classification and mechanisms. It defines pain and different types including nociceptive, neuropathic, and chronic pain. It describes peripheral and central sensitization mechanisms. It discusses evaluation and management of neuropathic pain including first-line options like gabapentin, pregabalin, amitriptyline and second-line options like duloxetine, tramadol, opioids. Adverse effects and considerations with long term use are also summarized.
This document discusses the use of antidepressants to treat neuropathic pain. It begins with background on depression and types of pain, focusing on neuropathic pain. Neuropathic pain results from nerve damage and is described as burning or shocking. The document then discusses the link between depression and pain, and the use of tricyclic antidepressants (TCAs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) to treat pain. TCAs like amitriptyline are effective for some neuropathic pain cases by inhibiting norepinephrine reuptake. SNRIs like duloxetine and venlafaxine may also help by increasing norepinephrine and serotonin levels in the descending pain pathway. The pharmacology, dos
1) An international collaboration identified a protein NOS1AP that is involved in the biological pathway of neuropathic pain. Disrupting the formation of this protein was able to reduce pain in rodent models of nerve damage and chemotherapy-induced pain without severe side effects of current drugs.
2) Neuropathic pain is caused by lesions or diseases of the somatosensory nervous system. Current pharmacological treatments include antidepressants, anticonvulsants, sodium channel blockers, and calcium channel modulators.
3) Research is exploring new potential treatment targets like changes in HCN channels, potassium channels, and interrupting signaling cascades downstream of glutamate receptors to develop improved neuropathic pain therapies.
This document summarizes information about neuropathic pain, including its classification, mechanisms, signs and symptoms, types, and current treatment options. It begins with definitions of neuropathic pain and its classification by the International Association for the Study of Pain. It then discusses the mechanisms, development, and pathophysiology of neuropathic pain. Following sections provide details on the signs and symptoms, types (peripheral vs central neuropathy), most common conditions, and current treatment options including tricyclic antidepressants, anticonvulsants, opioids, gabapentin, and pregabalin. It highlights the mechanisms, pharmacokinetics, dosing, and clinically proven efficacy of pregabalin for treating neuropathic pain conditions like diabetic peripheral neuropathy and fibromyalgia.
The document discusses neuropathic pain, including its pathophysiology, symptoms, causes, assessment, and treatment approaches. It provides details on pharmacological and non-pharmacological treatment options for peripheral and central neuropathic pain, including guidelines on first-line therapies such as antidepressants, anticonvulsants, and topical lidocaine. Emerging treatments currently under investigation are also mentioned.
This document discusses neuropathic pain, its causes, symptoms, and treatment options. It begins by defining neuropathic pain as pain resulting from damage or disease affecting the somatosensory nervous system, such as diabetic neuropathy or postherpetic neuralgia. Symptoms include abnormal sensations like tingling, burning, and pain from stimuli that are normally non-painful. Treatment options discussed include tricyclic antidepressants, gabapentin, pregabalin, serotonin-norepinephrine reuptake inhibitors, topical lidocaine, opioids, and emerging treatments like botulinum toxin, cannabinoids, spinal cord stimulation, and intrathecal drug delivery.
This document discusses neuropathic pain, its definition, symptoms, pathophysiology, assessment, and management. Some key points:
- Neuropathic pain is caused by damage or disease affecting the somatosensory nervous system. It is characterized by spontaneous ongoing pain, abnormal sensations, and hypersensitivity.
- Common causes include diabetic neuropathy, postherpetic neuralgia, spinal cord injury. Assessment involves history, exam, and tools like LANSS and DN4.
- Management includes non-pharmacological options like TENS, physical therapy, as well as drugs like gabapentin, pregabalin, tricyclic antidepressants.
- For severe cases, neurosurgical options like cord
Current concept for management of neuropathic painNeurologyKota
The document discusses pain classification and mechanisms. It defines pain and different types including nociceptive, neuropathic, and chronic pain. It describes peripheral and central sensitization mechanisms. It discusses evaluation and management of neuropathic pain including first-line options like gabapentin, pregabalin, amitriptyline and second-line options like duloxetine, tramadol, opioids. Adverse effects and considerations with long term use are also summarized.
This document discusses the use of antidepressants to treat neuropathic pain. It begins with background on depression and types of pain, focusing on neuropathic pain. Neuropathic pain results from nerve damage and is described as burning or shocking. The document then discusses the link between depression and pain, and the use of tricyclic antidepressants (TCAs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) to treat pain. TCAs like amitriptyline are effective for some neuropathic pain cases by inhibiting norepinephrine reuptake. SNRIs like duloxetine and venlafaxine may also help by increasing norepinephrine and serotonin levels in the descending pain pathway. The pharmacology, dos
1) An international collaboration identified a protein NOS1AP that is involved in the biological pathway of neuropathic pain. Disrupting the formation of this protein was able to reduce pain in rodent models of nerve damage and chemotherapy-induced pain without severe side effects of current drugs.
2) Neuropathic pain is caused by lesions or diseases of the somatosensory nervous system. Current pharmacological treatments include antidepressants, anticonvulsants, sodium channel blockers, and calcium channel modulators.
3) Research is exploring new potential treatment targets like changes in HCN channels, potassium channels, and interrupting signaling cascades downstream of glutamate receptors to develop improved neuropathic pain therapies.
Medical management of neuropathic painSudhir Kumar
This document discusses the medical management of neuropathic pain. It describes the clinical features and common causes of neuropathic pain, including central neuropathic pain from conditions like stroke and multiple sclerosis, and peripheral neuropathic pain from issues like diabetic neuropathy and post-herpetic neuralgia. It provides details on medical treatments for neuropathic pain such as pregabalin, gabapentin, tricyclic antidepressants, duloxetine, and topical agents like capsaicin and lidocaine. The document emphasizes starting low and gradually increasing drug doses to find the desired effect with mild and uncommon side effects primarily involving sedation and dizziness.
Sentra PM is a patented medical food designed specifically for the dietary management of the altered metabolic processes of sleep disorders.
The safety and efficacy of Sentra PM is supported by multiple clinical trials and over a decade of clinical use. Sentra PM is recommended by physicians as an alternative to addictive and dangerous prescription sleep aids.
For more information please visit www.medicalfoods.com or call (844)474-3111
The document discusses neuropathic pain management and treatment options. It defines neuropathic pain and differentiates it from acute pain. It describes the pathophysiology and possible descriptions of neuropathic pain. The goals of clinical assessment are to achieve diagnosis, identify underlying causes, evaluate comorbidities, and develop a targeted treatment plan. Treatment options discussed include nonpharmacological approaches, topical medications, systemic medications like anticonvulsants, antidepressants, and opioids. New treatments and applications of existing treatments are improving management of neuropathic pain conditions.
1. Ketamine and its derivative esketamine work as rapid-acting antidepressants through their action on the NMDA receptor and glutamate neurotransmission in the brain.
2. Intranasal esketamine has been FDA approved for treatment-resistant depression while intravenous ketamine remains off-label, both as adjunctive therapies.
3. Ketamine and esketamine have potential side effects involving the central nervous system and gastrointestinal tract but can effectively reduce suicidal ideation within hours of administration.
Neuropathic pain is caused by damage or disease affecting the somatosensory nervous system and is characterized by abnormal sensations such as burning or stabbing pain. It is estimated to affect 7-8% of adults. Common causes include diabetes, shingles, HIV, cancer treatments and injuries. Diagnosis involves medical history, exams and tests to rule out other conditions. Treatment involves pharmacologic options like antidepressants, anticonvulsants and opioids as well as non-pharmacologic therapies. However, neuropathic pain is difficult to treat and a multidisciplinary approach combining several therapies is often needed to provide effective relief.
This document summarizes medications used to treat pain and inflammation. It discusses non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, tramadol, anti-epileptic drugs, tricyclic antidepressants, muscle relaxants, and opiates. NSAIDs are first-line treatments that reduce inflammation and pain by inhibiting cyclooxygenase enzymes. Acetaminophen also reduces pain but lacks anti-inflammatory effects. Tramadol, anti-epileptics, tricyclics, and muscle relaxants may be used as adjuvants. Opiates are reserved for moderate to severe short-term pain. Careful patient screening and protocols are recommended when prescribing op
The document discusses management strategies for acute and subacute pain. It compares analgesic options and outlines the World Health Organization's three-step "pain ladder" approach. The pain ladder involves scheduled administration of medications ranging from non-steroidal anti-inflammatories to weak opioids like tramadol and strong opioids if needed. Proper use of analgesics requires considering factors like compliance, side effects, and risk of dependence.
Analgesics, also known as pain killers, are drugs that selectively relieve pain by acting in the central nervous system or peripheral pain mechanisms without affecting consciousness. There are two main types of analgesics - non-opioids and opioids. Non-opioids include nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and acetaminophen, which work by inhibiting cyclooxygenase enzymes. Opioids include drugs like morphine, codeine, and tramadol, which act as agonists at opioid receptors in the brain to reduce neuronal excitability and pain transmission. Both types of analgesics are used to treat mild to severe acute pain, while opioids are also used for moderate to severe
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
Hippocrates first suggested epilepsy was a brain disorder in 400 BC. It is defined as brief episodes of loss of consciousness due to abnormal brain neuron firing. Seizures can be focal or generalized. Common seizure types include generalized tonic-clonic, absence, myoclonic, complex partial, and simple partial. Antiepileptic drugs work by modifying ion conductances like sodium channels, increasing GABA effects, or blocking glutamate receptors. Common antiepileptic drugs include phenytoin, carbamazepine, valproic acid, ethosuximide, and phenobarbital. Adverse effects and drug interactions must be monitored with long-term antiepileptic treatment.
This document discusses recent advances in pain management, including multimodal analgesia using different drug classes and routes of administration to provide improved pain relief with fewer side effects. It describes pharmacological and non-pharmacological pain interventions, the WHO analgesic ladder for treating pain, and various opioid and non-opioid analgesics as well as adjuvants that have been developed or investigated for postoperative pain management, including several novel drug delivery methods for opioids. The goal is to reduce opioid requirements, side effects, and hasten recovery through multimodal approaches.
1362576458 new look at painful neuropathydfsimedia
This document discusses insights into painful neuropathy in diabetes. It notes that chronic neuropathic pain affects 20% of diabetics with over 10 years duration. The frequency of chronic painful neuropathy is similar in type 1 and type 2 diabetes. Several treatment options are discussed including tricyclic antidepressants, anticonvulsants like gabapentin and pregabalin, alpha-lipoic acid, capsaicin cream, and physical therapies like TENS and PENS. Tight glucose control is also emphasized as important for managing painful neuropathy.
This document discusses pain management in the emergency department. It outlines common pitfalls like withholding analgesics or using inappropriate routes or dosages. It then reviews specific analgesics like ketorolac, COX-2 inhibitors, tramadol, propoxyphene, opioids, and analgesics for procedural sedation. Case examples are provided and key points about dosing, efficacy, and side effects of analgesics like morphine, hydromorphone, fentanyl, ketamine, propofol, etomidate, and methohexital are summarized. The document emphasizes providing analgesics early and often to effectiveness rather than arbitrary dosage limits.
The key to a successful Acute Pain Service is not so much the use of sophisticated drugs and high technology equipment, but an excellent organisational structure and well trained medical and nursing personnel.
Anaesthetic considerations for intraoperative neurophysiological monitoringSamir Elkafrawy
The document discusses neurophysiologic intraoperative monitoring (NIOM) and its use during spinal and brain surgeries to reduce risks to peripheral nerves. It covers the basic NIOM techniques of electromyography, motor and somatosensory evoked potentials, motor evoked potentials, and electroencephalography. It also discusses the four phases of general anesthesia - premedication, induction, maintenance, and recovery - and considerations for each phase like medications administered. Finally, it provides details on ideal properties of anesthetic drugs and the history and use of inhalation, intravenous, and muscle relaxant anesthetics.
Glucocorticoids for optimizing its use 2021( f )SafwatElaraby
1. Prolonged, frequent, or high-dose GC use can suppress the HPA axis, potentially leading to adrenal insufficiency if used long-term.
2. The duration of HPA axis suppression generally approximates the anti-inflammatory effects of a given GC dose.
3. Strategies like using lower doses, shorter durations, and pulsed therapy can help minimize HPA axis disruption from GC use.
Repetitive transcanial magnetic stimulation(r tms) for depression treatmentGuru Prasath
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive treatment used for depression when common treatments do not work. rTMS uses rapidly changing magnetic fields to induce weak electric currents in neurons, targeting areas of the limbic system associated with depression. This triggers neurotransmitter secretion and facilitates neural activity in the targeted area. rTMS has advantages over antidepressants as it does not cause side effects and its effects can last beyond the stimulation period.
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
Medical management of neuropathic painSudhir Kumar
This document discusses the medical management of neuropathic pain. It describes the clinical features and common causes of neuropathic pain, including central neuropathic pain from conditions like stroke and multiple sclerosis, and peripheral neuropathic pain from issues like diabetic neuropathy and post-herpetic neuralgia. It provides details on medical treatments for neuropathic pain such as pregabalin, gabapentin, tricyclic antidepressants, duloxetine, and topical agents like capsaicin and lidocaine. The document emphasizes starting low and gradually increasing drug doses to find the desired effect with mild and uncommon side effects primarily involving sedation and dizziness.
Sentra PM is a patented medical food designed specifically for the dietary management of the altered metabolic processes of sleep disorders.
The safety and efficacy of Sentra PM is supported by multiple clinical trials and over a decade of clinical use. Sentra PM is recommended by physicians as an alternative to addictive and dangerous prescription sleep aids.
For more information please visit www.medicalfoods.com or call (844)474-3111
The document discusses neuropathic pain management and treatment options. It defines neuropathic pain and differentiates it from acute pain. It describes the pathophysiology and possible descriptions of neuropathic pain. The goals of clinical assessment are to achieve diagnosis, identify underlying causes, evaluate comorbidities, and develop a targeted treatment plan. Treatment options discussed include nonpharmacological approaches, topical medications, systemic medications like anticonvulsants, antidepressants, and opioids. New treatments and applications of existing treatments are improving management of neuropathic pain conditions.
1. Ketamine and its derivative esketamine work as rapid-acting antidepressants through their action on the NMDA receptor and glutamate neurotransmission in the brain.
2. Intranasal esketamine has been FDA approved for treatment-resistant depression while intravenous ketamine remains off-label, both as adjunctive therapies.
3. Ketamine and esketamine have potential side effects involving the central nervous system and gastrointestinal tract but can effectively reduce suicidal ideation within hours of administration.
Neuropathic pain is caused by damage or disease affecting the somatosensory nervous system and is characterized by abnormal sensations such as burning or stabbing pain. It is estimated to affect 7-8% of adults. Common causes include diabetes, shingles, HIV, cancer treatments and injuries. Diagnosis involves medical history, exams and tests to rule out other conditions. Treatment involves pharmacologic options like antidepressants, anticonvulsants and opioids as well as non-pharmacologic therapies. However, neuropathic pain is difficult to treat and a multidisciplinary approach combining several therapies is often needed to provide effective relief.
This document summarizes medications used to treat pain and inflammation. It discusses non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, tramadol, anti-epileptic drugs, tricyclic antidepressants, muscle relaxants, and opiates. NSAIDs are first-line treatments that reduce inflammation and pain by inhibiting cyclooxygenase enzymes. Acetaminophen also reduces pain but lacks anti-inflammatory effects. Tramadol, anti-epileptics, tricyclics, and muscle relaxants may be used as adjuvants. Opiates are reserved for moderate to severe short-term pain. Careful patient screening and protocols are recommended when prescribing op
The document discusses management strategies for acute and subacute pain. It compares analgesic options and outlines the World Health Organization's three-step "pain ladder" approach. The pain ladder involves scheduled administration of medications ranging from non-steroidal anti-inflammatories to weak opioids like tramadol and strong opioids if needed. Proper use of analgesics requires considering factors like compliance, side effects, and risk of dependence.
Analgesics, also known as pain killers, are drugs that selectively relieve pain by acting in the central nervous system or peripheral pain mechanisms without affecting consciousness. There are two main types of analgesics - non-opioids and opioids. Non-opioids include nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and acetaminophen, which work by inhibiting cyclooxygenase enzymes. Opioids include drugs like morphine, codeine, and tramadol, which act as agonists at opioid receptors in the brain to reduce neuronal excitability and pain transmission. Both types of analgesics are used to treat mild to severe acute pain, while opioids are also used for moderate to severe
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
Hippocrates first suggested epilepsy was a brain disorder in 400 BC. It is defined as brief episodes of loss of consciousness due to abnormal brain neuron firing. Seizures can be focal or generalized. Common seizure types include generalized tonic-clonic, absence, myoclonic, complex partial, and simple partial. Antiepileptic drugs work by modifying ion conductances like sodium channels, increasing GABA effects, or blocking glutamate receptors. Common antiepileptic drugs include phenytoin, carbamazepine, valproic acid, ethosuximide, and phenobarbital. Adverse effects and drug interactions must be monitored with long-term antiepileptic treatment.
This document discusses recent advances in pain management, including multimodal analgesia using different drug classes and routes of administration to provide improved pain relief with fewer side effects. It describes pharmacological and non-pharmacological pain interventions, the WHO analgesic ladder for treating pain, and various opioid and non-opioid analgesics as well as adjuvants that have been developed or investigated for postoperative pain management, including several novel drug delivery methods for opioids. The goal is to reduce opioid requirements, side effects, and hasten recovery through multimodal approaches.
1362576458 new look at painful neuropathydfsimedia
This document discusses insights into painful neuropathy in diabetes. It notes that chronic neuropathic pain affects 20% of diabetics with over 10 years duration. The frequency of chronic painful neuropathy is similar in type 1 and type 2 diabetes. Several treatment options are discussed including tricyclic antidepressants, anticonvulsants like gabapentin and pregabalin, alpha-lipoic acid, capsaicin cream, and physical therapies like TENS and PENS. Tight glucose control is also emphasized as important for managing painful neuropathy.
This document discusses pain management in the emergency department. It outlines common pitfalls like withholding analgesics or using inappropriate routes or dosages. It then reviews specific analgesics like ketorolac, COX-2 inhibitors, tramadol, propoxyphene, opioids, and analgesics for procedural sedation. Case examples are provided and key points about dosing, efficacy, and side effects of analgesics like morphine, hydromorphone, fentanyl, ketamine, propofol, etomidate, and methohexital are summarized. The document emphasizes providing analgesics early and often to effectiveness rather than arbitrary dosage limits.
The key to a successful Acute Pain Service is not so much the use of sophisticated drugs and high technology equipment, but an excellent organisational structure and well trained medical and nursing personnel.
Anaesthetic considerations for intraoperative neurophysiological monitoringSamir Elkafrawy
The document discusses neurophysiologic intraoperative monitoring (NIOM) and its use during spinal and brain surgeries to reduce risks to peripheral nerves. It covers the basic NIOM techniques of electromyography, motor and somatosensory evoked potentials, motor evoked potentials, and electroencephalography. It also discusses the four phases of general anesthesia - premedication, induction, maintenance, and recovery - and considerations for each phase like medications administered. Finally, it provides details on ideal properties of anesthetic drugs and the history and use of inhalation, intravenous, and muscle relaxant anesthetics.
Glucocorticoids for optimizing its use 2021( f )SafwatElaraby
1. Prolonged, frequent, or high-dose GC use can suppress the HPA axis, potentially leading to adrenal insufficiency if used long-term.
2. The duration of HPA axis suppression generally approximates the anti-inflammatory effects of a given GC dose.
3. Strategies like using lower doses, shorter durations, and pulsed therapy can help minimize HPA axis disruption from GC use.
Repetitive transcanial magnetic stimulation(r tms) for depression treatmentGuru Prasath
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive treatment used for depression when common treatments do not work. rTMS uses rapidly changing magnetic fields to induce weak electric currents in neurons, targeting areas of the limbic system associated with depression. This triggers neurotransmitter secretion and facilitates neural activity in the targeted area. rTMS has advantages over antidepressants as it does not cause side effects and its effects can last beyond the stimulation period.
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Neuropathic Pain
Causes, Mechanisms and Treatment of Neuropathic Pain
Presented At Primed, QE2 Conference Centre, Westminster, London to National Audience of Primary Care Doctors
5th November 2009
PEG (Pain, Enjoyment, General activity) scale (0-10)
1. What number best describes your Pain on average in the past week? 5 → 5 (no change)
2. What number best describes how much you are Enjoying life?
3 → 7 (worsening)
3. What number best describes your General activity level?
4 → 9 (worsening)
This document summarizes the treatment of neuropathic pain. It discusses the various causes of neuropathic pain including diabetes, shingles, and spinal cord injuries. It then describes common neuropathic pain conditions and symptoms. The document outlines the pathophysiology of neuropathic pain in both the peripheral and central nervous systems. It provides details on different drug classes used to manage neuropathic pain such as antidepressants, antiepileptics, opioids, topical agents, and other possibilities. The summary notes that neuropathic pain has no single highly effective treatment and often requires a trial-and-error process to determine the appropriate polypharmacy regimen for each patient.
Orthotics are devices added to the body to stabilize, immobilize, or assist body parts. This document discusses different types of orthotics for the lower extremities, upper extremities, and spine. Common orthotics include foot orthotics, ankle foot orthotics, knee orthotics, and cervical orthotics. The document provides examples and descriptions of various orthotics, their purposes, and conditions they are used to treat.
The document discusses neuropathic pain, its etiology and treatment. It notes that chronic pain often has an unknown cause, persists after healing for at least 3 months, and requires treatment of both the underlying disease and pain disorder. It also categorizes neuropathies as focal like mononeuritis or entrapment, or diffuse like proximal or distal neuropathies affecting large or small fibers. Additionally, it states that many neuropathic pain patients continue suffering despite therapy and developing new rational treatments has been slow.
This document discusses Advanced Trauma Life Support (ATLS), a protocol for trauma care. It outlines the history and growth of ATLS since its introduction in 1988. While ATLS protocols align well with recommendations from reviews of trauma care, the document calls for strengthening ATLS training requirements and ensuring protocols fit current local practice. The future of ATLS would benefit from formal introduction into postgraduate medical education and commitment to ongoing skills retention.
The document discusses neuropathic pain and its treatment. It defines neuropathic pain as pain initiated or caused by primary lesions or dysfunction in the nervous system. Some examples of neuropathic pain given are postherpetic neuralgia, diabetic peripheral neuropathy, and post-surgical neuropathy. The document outlines approaches to diagnosing neuropathic pain, including listening to the patient's description of their pain, looking for sensory abnormalities, and locating the region of pain to a neuroanatomical area. It discusses treating neuropathic pain with topical medications, systemic medications like anticonvulsants, antidepressants and opioids.
This document discusses pediatric multiple sclerosis. It begins with defining pediatric MS as occurring in children under 18 years old. It then covers the epidemiology, finding the incidence is highest between 13-16 years old and females are more commonly affected than males. Risk factors discussed include genetics, obesity, and passive smoking. The pathophysiology in pediatric MS involves less axonal damage and innate immune response dominance over adaptive. Clinical features can include polysymptomatic or monosymptomatic presentations, and differential diagnosis must consider ADEM, CIS, and other conditions. MRI and CSF findings are discussed. Treatment involves steroids for attacks and first-line DMTs like interferons and glatiramer acetate.
This document provides information on neuropathic pain diagnosis and management, with a focus on diabetic peripheral neuropathy. It discusses:
- The different types of pain (nociceptive, neuropathic, central sensitization) and characteristics of each. Neuropathic pain is caused by damage to the somatosensory nervous system and is often chronic.
- Neuropathic pain is prevalent in many conditions including diabetes, cancer, HIV, post-surgical, and postherpetic neuralgia. Over 50% of people with diabetes experience painful diabetic peripheral neuropathy.
- The pathophysiology of neuropathic pain involves peripheral and central nervous system changes that lead to hypersensitivity and abnormal pain response. Sleep disruption and anxiety/depression can
Ankle-foot orthoses (AFOs) are external devices that attach to the lower leg and foot to improve function by controlling motion and providing support. The main components are a calf band, medial and lateral bars that articulate with ankle joints, and a stirrup that anchors to the shoe. There are 5 types of artificial ankle joints prescribed according to muscle strength: free ankle, dorsiflexion stop, plantarflexion stop, fixed dorsiflexion stop, and fixed hinge. AFOs are used to treat drop foot and other conditions involving muscle weakness, deformities, or instability by maintaining proper foot and ankle positioning during gait.
Orthosis are devices used to support weak joints and correct deformities. They work by applying three point pressure and distributing weight across a wide surface area. Common orthosis include ankle foot orthosis (AFO) which support the ankle and foot, knee ankle foot orthosis (KAFO) which stabilize the knee and lower leg, and hip knee ankle foot orthosis (HKAFO) which provide support from the hip to the foot. Orthosis are made of plastic or metal and their design depends on the joints needing support and the individual's condition.
Tricyclic antidepressants (TCAs) share similar chemical structures and biological properties. They are highly lipophilic and tissue-bound outside the central nervous system. Their anticholinergic and noradrenergic effects can cause unpleasant or dangerous side effects. Examples of TCAs described include imipramine, desipramine, clomipramine, amitriptyline, nortriptyline, protriptyline, trimipramine, doxepin, and maprotiline. Selective serotonin reuptake inhibitors have a different structure but some TCAs are metabolized into compounds that are selective norepinephrine reuptake inhibitors. Examples given are flu
TCA cycle- steps, regulation and significanceNamrata Chhabra
The document discusses the citric acid cycle (TCA cycle), including its 8 steps, regulation, and significance. The TCA cycle occurs in the mitochondria and is the final common pathway for the oxidation of fuels like carbohydrates, fatty acids, and amino acids. It harvests electrons from these fuels to produce NADH and FADH2, which are then used in the electron transport chain to produce ATP through oxidative phosphorylation. The cycle plays a crucial role in cellular respiration and the production of cellular energy.
craniofacial_pain EXCELLENTSLIDES PLUS TRIGEMINAL.pptDeniseMathre1
This document provides information on the diagnosis and management of craniofacial pain. It begins by emphasizing the importance of establishing the correct diagnosis, as the wrong diagnosis can lead to wrong treatment. It then covers various pain syndromes involving the face and head, including neuropathic, headache and dental conditions. The document discusses the pharmacological and surgical treatment options for craniofacial pain in detail, focusing on antiepileptic drugs, antidepressants, opioids, botulinum toxin injections, and peripheral nerve stimulation techniques. It stresses that successful treatment depends on making an accurate diagnosis of the underlying cause of the patient's pain.
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
This document discusses the evaluation of analgesic agents. It begins by classifying pain based on its source, location, duration and type. It then describes the neural mechanisms of pain transmission, including the different types of nerve fibers involved and modulation that occurs in the nociceptive pathway. The document discusses various chemical mediators involved in pain signaling and transmission to higher brain centers. It also covers endogenous opioid peptides and opioid receptors, and describes various in vitro and in vivo tests used to evaluate potential analgesic agents.
GP Palliative Care Update 2019 Neuropathic Pain Dr. Paul McNamara with thanks...St Oswald's Hospice
Dr. Paul McNamara's presentation aimed to define neuropathic pain, describe its underlying pathophysiology, and discuss pharmacological and non-pharmacological therapies for managing neuropathic pain in palliative care patients. The presentation covered the clinical characteristics of neuropathic pain, pharmacological options including TCAs, gabapentinoids, and ketamine, as well as non-drug therapies like TENS and acupuncture. Case studies were also presented to demonstrate practical application of neuropathic pain management principles.
1) Chronic pain affects 19% of people and often leads to reduced ability to work or job loss due to inadequate pain management. Ketamine is an NMDA receptor antagonist that has been used as an anesthetic and analgesic drug since the 1960s.
2) A study looked at the efficacy and safety of ketamine treatment for chronic pain in healthy volunteers and patients with Complex Regional Pain Syndrome type 1 (CRPS-1). The study found ketamine reduced experimental and chronic pain in CRPS patients with no changes in vital signs or liver function.
3) The difference in timing between the onset and offset of ketamine's analgesic effects suggests it has a modulatory effect on chronic pain processes beyond just acute pain relief.
This document discusses mechanisms of pain transmission and modulation as well as recent advances in pharmacological pain therapy. It begins by outlining various mechanisms including transduction, sensitization, and descending pain pathways. It then summarizes common analgesic classes like opioids, NSAIDs, acetaminophen, gabapentinoids, local anesthetics, antidepressants and their mechanisms of action. The document concludes by mentioning new modalities like patient-controlled analgesia that provide better pain relief than conventional methods.
Multimodal pain management following surgical proceduresDrYaminiVS
1. The document discusses concepts related to nociception, central sensitization, and multimodal analgesia for perioperative pain management.
2. It provides definitions of terms like nociception and describes the types of pain and sensory receptors involved in pain perception.
3. The key aspects of multimodal analgesia involve combining different analgesics that act through different mechanisms in the nervous system to provide improved analgesia and fewer side effects than individual analgesics alone.
Neuropathic pain is caused by damage or dysfunction in the nervous system. It is initiated or caused by a primary lesion or dysfunction in either the peripheral or central nervous system. Common causes include diabetes, shingles, spinal cord injury, stroke, alcoholism and medications. This document discusses various types of neuropathic pain such as peripheral nerve damage and peripheral neuropathies. It also covers symptoms, diagnosis, examination tests and management options. The management of neuropathic pain focuses on treating underlying causes, reducing pain, improving function and quality of life. Pregabalin and gabapentin are considered first-line treatments and one study found that pregabalin was as effective as gabapentin for neuropathic pain associated with spinal cord injury.
yes this is my first presentation just prepared for my wkly presentation of oncology department RAJSHAHI MEDICAL COLLEGE. Though it was not that much good.
This document discusses medication options for low back pain. It begins by outlining first-line treatments including non-opioid analgesics like paracetamol and NSAIDs. Combination therapy using both is recommended if pain persists. The document then discusses second-line options if pain involves neuropathic components, such as tricyclic antidepressants, tramadol, or tapentadol. Strong opioids are a fourth-line treatment option if other medications are ineffective.
Basics of acute and chronic pain medicine for the Otolaryngologist (ENT)yury
This document summarizes key topics in acute and chronic pain medicine relevant to otolaryngologists. It discusses the differences between acute and chronic pain, as well as nociceptive and non-nociceptive pain. The benefits of effective postoperative analgesia are outlined. Different types of central facial pain, neuralgias, cancer pain, and headache are briefly described along with their typical treatments.
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This document discusses chronic pain management. It defines chronic pain as pain persisting for over 3 months or associated with a chronic pathological process. Chronic pain can be nociceptive (from damaged tissue) or neuropathic (from damaged nerves). Treatment involves a multimodal approach including medications like opioids, antidepressants, anticonvulsants, steroids and procedures like nerve blocks. Nerve blocks discussed include trigeminal, facial, glossopharyngeal, phrenic and cervical nerve blocks. Complications of nerve blocks include intravascular injection and nerve injury.
The document discusses pain management and analgesia. It outlines the consequences of untreated pain such as wasting, immune suppression, and increased risk of complications. It then covers the physiology of pain, types of pain responses, signs of pain, behavioral responses, and methods of pain assessment. Finally, it discusses various pharmacological agents for perioperative pain management including opioids, NSAIDs, local anesthetics, and other drugs, outlining their mechanisms of action, uses, and potential adverse effects.
This document discusses diabetic neuropathy and its management. It provides definitions of diabetic neuropathy and outlines its causes, types, risk factors, features, burden, and management approaches. Pregabalin is established as an effective first-line treatment based on evidence from multiple clinical trials. Trials showed that pregabalin across dosage ranges of 150-600 mg/day significantly reduced neuropathic pain in patients with diabetic peripheral neuropathy.
Acute pain management & preemptive analgesia (3)DR SHADAB KAMAL
This document discusses acute pain management and pre-emptive analgesia. It defines acute pain as pain caused by actual or potential tissue damage that is usually nociceptive in nature. Acute pain management primarily deals with patients recovering from surgery or acute medical conditions. Pre-emptive analgesia aims to prevent central neural sensitization by administering analgesics before a painful stimulus occurs, which can reduce both acute postoperative pain and the risk of chronic postsurgical pain. The document outlines various treatment approaches for acute pain management, including opioids, non-opioid analgesics, regional anesthetic techniques, and multimodal analgesia.
Acute pain management involves classifying pain and identifying its underlying cause. Treatment options include nonopioid medications like acetaminophen and NSAIDs, opioids, and adjuvant analgesics. Opioids are effective for moderate to severe acute pain but can cause adverse effects like respiratory depression, nausea, and constipation. Adjuvant analgesics like gabapentin, pregabalin, and ketamine may enhance opioid analgesia and reduce opioid requirements and side effects. Close monitoring is important when using opioids to manage acute pain.
This document discusses acute pain management. It begins by classifying pain and then focuses on acute pain, which is defined as lasting less than 12 weeks and being caused by surgery, injury, or acute illness. The pharmacologic treatment of acute pain includes nonopioid drugs like acetaminophen, NSAIDs, and adjuvants/coanalgesics. Opioids are also discussed, including routes of administration, mechanisms of action, effects on organ systems, indications, dosing, and adverse effects. Specific opioids like morphine, fentanyl, and tramadol are covered in more detail. Adjuvant analgesics that may enhance opioid effects like antidepressants, anticonvulsants, local anesthetics,
This document discusses three neurological conditions: Guillain Barre Syndrome, Multiple Sclerosis, and Myasthenia Gravis.
Guillain Barre Syndrome is a condition causing rapid demyelination of peripheral nerves resulting in ascending weakness. It can be caused by infections or injuries and leads to impaired nerve signaling. Clinical features include muscle weakness and diminished reflexes.
Multiple Sclerosis is an immune-mediated disease causing destruction of the myelin sheath in the central nervous system. It has autoimmune and genetic risk factors and results in plaques forming on the myelin sheath, interrupting nerve signals. Common symptoms are fatigue, weakness, numbness, and lack of coordination.
Myasthen
This document provides a summary of examination findings and differential diagnoses for a patient presenting with low back pain. Key examination findings included limited range of motion of the lumbar spine, diffuse tenderness over the lumbar paraspinals and bilateral greater trochanters/SI joints, and normal strength and sensation tests. The document then reviews gait, provocative tests, and muscle grading to further evaluate the patient. Common differential diagnoses for low back pain are listed, along with descriptions of relevant anatomy and neurological patterns.
This document provides an overview of balloon kyphoplasty as an orthopaedic treatment for vertebral compression fractures. It describes how balloon kyphoplasty can stabilize fractures and correct spinal deformity by using an inflatable balloon to restore height to a fractured vertebra before injecting bone cement. Clinical studies discussed show that balloon kyphoplasty provides significant pain reduction, mobility improvements, and a low complication rate compared to alternative treatments like vertebroplasty.
This document discusses urine toxicology testing for drugs of abuse. It describes the types of drugs that can be detected through urine testing, including amphetamines, barbiturates, benzodiazepines, cannabinoids, cocaine, methadone, opiates, and PCP. It outlines the normal detection windows for these drugs in urine and discusses specimen collection and screening versus confirmatory testing methods. The document also addresses issues like interferences, adulterants that can produce false negatives, and challenges in drug testing. It provides details on opiate detection specifically and introduces the Ameritox Rx Guardian urine drug monitoring program.
The document summarizes opioids and their use in pain management. It describes the scheduling of controlled substances including opioids, endogenous and receptor systems, metabolism and excretion pathways, routes of administration considerations, adverse effects and selected opioids like morphine, fentanyl, methadone.
This document discusses different types of back pain and potential treatment options. It distinguishes between acute versus chronic back pain, axial versus radiating pain, and discogenic versus spondylitic pain. Diagnostic considerations include determining if the pain is referred or radicular, and whether it is caused by spondylosis or a herniated disc. Potential treatments discussed include medications, physical therapy, injections, and surgeries.
The document provides information and guidelines around evaluation and management documentation, including documentation of the chief complaint, history of present illness, review of systems, past medical history, physical exam, and medical decision making. It discusses the components needed for different levels of evaluation and management services and how to tally the level of service based on the history, exam, and medical decision making complexity.
Trigeminal neuralgia is a neuropathic disorder characterized by severe, sporadic facial pain. It is caused most commonly by vascular compression of the trigeminal nerve near the brainstem. Carbamazepine is first-line medical treatment but has side effects. Interventional treatments include microvascular decompression, rhizotomy, and gamma knife radiosurgery which provide initial pain relief in the majority but have risks of sensory deficits. Treatment is aimed at pain control and improving quality of life.
The document discusses various interventional procedures for treating back pain, including discography, intradiscal electrothermal therapy (IDET), and percutaneous disc decompression. It provides information on indications and contraindications for these procedures, techniques, interpretation of discography results, risks/complications, efficacy evidence, and mechanisms of action. Discography involves injecting dye into intervertebral discs to reproduce pain, help identify painful discs, and predict fusion outcomes. IDET uses heat to shrink collagen fibers in painful discs. Percutaneous decompression techniques aim to remove disc material for radicular pain.
This document summarizes rational use of opioids in anesthesiology. It discusses the mechanisms of action of opioids in inhibiting neurotransmitter release and altering ion conductance. It notes that opioids can block the stress response, allow for balanced anesthesia using reduced doses of other agents, and provide postoperative analgesia. However, opioids can also cause issues like histamine release, hypotension, urinary retention, decreased GI motility, and respiratory depression when combined with other sedatives. The effects of specific opioids like fentanyl, hydromorphone, methadone, remifentanil, and their properties, dosing, and comparisons are outlined. It emphasizes administering balanced anesthesia and avoiding morphine in some patients,
This document discusses opioids and their mechanism of action, pharmacokinetics, metabolism, effects on circulation and respiration, side effects, and indications/contraindications. It notes opioids act on mu, kappa, delta, and sigma receptors and details their liver metabolism and renal excretion. Specific opioids like morphine, fentanyl, and meperidine are mentioned. Side effects include nausea, vomiting, respiratory depression, constipation, immune suppression, and addiction risk. Opioids are indicated for cancer pain and the perioperative period but have contraindications like opioid hypersensitivity or use with MAOIs.
CRPS Type I, also known as complex regional pain syndrome, is a chronic pain condition that usually affects the arms or legs after an injury. It is characterized by ongoing pain that is disproportionate to the injury, as well as changes in skin temperature, color, and swelling. While the exact pathophysiology is unknown, it likely involves changes in the peripheral and central nervous systems. Diagnosis is based on ongoing pain and symptoms in the affected area that cannot be explained by another condition. Treatments include medications, nerve blocks, physical therapy, and spinal cord stimulation, with the goals of reducing pain and improving function. Early intervention is recommended to prevent long-term disability.
This document contains 6 cases involving patients with pain issues following various surgeries requiring management of epidural or PCA analgesia. Case 1 involves a patient whose spinal anesthesia is wearing off after hip replacement. Case 2 discusses standard PCEA settings and concerns about stopping an epidural due to low blood pressure. Case 3 involves pain management for a very large patient after bowel surgery. Case 4 reviews considerations for removing an epidural catheter in a patient on anticoagulants. Cases 5 and 6 discuss managing worsening pain at different post-op times and the innervation of the lower extremity and knee.
Pediatric Neuraxial Anesthesia and Postoperative Pain Managementyury
This document discusses neuraxial anesthesia/analgesia benefits such as hemodynamic stability, decreased anesthetic requirements, and improved pain relief compared to IV opioids. It also compares pediatric and adult spine anatomy differences like conus medullaris level and CSF volume. Guidelines are provided for epidural solutions and dosages in children, including maximal bupivacaine bolus and infusion doses. Adjuvants like opioids, clonidine and ketamine are reviewed. Pediatric pain assessment tools and postoperative pain medication options and dosages are also summarized. Case examples demonstrate application of epidural and other analgesic techniques for different pediatric surgical scenarios.
Human: Thank you for the summary. You captured the key points effectively in 3 conc
This document provides information on patient selection criteria, candidate types, and contraindications for spinal cord stimulation (SCS). Good candidates tend to have neuropathic or complex regional pain syndrome. Psychological screening is important, and those with untreated disorders like depression are poor candidates. The document also summarizes SCS techniques, types of implant systems, lead types, and trial lead placement procedures.
This document provides an overview of patient selection considerations for intrathecal infusion therapy. It discusses recommended physician qualifications and clinic setup. Key factors in patient selection include failure of conservative treatments, a positive psychological evaluation, ability to afford refills, and a successful screening trial. Contraindications include untreated depression or substance abuse, pre-existing infections or edema, and inability to tolerate an implanted pump. The document also reviews pump complications seen in studies.
This document discusses anticoagulation and neuraxial anesthesia/analgesia. It provides an overview of case reports of epidural hematomas occurring with the anticoagulant Lovenox. It then reviews indications for antithrombotic therapy and recommended prophylaxis for DVT/VTE. The properties and monitoring of various anticoagulants including heparin, warfarin, low molecular weight heparin, and antiplatelet medications are discussed. Guidelines for the use of neuraxial techniques in patients on different anticoagulation regimens are provided.
Placebos can produce real physiological effects through mechanisms like decreased anxiety, learning, expectations, and the body's natural painkilling endorphins. Studies show placebo interventions relieve symptoms in 5-55% of patients across conditions like asthma, ulcers, angina, postoperative pain, and back pain. Certain patient and provider factors influence placebo responses; warmth, empathy, and positively conveying realistic optimism about treatment are important.
- Pediatric pain management requires a multidisciplinary team approach to properly assess and treat a child's pain. This includes addressing physiological, sensory, cognitive, behavioral, and affective components of pain.
- It is important to believe the child's reports of pain, listen to parents and children, and consult other experts when needed. Treatment should be individualized and non-pharmacological options considered in addition to pharmacological interventions.
- Common opioid medications used for pediatric pain include morphine, hydromorphone, fentanyl, and methadone. Non-opioid options also have a role to play depending on the situation. Proper protocols and guidelines help ensure children's pain is well-managed
Tricyclic antidepressants are generally the first choice treatment for post-herpetic neuralgia (PHN) due to their efficacy and lack of dependency. Opioids or anticonvulsants like gabapentin can also provide relief. Topical capsaicin may help but is often poorly tolerated, while intrathecal steroids can be considered for intractable cases affecting nerves other than the trigeminal nerve. Treatment aims to improve sleep, which can significantly decrease overall suffering from PHN.
Cancer Pain: Introduction and Medical Managementyury
This document provides an overview of cancer pain management. It discusses that pain can be caused by the tumor or its treatment. Prevalence of pain increases with late stage malignancy, with up to 80% of terminal patients experiencing significant pain. Treatment involves a multimodal approach including antitumor therapies, pharmacological options, and interventional procedures. The WHO ladder recommends a three step approach using nonopioids, then adding opioids for increasing pain, and more potent opioids for severe pain. Proper pain assessment and a variety of pharmacological options are discussed.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
The benefits of an ePCR solution should extend to the whole EMS organization, not just certain groups of people or certain departments. It should provide more than just a form for entering and a database for storing information. It should also include a workflow of how information is communicated, used and stored across the entire organization.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
1. Joshua H. Pozner, M.D. Mount Sinai School of Medicine Department of Anesthesiology Division of Pain medicine Neuropathic Agents
2. Neuropathic Pain Pain initiated or caused by a primary lesion or dysfunction in the nervous system Onset secondary to viral infection, trauma, certain medications, or metabolic insults Typically serves no protective purpose Nerves that remain intact following disease or injury are often hyperactive, signaling pain in the absence of painful stimuli Often described as a burning in quaility May or may not follow a dermatomal distribution
3. Neuropathic Pain States Diabetic painful neuropathy Non-diabetic painful polyneuropathy HIV-related distal sensory polyneuropathy Antiretroviral toxic neuropathy Post-herpetic neuralgia Classical trigeminal neuralgia Central pain Multiple sclerosis Central poststroke pain Spinal cord injury Cancer neuropathic pain Radiculopathy Phantom limb pain Stump pain Complex regional pain syndrome types I & II
26. TCA - Mechanisms Noradrenergic effect Acts at level of descending bulbospinal pathway Inhibitory influence on spinal neural activity Evidence: Depletion of central norepinephrine systems with alpha-methyl p-tyrosine inhibits the antinociceptive actions of TCAs Alpha-adrenoreceptor antagonists such as phentolamine (alpha-1 and alpha-2 blocker) inhibit antinociceptive action of TCAs Alpha-1 blocker, prazosin + amitriptyline = antinociception Alpha-2 blocker, RX821002 + amitriptyline ≠ antinociception Suggests TCAs derive part of antinociceptive effect at the level of the alpha-2 receptor
27. TCA - Mechanisms Opioidergic effect Evidence Naloxone has been shown to antagonize antinociceptive effect of clomipramine in rats Naltrindole (delta-opioid antagonist) has been shown to antagonize antinociceptive effects of TCAs Chronic TCA administration can modify opioid receptor densities and increase opioid levels in rats
28. TCA - Mechanisms NMDA receptor effect Evidence: TCAs bind NMDA receptor complex Chronic administration alters NMDA binding characteristics Imipramine has been shown to prevent Ca2+ influx via NMDA receptor in rat brain
29. TCA - Mechanisms Adenosine receptor effect Inhibit reuptake into neuronal tissue Adenosine has known analgesic effects both peripherally and centrally α1 receptor activation produces antinociception by decreasing cAMP Evidence: Adenosine receptor antagonists (i.e.: caffeine) inhibit antinociceptive effect of TCAs
30. TCA - Mechanisms Sodium channel effect Local anesthetic-type mechanism Demonstrated in animal models Injection into rat sciatic notch comparable to bupivacaine Topical application comparable to lidocaine Anecdotal evidence of holding TCA tablet over sore tooth causing localized numbness Case studies of efficacy with 5% doxepin cream in CRPS I and with doxepin rinse in oral pain from cancer or cancer treatment
31. TCA - Mechanisms Calcium channel effect Chronic treatment has been shown to increase density of L-type channels Antinociceptive effect nullified by nifedipine administration
32. TCA - Mechanisms Anti-inflammatory effect Evidence Experimental model showed imipramine to reduce inflammation induced by carrageenin in rats Dose dependent Clomipramine reduces carrageenin-induced skin inflammation, PGE2 biologic activity and substance P concentration in rat inflammatory exudate
33. TCA – Side Effects Linked to inhibitory interactions with histaminic, cholinergic muscarinic, and cholinergic nicotinic receptors Adverse effects Dry mouth Sedation Dizziness Lethargy Urinary retention Weight gain Most common antidepressants used in suicide attempts
34. TCAs - Indications Numerous studies have demonstrated efficacy in neuropathic pain models Features of neuropathic pain are not dependent on the causal disease Has become accepted that the evidence of analgesia with specific conditions is strong enough to allow uniform use for any condition manifesting the symptoms of neuropathic pain
59. SSRIs Animal models Paroxetine & Fluvoxamine: dose dependent antinociception in mouse hot plate pain test (weak association fluoxetine and citalopram; none with escitalopram) Paroxetine antinociceptive effect Inhibition by naloxone Inhibition by ondansetron (5-HT3 antagonist) No inhibition by ketanserin (5-HT2 antagonist) NNT Paroxetine: 5 Fluoxetine: 15.3
60. SSRIs Human pain studies PDN Sindrup et al.: paroxetine did produce pain relief but less than with imipramine Paroxetine was associated with fewer side effects Fibromyalgia Norregaard et al.: no changes observed in any pain parameter on citalopram after 8 weeks of treatment Caution with concomitant use of NSAIDs May be associated with higher incidence of gastritis/PUD
83. Anticonvulsants - Mechanisms Voltage-gated calcium channels N-type high voltage channel largely responsible for neurotransmitter release from presynaptic nerve terminals L-type high voltage channel found in high concentration in skeletal and smooth muscle T-type low-voltage channel also implicated in transmission of neuropathic pain in periphery and in spinal cord and in central pain α2-δ subunit Increased expression in DRG secondary to peripheral nerve injury in animal models Upregulation noted primarily in neuropathic- and inflammatory-mediated hyperalgesia Binding of gabapentin and pregabalin inhibits calcium influx Selective primarily in above pain states
84. Anticonvulsants - Mechanisms Voltage-gated sodium channels Increased expression has been demonstrated in peripheral and central sensory neurons in neuropathic pain Na channels 1.2, 1.8, 1.9 are preferentially expressed on peripheral sensory neurons Role in nociception Greater inhibition of the channel when membrane is depolarized Binding of fast current of the open channel by AED is slow compared to that of local anesthetics Ensures that kinetic properties of normal action potential are not altered May also regulate excitability by blocking persistent sodium current
85. Anticonvulsants - Mechanisms GABA modulation Main inhibitory neurotransmitter in CNS GABA-A receptors: Cl--permeable ionotropic channel pores GABA-B receptors: metabotropic G-protein-coupled Activity terminated at synapse by reuptake into nerve terminals and metabolized by GABA tramsaminase Activity potentiated by many AEDs Direct action on GABA-A receptors (benzos) Increase synthesis Inhibit reuptake Inhibit GABA-T
86. Anticonvulsants - Mechanisms Glutamate modulation Main excitatory neurotransmitter in CNS Action primarily mediated through inotropic ligand-gated receptors NMDA – slow-gating and desensitize weakly Agonist action requires coagonist glycine Antagonized by ketamine (role in status epilepticus) AMPA – fast-gating and desensitize strongly Kainate Act secondarily through metabotropic G-protein-coupled receptors
88. Anticonvulsants Phenytoin/Fosphenytoin First AED to be used for neuropathic pain (trigeminal neuralgia) Subsequent RCTs have shown little analgesic efficacy Numerous drawbacks Highly protein-bound Only free drug is metabolically active Multiple drug-drug interactions Nonlinear metabolism and elimination AE: hypersensitivity reaction (rash, fever, LAD), hypotension, nystagmus, ataxia, encephalopathy, osteoporosis, teratogenicity
89. Anticonvulsants Carbamazepine First approved for trigeminal neuralgia (later for epilepsy) Chemically related to TCAs Has been studied in PHN, PDN, poststroke pain, pain in GBS Nonlinear time-dependent kinetics due to autoinduction Half-life can shorten considerably 38 hours after single dose to 12 hours after chronic therapy Often requires increase in dose after weeks of treatment Autoinduction quickly reversed with discontinuation Therapeutic range: 4-12 mg/dL Typically dosed twice daily AE: rash, neurotoxicity, diplopia, hyponatremia, agranulocytosis Primarily attributable to 10,11-epoxide metabolite
90. Anticonvulsants Oxcarbazepine Structure similar to carbamazepine Modulates sodium and calcium channels May act at level of adenosine receptor Antinociception reduced with adenosine receptor antagonists Limited but increasing evidence of use for treatment of pain RCTs have shown efficacy in alleviating TGN Pain relief may be apparent within 24-48 hours Some have shown pain relief despite lack of response to carbamazepine May also have a role in PDN At therapeutic dose, metabolism is not induced nor inhibited by CYP system 95% bioavailability AE: rash, hyponatremia, neurotoxicity, hypothyroidism Less frequent than with carbamazepine
91. Anticonvulsants Gabapentin Binds α2-δ subunit of voltage-gated calcium channel Decreases release of monoamines Nonlinear kinetics Absorption via facilitated transport is saturable Bioavailability is related to dose Drug is not metabolized and does not induce enzymes Lack of drug-drug interactions Low protein binding Eliminated unchanged via kidneys Adjust dose in renal impairment Removed during HD Implies CRCL < 15 mL/min: dose 100-300 mg/day with supplemental dose of 100-300mg after dialysis Elimination half-life: 6 hours
92. Anticonvulsants Gabapentin Studied in numerous pain syndromes: Multiple sclerosis-related central pain, CRPS I & II, migraine, TGN, HIV neuropathy, SCI, cluster HA, DPN, PHN May reduce opioid requirements postoperatively Synergistic Best analgesia in PDN and PHN with gabapentin-morphine combination Reduced doses than when either is used alone AE: dizziness, fatigue, somnolence, weight gain, peripheral edema
93. Anticonvulsants Pregabalin Anticonvulsant, anxiolytic, and analgesic activity Binds α2-δ subunit of voltage-gated calcium channel Predictable pharmacokinetics High bioavailability Elimination half-life: 6.3 hours Not protein-bound No effect on CYP450 system 90% excreted unchanged in urine Adjust dose in renal impairment Numerous RCTs Improved pain and sleep scores in PDN after one week Also effective in PHN, fibromyalgia AE: dizziness, fatigue, somnolence, weight gain, peripheral edema
94. Anticonvulsants Topiramate Derivative of D-fructose Mechanism Blocks voltage-sensitive sodium channels Potentiates GABA at level of GABA-A receptor Increases opening frequency Cl- ion channels Blocks glutamate receptors Reduces activity of L-type Ca++ channels Linear pharmacokinetics Half-life: 19-25 hours 85% bioavailability Mild enzyme inducer Indication: migraine prophylaxis Inhibits trigeminocervical pain transmission No demonstrable analgesia in PDN AE: paresthesias, drowsiness, cognitive effects, nephrolithiasis, weight loss
95. Anticonvulsants Divalproex Mechanism: Inhibits GABA catabolism Increases synaptic release of GABA Sodium valproate and valproic acid in 1:1 ratio FDA approved for migraine prophylaxis Also used as acute treatment in migraine, but evidence is lacking Highly protein bound Half-life: 16 hours Extensively metabolized Lack of enzyme induction Multiple drug-drug interactions with other AEDs AE: drowsiness, tremor, nausea, weight gain, alopecia, peripheral edema, hepatotoxicity, pancreatitis, encephalopathy, teratogenicity
96. Anticonvulsants Lamotrigine Fewer side effects relative to carbamazepine and phenytoin Little dose-dependent toxicity No need to monitor lab values No effect on liver enzymes 55% protein-bound Half-life: 30 hours Requires slow titration (4-6 weeks) Serum levels reduced by enzyme-inducing drugs Reportedly useful in lumbar radicular pain RCTs have shown benefit in HIV-associated distal sensory polyneuropathy, antiretroviral toxic neuropathy, SCI pain, central poststroke pain AE: rash, Stevens-Johnson syndrome
97. Anticonvulsants Others requiring further investigation to support analgesic activity: Levetiracetam Tiagabine May have a role in pain resulting from tonic spasm of multiple sclerosis Zonisamide May have a role in PDN RCTs showed improvement, but not significantly better than placebo Benzodiazepines Clonazepam has been reportedly used in chronic facial pain
98. Local Anesthetics Uses: Neuropathic pain that arises from abnormally developed sodium channels at site of neuronal injury Persistent spontaneous ectopic discharges along an injured peripheral nerve, in neuromas, in DRG, in a central hyperexcitable state Repeated activation of peripheral nociceptors leading to central sensitization, resulting in hyperalgesia, allodynia Can block aberrant discharges at concentrations below those necessary to produce conduction blockade
99. Local Anesthetics Lidocaine Binds abnormally developed sodium channels Reduces frequency of ectopic discharges Intravenous Meta-analysis of numerous neuropathic pain states Typical dose: 5mg/kg over 30-60 minutes Effect more consistent in patients with pain secondary to trauma, PDN, and central pain Also effective in PHN, stump pain Less effective in phantom pain than morphine Ineffective in HIV-related polyneuropathy Consider transitioning to mexilitine if positive response AE: nausea, vomiting, abdominal pain, diarrhea, dizziness, perioral numbness, tremor, dry mouth, metallic taste, insomia, tachycardia
100. Local Anesthetics Lidocaine patch Topical application limits systemic effects Up to 5% of total dose applied is absorbed systemically Maximum plasma concentration is achieved by day 2 Systemically absorbed lidocaine is primarily metabolized by liver Efficacy demonstrated in PHN – FDA approved Has also been used in myofascial pain, LBP, OA, PDN 10 x 14cm, 700mg, nonwoven polyethylene backing Maximum of three patches to intact skin 12 hours on, 12 hours off Those who are responsive feel relief within days Some have delayed relief – trial period of 2 weeks recommended 1/3 report continued pain relief when patch is not applied Minimal AE (skin irritation); minimal drug-drug interactions; may be used indefinitely
101. Local Anesthetics Mexilitine Oral bioavailable analogue of lidocaine Most effective in neuropathic pain due to PDN, trauma and central pain Has also been used in postoperative pain 600mg night before breast cancer surgery and for 10 days reduced analgesic requirements from postoperative days 2-10 AE: similar to lidocaine; more nausea, fewer CNS symptoms; fever, eosinophilia, lymphocytosis, liver dysfunction 90% bioavailable 40% protein-bound Eliminated primarily by hepatic metabolism Caution in liver dysfunction Half-life: 6.7-17.2 hours Lack of predictable dose-response relationship Titrate over days to weeks
102. Ketamine Mechanisms Non-competitive NMDA receptor antagonist Inhibition of voltage gated Na+ and K+ channels Inhibition serotonin, dopamine reuptake Formulations Injectable, oral, topical, intrathecal, epidural May be useful in instances in which “wind-up” is presumed to have already occurred Evidence for efficacy is moderate to weak Described uses Central pain Complex regional pain syndromes Fibromyalgia Ischemic pain Phantom limb pain Postherpetic neuralgia Cancer pain AE: psychomimetic reactions, sensorimotor disturbances, hyperactivity
103. Capsaicin Mechanisms Causes neurotoxic cellular degeneration of primary afferent nociceptors Results in activation, desensitization, and occasionally, destruction of lightly myelinated or unmyelinated primary afferent fibers Uses Possible clinical role for topical capsaicin at high doses Applications of 5-10% PHN HIV associated neuropathy Arthritic pain; LBP; post-surgical pain At low doses, compliance may be a problem because prolonged and frequent applications are required, and application is marked by intense initial burning effects
104. Clonidine Mechanisms Alpha-2 adrenergic agonist Increases GABA-A activity Stimulates cholinergic interneurons in the spinal cord when given intrathecally and epidurally Sites of action: periphery, supraspinal CNS, spinal cord Most data reflect the effectiveness of the intrathecal and epidural administration of clonidine Newer data may support efficacy in various neuropathic pain states with use of oral and topical administration Diabetic neuropathy Postherpetic neuralgia Dose should be tapered to avoid rebound hypertension AE: sedation, hypotension, dry mouth, dizziness, constipation, orthostasis, sexual dysfunction
105. Botulinum Toxin Neurotoxin with affinity for cholinergic synapses Endocytosed into motor neuron terminal Inhibits exocytosis of synaptic vesicles containing acetylcholine Role in pain modulation Inhibits exocytosis of other neuropeptides such as substance P In vitro: reduces stimulated release of CGRP Decreases the inflammatory response and release of glutamate induced by SQ formalin in mice paws Reduced activity of dorsal horn neurons May mitigate peripheral and central sensitization Uses PDN TGN PHN Migraine
106. Conclusion Complex chronic pain state Numerous etiologies Difficult to treat Multimodal/multiagent approach Trial and error