The document discusses peripheral neuropathy including definitions, symptoms, classifications, epidemiology, differential diagnosis, diagnostic workup, and case examples. It provides an overview of peripheral neuropathy including common causes like diabetes and idiopathic neuropathy as well as diagnostic testing and examination techniques. Specific case examples are used to demonstrate the clinical presentation and workup of peripheral neuropathy.
The document provides information about protocols for treating patients exhibiting signs of an acute stroke or CVA. It outlines assessments and tests to determine if a patient is having a stroke, including the Cincinnati Pre-hospital Stroke Scale (CPSS) and Rapid Arterial Occlusion Evaluation (RACE). It describes treating potential underlying causes of stroke symptoms like hypoglycemia. It also notes the differences between primary and comprehensive stroke centers in terms of capabilities for treating patients.
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive weakness and impaired sensory function caused by damage to the peripheral nervous system. It has an incidence rate of 1-2 per 100,000 people and predominantly affects males over 50 years old. CIDP is diagnosed based on progressive muscle weakness, reduced reflexes, nerve conduction studies showing demyelination, elevated CSF protein, and nerve biopsy with signs of demyelination. Treatment involves intravenous immunoglobulin, plasma exchange, steroids, or other immunosuppressants, with around 50% of patients experiencing improvement with therapy.
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by restricted blood flow. TIAs last less than 24 hours and have an annual incidence of 3 per 10,000 people. Approximately 10% of patients experience a TIA before having a stroke. Management involves identifying risk factors like hypertension and treating the underlying cause, often through antiplatelet agents, anticoagulation, or carotid endarterectomy to prevent future strokes.
This document summarizes various neurological effects of alcoholism. It discusses acute alcoholic intoxication, alcohol withdrawal including seizures, hallucinations, and delirium tremens. It also covers nutritional deficiencies that can occur like Wernicke-Korsakoff syndrome and neurological complications of uncertain etiology. Specific conditions related to alcoholism are explained such as encephalopathy, trauma, strokes and others. The effects of alcohol on neurotransmitter systems are outlined. Features of alcohol withdrawal syndrome and delirium tremens are defined. Management of withdrawal and complications are addressed.
The document discusses the definition, classification, features, and pathophysiology of dystonia. It is classified based on age of onset, distribution, and etiology. Primary dystonias have no known underlying brain lesion and can be hereditary or idiopathic in nature, while secondary dystonias have an identifiable cause such as drugs, toxins, or other neurological conditions. The pathophysiology of primary dystonias involves subtle changes in neuronal signaling and communication in basal ganglia circuits that lead to abnormal patterns of muscle contraction.
This document provides information on spinal tuberculosis, including its history, types of lesions, clinical presentation, imaging findings, treatment, and indications for surgery. It discusses how spinal tuberculosis is usually secondary to a primary infection elsewhere in the body that spreads hematogenously to the spine. The most common type of spinal lesion is a paradiscal lesion that begins in the vertebral body. Clinical presentation varies from asymptomatic to paraplegia. Imaging like CT and MRI are useful to identify bone destruction and abscesses. Treatment involves anti-tuberculosis medications for 18 months along with rest. Surgery is indicated for neurological deterioration, advanced disease, or diagnostic uncertainty.
1. Stroke is defined as a nontraumatic brain injury caused by occlusion or rupture of cerebral blood vessels that results in sudden neurological deficits.
2. The most common types of stroke are ischemic (85%) and hemorrhagic (15%). Ischemic strokes are further classified as thrombotic, embolic, or lacunar.
3. Major risk factors for stroke include hypertension, heart disease, diabetes, smoking, and older age. Location of brain injury determines the specific neurological symptoms, such as deficits on one side of the body for middle cerebral artery strokes.
This presentation provides information on Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). It discusses their etiology, clinical presentation, diagnosis, and physiotherapy management. Both GBS and CIDP result from an autoimmune attack on peripheral nerves causing demyelination. While GBS is acute, CIDP is chronic with progressive symptoms over time. Clinical features include weakness, numbness, and sensory loss. Physiotherapy focuses on maintaining function, mobility, and recovery through various exercises depending on the patient's stage of illness. Prognosis is generally good, with around 65% of GBS patients achieving near complete recovery within a year.
The document provides information about protocols for treating patients exhibiting signs of an acute stroke or CVA. It outlines assessments and tests to determine if a patient is having a stroke, including the Cincinnati Pre-hospital Stroke Scale (CPSS) and Rapid Arterial Occlusion Evaluation (RACE). It describes treating potential underlying causes of stroke symptoms like hypoglycemia. It also notes the differences between primary and comprehensive stroke centers in terms of capabilities for treating patients.
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive weakness and impaired sensory function caused by damage to the peripheral nervous system. It has an incidence rate of 1-2 per 100,000 people and predominantly affects males over 50 years old. CIDP is diagnosed based on progressive muscle weakness, reduced reflexes, nerve conduction studies showing demyelination, elevated CSF protein, and nerve biopsy with signs of demyelination. Treatment involves intravenous immunoglobulin, plasma exchange, steroids, or other immunosuppressants, with around 50% of patients experiencing improvement with therapy.
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by restricted blood flow. TIAs last less than 24 hours and have an annual incidence of 3 per 10,000 people. Approximately 10% of patients experience a TIA before having a stroke. Management involves identifying risk factors like hypertension and treating the underlying cause, often through antiplatelet agents, anticoagulation, or carotid endarterectomy to prevent future strokes.
This document summarizes various neurological effects of alcoholism. It discusses acute alcoholic intoxication, alcohol withdrawal including seizures, hallucinations, and delirium tremens. It also covers nutritional deficiencies that can occur like Wernicke-Korsakoff syndrome and neurological complications of uncertain etiology. Specific conditions related to alcoholism are explained such as encephalopathy, trauma, strokes and others. The effects of alcohol on neurotransmitter systems are outlined. Features of alcohol withdrawal syndrome and delirium tremens are defined. Management of withdrawal and complications are addressed.
The document discusses the definition, classification, features, and pathophysiology of dystonia. It is classified based on age of onset, distribution, and etiology. Primary dystonias have no known underlying brain lesion and can be hereditary or idiopathic in nature, while secondary dystonias have an identifiable cause such as drugs, toxins, or other neurological conditions. The pathophysiology of primary dystonias involves subtle changes in neuronal signaling and communication in basal ganglia circuits that lead to abnormal patterns of muscle contraction.
This document provides information on spinal tuberculosis, including its history, types of lesions, clinical presentation, imaging findings, treatment, and indications for surgery. It discusses how spinal tuberculosis is usually secondary to a primary infection elsewhere in the body that spreads hematogenously to the spine. The most common type of spinal lesion is a paradiscal lesion that begins in the vertebral body. Clinical presentation varies from asymptomatic to paraplegia. Imaging like CT and MRI are useful to identify bone destruction and abscesses. Treatment involves anti-tuberculosis medications for 18 months along with rest. Surgery is indicated for neurological deterioration, advanced disease, or diagnostic uncertainty.
1. Stroke is defined as a nontraumatic brain injury caused by occlusion or rupture of cerebral blood vessels that results in sudden neurological deficits.
2. The most common types of stroke are ischemic (85%) and hemorrhagic (15%). Ischemic strokes are further classified as thrombotic, embolic, or lacunar.
3. Major risk factors for stroke include hypertension, heart disease, diabetes, smoking, and older age. Location of brain injury determines the specific neurological symptoms, such as deficits on one side of the body for middle cerebral artery strokes.
This presentation provides information on Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). It discusses their etiology, clinical presentation, diagnosis, and physiotherapy management. Both GBS and CIDP result from an autoimmune attack on peripheral nerves causing demyelination. While GBS is acute, CIDP is chronic with progressive symptoms over time. Clinical features include weakness, numbness, and sensory loss. Physiotherapy focuses on maintaining function, mobility, and recovery through various exercises depending on the patient's stage of illness. Prognosis is generally good, with around 65% of GBS patients achieving near complete recovery within a year.
This document provides guidelines for treating radiculopathy and back pain. It discusses:
- Common causes of back pain including ligament/muscle strains and spinal issues
- Nonsurgical and pharmacological treatment options for acute, subacute, and chronic back pain including exercise, NSAIDs, muscle relaxants, and opioids
- Surgical indications and procedures for severe or persistent back pain such as spinal fusion, disc replacement, and microdiscectomy
- Approaches to acute radiculopathy including imaging, glucocorticoids, opioids, and exercise-based rehabilitation
Dr. Ankur Mittal's presentation discusses stenosing tenosynovitis, also known as trigger finger. The anatomy of the flexor tendon sheath and pulley system is described. Trigger finger occurs when a thickened flexor tendon catches on the A1 pulley, most commonly in the ring finger. Conservative treatments include splinting, steroid injections, and exercises, while surgery involves open or percutaneous release of the A1 pulley. Postoperative care focuses on early mobilization while avoiding complications like nerve damage or bowstringing. Surgical synovectomy may be required in rheumatoid patients to address underlying synovitis.
Dysautonomia refers to a malfunction of the autonomic nervous system that controls involuntary body functions like heart rate, blood pressure, digestion, and sweating. The document discusses the anatomy and functions of the autonomic nervous system and its divisions. It then defines dysautonomia and lists various causes like diabetes, multiple sclerosis, and injuries. Common symptoms involve fatigue, dizziness, digestive issues, urinary problems, and temperature regulation difficulties. Tests of autonomic function are described that measure responses like heart rate and blood pressure during maneuvers to identify autonomic dysfunction.
The document provides information about spondylosis, a degenerative disorder of the spine. It defines spondylosis as general wear and tear that occurs in the joints and bones of the spine with age. Over 85% of people over age 60 are affected. Spondylosis causes loss of normal spinal shape and function and can affect the cervical, thoracic, or lumbar regions. Non-surgical treatments include soft collars, physiotherapy like heat/cold therapy and electrical stimulation, and medications like acetaminophen and NSAIDs. Surgery is reserved for severe cases not relieved by other treatments.
The document discusses HIV infection and encephalitis. Some key points:
- HIV is a retrovirus that causes AIDS and can affect the nervous system directly or indirectly through opportunistic infections.
- Neurological features develop in 80% of infected individuals, manifesting as effects of HIV or infections/tumors due to immunodeficiency.
- HIV encephalitis refers to cognitive impairment from cerebral HIV infection and does not include opportunistic infections from immunodeficiency.
- Symptoms of HIV encephalitis include decreased cognition, psychomotor slowing, and motor symptoms like gait instability. Diagnosis involves neuropsychological testing and neuroimaging. Treatment includes antiretroviral therapy and
Polymyalgia rheumatica and giant cell arteiritisdattasrisaila
Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are two closely related inflammatory conditions that often occur in the same patient population. GCA causes inflammation of medium and large arteries and can lead to vision loss, strokes, and other ischemic symptoms. It predominantly affects women over 50 and is diagnosed based on clinical features, elevated inflammatory markers like ESR, and positive temporal artery biopsy. Imaging plays an important role in diagnosis and monitoring disease involving large arteries like the aorta. High-dose corticosteroids are the primary treatment.
Central nervous system tuberculosis (CNS TB) is a severe form of TB infection that can affect the brain and spinal cord. It is most common in children under 5 years old. Left untreated, CNS TB has an almost 100% fatality rate and can cause permanent neurological damage even with treatment. Diagnosis involves examination of cerebrospinal fluid which shows increased white blood cells and protein with low glucose. Brain imaging also helps with diagnosis. Treatment requires a multi-drug regimen administered over 9-12 months. Adjunctive steroids are also often used to reduce inflammation and complications. Even with treatment, CNS TB has poor outcomes with only one third of patients fully recovering neurologically.
Osteoarthritis is a degenerative joint disease characterized by cartilage breakdown. It is the most common form of arthritis, often affecting the knees in 70% of people over age 60. Osteoarthritis can cause functional impairment and disability in older adults and is a leading cause of joint replacement surgery. Risk factors include age, obesity, genetics, and joint trauma. Treatment focuses on reducing pain and preserving function through lifestyle changes, physical therapy, braces, and medications like acetaminophen, NSAIDs, and opioids. Surgery is considered for severe, treatment-resistant cases.
A 70-year-old female presented with new onset headache, visual impairment, jaw pain with chewing, and temporal tenderness. She had an elevated ESR. Giant cell arteritis (temporal arteritis) most commonly affects those over age 50 and is a vasculitis involving large and medium arteries, principally the temporal arteries. Diagnosis is based on clinical features and biopsy showing necrotizing arteritis. Treatment involves high-dose steroids to prevent vision loss, with gradual tapering over months to years to prevent relapse. Imaging such as ultrasound and MRI can also help with diagnosis when biopsy is inconclusive or not possible.
Guillain Barre Syndrome (GBS) is a serious disorder that occurs when the body’s defense (immune) system mistakenly attacks part of the nervous system i.e Autoimmune Disorder.
This document discusses status epilepticus, which is defined as prolonged or repeated seizures without recovery between seizures. It classifies status epilepticus, explores its pathophysiology and etiology, and outlines its presentation, differential diagnosis, workup, and management. Status epilepticus results from either failed seizure termination mechanisms or initiation of mechanisms leading to prolonged seizures. It can cause neuronal death or injury if not promptly treated. Management involves initial treatment with benzodiazepines followed by anti-seizure medications like fosphenytoin or anesthetic doses if seizures persist over 40 minutes.
Fibromyalgia is a syndrome characterized by chronic widespread pain, stiffness, and tenderness in the muscles and joints without signs of inflammation. It predominantly affects women between 35-55 years old and causes significant pain and fatigue that interferes with daily activities. While the exact cause is unknown, fibromyalgia is diagnosed by identifying tender points on the body and treatment focuses on managing symptoms through exercise, stress reduction, medications, and alternative therapies as there is no cure.
This document provides an overview of peripheral neuropathies. It discusses that peripheral neuropathies can involve sensory nerves, motor nerves, or both, and may affect single or multiple nerves. The document then covers the clinical presentation and classification of different types of neuropathies, including those that primarily affect the cell body, myelin, or axon. It also lists common causes of peripheral neuropathies like diabetes, paraproteinemia, alcohol misuse, and discusses their prevalence. The temporal course, symptoms, and assessment of peripheral neuropathies are discussed in detail.
This document discusses polymyalgia rheumatica (PMR), a clinical syndrome characterized by severe aching and stiffness in the neck, shoulder, and pelvic areas. It affects people over age 50, especially whites and females. Symptoms include morning stiffness and pain in proximal muscles that is worse with inactivity. Treatment involves corticosteroids like prednisone to reduce inflammation over 2-4 years as the average length of the disease is 3 years and relapses are common if steroids are tapered too quickly.
Cervical myelopathy is caused by compression of the cervical spinal cord, most commonly from cervical spondylosis. Cervical spondylosis involves degenerative changes to the spine that decrease space for the spinal cord. This can lead to static or dynamic compression of the cord, impairing circulation. Patients experience symptoms like neck pain, weakness, spasticity and sensory changes. Diagnosis involves assessing severity using scales and investigating spinal changes through imaging like CT which shows stenosis and compression more clearly than x-rays.
1) Tuberculosis is caused by Mycobacterium tuberculosis and commonly affects the lungs and lymph nodes. It spreads hematogenously to other sites like bones.
2) The mycobacterial cell wall structure makes it highly impermeable, reducing the effectiveness of most antibiotics. Diagnosis involves clinical signs, radiology, microbiological tests, and molecular techniques.
3) Spinal tuberculosis commonly affects the thoracic and lumbar regions. Paradiscal lesions involving the disc are most common. Management involves antitubercular drugs, drainage of abscesses, and surgery.
OP Poisoning - Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kole...Dr Ajith Venugopalan
Organophosphate Poisoning - Evaluation & Management
Toxicology
Emergency Medicine
- Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kolenchery, Ernakulam, Kerala, India
Peripheral neuropathies can be classified into several types based on the pattern of nerve involvement:
1) Mononeuropathy affects a single nerve and can be caused by direct injury, ischemia, or inflammation. Carpal tunnel syndrome is an example.
2) Mononeuritis multiplex involves multiple individual nerves developing lesions over time and is often seen in vasculitis.
3) Polyneuropathy damages many nerve cells across the body symmetrically and can be caused by systemic processes like diabetes or toxins.
Neuropathies are caused by a wide range of factors including metabolic diseases, infections, nutritional deficiencies, autoimmune disease, drugs, and toxins. Identifying the pattern of nerve
This document discusses whiplash, which refers to injuries to the neck caused by sudden acceleration-deceleration movements like those in car accidents. It begins by outlining the history and terminology of whiplash. The mechanism of injury involves cervical acceleration and deceleration, stretching and tearing muscles and tendons. Common causes are car accidents and falls. Injuries can range from muscle strains to fractures. Symptoms include neck pain and stiffness. Treatment involves immobilization, medications, physical therapy, and sometimes surgery for severe cases. Most patients see gradual improvement over 3 months to a year.
Peripheral neuropathy can be caused by damage to peripheral nerves outside of the brain and spinal cord. Symptoms may include numbness, tingling, pain or weakness in the hands, feet, arms and legs. Peripheral neuropathy has many potential causes including diabetes, nutritional deficiencies, toxins, infections and autoimmune disorders. Evaluation may involve neurological exams, nerve conduction studies and biopsies. Treatment depends on the underlying cause but aims to relieve symptoms and prevent further nerve damage when possible.
Plexopathy is a disorder affecting nerve networks like the brachial or lumbosacral plexus. Symptoms include pain, motor control loss, and sensory deficits. It is usually caused by localized trauma or compression. Brachial plexopathy specifically affects the network of nerves from the cervical spine to the shoulder, arm, and hand. Lumbosacral plexopathy affects the network of nerves from the lumbar spine and sacral spine. Diabetic plexopathy commonly affects the lumbosacral plexus and causes anterior thigh pain and proximal leg muscle weakness.
This document provides guidelines for treating radiculopathy and back pain. It discusses:
- Common causes of back pain including ligament/muscle strains and spinal issues
- Nonsurgical and pharmacological treatment options for acute, subacute, and chronic back pain including exercise, NSAIDs, muscle relaxants, and opioids
- Surgical indications and procedures for severe or persistent back pain such as spinal fusion, disc replacement, and microdiscectomy
- Approaches to acute radiculopathy including imaging, glucocorticoids, opioids, and exercise-based rehabilitation
Dr. Ankur Mittal's presentation discusses stenosing tenosynovitis, also known as trigger finger. The anatomy of the flexor tendon sheath and pulley system is described. Trigger finger occurs when a thickened flexor tendon catches on the A1 pulley, most commonly in the ring finger. Conservative treatments include splinting, steroid injections, and exercises, while surgery involves open or percutaneous release of the A1 pulley. Postoperative care focuses on early mobilization while avoiding complications like nerve damage or bowstringing. Surgical synovectomy may be required in rheumatoid patients to address underlying synovitis.
Dysautonomia refers to a malfunction of the autonomic nervous system that controls involuntary body functions like heart rate, blood pressure, digestion, and sweating. The document discusses the anatomy and functions of the autonomic nervous system and its divisions. It then defines dysautonomia and lists various causes like diabetes, multiple sclerosis, and injuries. Common symptoms involve fatigue, dizziness, digestive issues, urinary problems, and temperature regulation difficulties. Tests of autonomic function are described that measure responses like heart rate and blood pressure during maneuvers to identify autonomic dysfunction.
The document provides information about spondylosis, a degenerative disorder of the spine. It defines spondylosis as general wear and tear that occurs in the joints and bones of the spine with age. Over 85% of people over age 60 are affected. Spondylosis causes loss of normal spinal shape and function and can affect the cervical, thoracic, or lumbar regions. Non-surgical treatments include soft collars, physiotherapy like heat/cold therapy and electrical stimulation, and medications like acetaminophen and NSAIDs. Surgery is reserved for severe cases not relieved by other treatments.
The document discusses HIV infection and encephalitis. Some key points:
- HIV is a retrovirus that causes AIDS and can affect the nervous system directly or indirectly through opportunistic infections.
- Neurological features develop in 80% of infected individuals, manifesting as effects of HIV or infections/tumors due to immunodeficiency.
- HIV encephalitis refers to cognitive impairment from cerebral HIV infection and does not include opportunistic infections from immunodeficiency.
- Symptoms of HIV encephalitis include decreased cognition, psychomotor slowing, and motor symptoms like gait instability. Diagnosis involves neuropsychological testing and neuroimaging. Treatment includes antiretroviral therapy and
Polymyalgia rheumatica and giant cell arteiritisdattasrisaila
Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are two closely related inflammatory conditions that often occur in the same patient population. GCA causes inflammation of medium and large arteries and can lead to vision loss, strokes, and other ischemic symptoms. It predominantly affects women over 50 and is diagnosed based on clinical features, elevated inflammatory markers like ESR, and positive temporal artery biopsy. Imaging plays an important role in diagnosis and monitoring disease involving large arteries like the aorta. High-dose corticosteroids are the primary treatment.
Central nervous system tuberculosis (CNS TB) is a severe form of TB infection that can affect the brain and spinal cord. It is most common in children under 5 years old. Left untreated, CNS TB has an almost 100% fatality rate and can cause permanent neurological damage even with treatment. Diagnosis involves examination of cerebrospinal fluid which shows increased white blood cells and protein with low glucose. Brain imaging also helps with diagnosis. Treatment requires a multi-drug regimen administered over 9-12 months. Adjunctive steroids are also often used to reduce inflammation and complications. Even with treatment, CNS TB has poor outcomes with only one third of patients fully recovering neurologically.
Osteoarthritis is a degenerative joint disease characterized by cartilage breakdown. It is the most common form of arthritis, often affecting the knees in 70% of people over age 60. Osteoarthritis can cause functional impairment and disability in older adults and is a leading cause of joint replacement surgery. Risk factors include age, obesity, genetics, and joint trauma. Treatment focuses on reducing pain and preserving function through lifestyle changes, physical therapy, braces, and medications like acetaminophen, NSAIDs, and opioids. Surgery is considered for severe, treatment-resistant cases.
A 70-year-old female presented with new onset headache, visual impairment, jaw pain with chewing, and temporal tenderness. She had an elevated ESR. Giant cell arteritis (temporal arteritis) most commonly affects those over age 50 and is a vasculitis involving large and medium arteries, principally the temporal arteries. Diagnosis is based on clinical features and biopsy showing necrotizing arteritis. Treatment involves high-dose steroids to prevent vision loss, with gradual tapering over months to years to prevent relapse. Imaging such as ultrasound and MRI can also help with diagnosis when biopsy is inconclusive or not possible.
Guillain Barre Syndrome (GBS) is a serious disorder that occurs when the body’s defense (immune) system mistakenly attacks part of the nervous system i.e Autoimmune Disorder.
This document discusses status epilepticus, which is defined as prolonged or repeated seizures without recovery between seizures. It classifies status epilepticus, explores its pathophysiology and etiology, and outlines its presentation, differential diagnosis, workup, and management. Status epilepticus results from either failed seizure termination mechanisms or initiation of mechanisms leading to prolonged seizures. It can cause neuronal death or injury if not promptly treated. Management involves initial treatment with benzodiazepines followed by anti-seizure medications like fosphenytoin or anesthetic doses if seizures persist over 40 minutes.
Fibromyalgia is a syndrome characterized by chronic widespread pain, stiffness, and tenderness in the muscles and joints without signs of inflammation. It predominantly affects women between 35-55 years old and causes significant pain and fatigue that interferes with daily activities. While the exact cause is unknown, fibromyalgia is diagnosed by identifying tender points on the body and treatment focuses on managing symptoms through exercise, stress reduction, medications, and alternative therapies as there is no cure.
This document provides an overview of peripheral neuropathies. It discusses that peripheral neuropathies can involve sensory nerves, motor nerves, or both, and may affect single or multiple nerves. The document then covers the clinical presentation and classification of different types of neuropathies, including those that primarily affect the cell body, myelin, or axon. It also lists common causes of peripheral neuropathies like diabetes, paraproteinemia, alcohol misuse, and discusses their prevalence. The temporal course, symptoms, and assessment of peripheral neuropathies are discussed in detail.
This document discusses polymyalgia rheumatica (PMR), a clinical syndrome characterized by severe aching and stiffness in the neck, shoulder, and pelvic areas. It affects people over age 50, especially whites and females. Symptoms include morning stiffness and pain in proximal muscles that is worse with inactivity. Treatment involves corticosteroids like prednisone to reduce inflammation over 2-4 years as the average length of the disease is 3 years and relapses are common if steroids are tapered too quickly.
Cervical myelopathy is caused by compression of the cervical spinal cord, most commonly from cervical spondylosis. Cervical spondylosis involves degenerative changes to the spine that decrease space for the spinal cord. This can lead to static or dynamic compression of the cord, impairing circulation. Patients experience symptoms like neck pain, weakness, spasticity and sensory changes. Diagnosis involves assessing severity using scales and investigating spinal changes through imaging like CT which shows stenosis and compression more clearly than x-rays.
1) Tuberculosis is caused by Mycobacterium tuberculosis and commonly affects the lungs and lymph nodes. It spreads hematogenously to other sites like bones.
2) The mycobacterial cell wall structure makes it highly impermeable, reducing the effectiveness of most antibiotics. Diagnosis involves clinical signs, radiology, microbiological tests, and molecular techniques.
3) Spinal tuberculosis commonly affects the thoracic and lumbar regions. Paradiscal lesions involving the disc are most common. Management involves antitubercular drugs, drainage of abscesses, and surgery.
OP Poisoning - Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kole...Dr Ajith Venugopalan
Organophosphate Poisoning - Evaluation & Management
Toxicology
Emergency Medicine
- Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kolenchery, Ernakulam, Kerala, India
Peripheral neuropathies can be classified into several types based on the pattern of nerve involvement:
1) Mononeuropathy affects a single nerve and can be caused by direct injury, ischemia, or inflammation. Carpal tunnel syndrome is an example.
2) Mononeuritis multiplex involves multiple individual nerves developing lesions over time and is often seen in vasculitis.
3) Polyneuropathy damages many nerve cells across the body symmetrically and can be caused by systemic processes like diabetes or toxins.
Neuropathies are caused by a wide range of factors including metabolic diseases, infections, nutritional deficiencies, autoimmune disease, drugs, and toxins. Identifying the pattern of nerve
This document discusses whiplash, which refers to injuries to the neck caused by sudden acceleration-deceleration movements like those in car accidents. It begins by outlining the history and terminology of whiplash. The mechanism of injury involves cervical acceleration and deceleration, stretching and tearing muscles and tendons. Common causes are car accidents and falls. Injuries can range from muscle strains to fractures. Symptoms include neck pain and stiffness. Treatment involves immobilization, medications, physical therapy, and sometimes surgery for severe cases. Most patients see gradual improvement over 3 months to a year.
Peripheral neuropathy can be caused by damage to peripheral nerves outside of the brain and spinal cord. Symptoms may include numbness, tingling, pain or weakness in the hands, feet, arms and legs. Peripheral neuropathy has many potential causes including diabetes, nutritional deficiencies, toxins, infections and autoimmune disorders. Evaluation may involve neurological exams, nerve conduction studies and biopsies. Treatment depends on the underlying cause but aims to relieve symptoms and prevent further nerve damage when possible.
Plexopathy is a disorder affecting nerve networks like the brachial or lumbosacral plexus. Symptoms include pain, motor control loss, and sensory deficits. It is usually caused by localized trauma or compression. Brachial plexopathy specifically affects the network of nerves from the cervical spine to the shoulder, arm, and hand. Lumbosacral plexopathy affects the network of nerves from the lumbar spine and sacral spine. Diabetic plexopathy commonly affects the lumbosacral plexus and causes anterior thigh pain and proximal leg muscle weakness.
This document discusses chemotherapy-induced peripheral neuropathy (CIPN). It begins by explaining that CIPN results from nerve damage caused by certain chemotherapy drugs and causes sensory symptoms like numbness, tingling and pain. It then notes that 30-60% of patients receiving neurotoxic chemotherapy will experience CIPN. The document outlines several chemotherapy agents commonly associated with CIPN and their risk levels. It describes the pathogenesis of CIPN and discusses factors that can contribute to its development. The clinical manifestations and potential consequences of CIPN are also summarized. The document reviews methods for assessing CIPN and discusses some pharmacological and non-pharmacological treatment strategies, noting that prevention and management options remain limited.
This document discusses peripheral neuropathy and provides guidance on evaluating and diagnosing peripheral nerve disorders. It defines peripheral neuropathy as disorders affecting the peripheral nervous system, which can involve sensory nerves, motor nerves, or both. The document outlines that peripheral neuropathies can be classified based on whether they primarily affect the cell body, myelin, or axon. It also lists common causes of peripheral neuropathy like diabetes, paraproteinemia, alcohol misuse, and vitamin B12 deficiency. The document provides guidance on clinical assessment, laboratory and electrodiagnostic testing, skin or nerve biopsy, and treatment approaches for peripheral neuropathy.
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.
This document provides information on complications that can occur after femoral access for catheterization procedures. The major complications discussed include hematoma, pseudoaneurysm, arteriovenous fistula, and arterial occlusion. For each complication, the summary describes typical physical findings and recommended nursing interventions. Studies comparing different approaches to hemostasis and sheath removal are also summarized, finding no significant difference in vascular complication rates between sandbag compression and bandage dressings.
The document discusses various types of peripheral neuropathy, including definitions, mechanisms of damage, classification based on examination findings, associated laboratory and diagnostic testing, and treatment approaches. Peripheral neuropathy can be caused by numerous systemic diseases and conditions and presents with a variety of symptoms depending on the affected nerve fibers and distribution of the neuropathy. A thorough evaluation is required to determine the underlying cause and guide management strategies.
Diabetic neuropathy is nerve damage caused by diabetes. It has many forms including distal symmetrical polyneuropathy (most common), proximal motor neuropathy, and autonomic neuropathy. The pathogenesis involves multiple mechanisms from hyperglycemia like increased polyol pathway flux, oxidative stress, and vascular dysfunction. Risk factors include poor glycemic control, obesity, older age, male sex, and family history. Symptoms vary by type but may include pain, numbness, weakness, gastrointestinal issues, and cardiovascular problems. Diagnosis involves clinical exam and electrodiagnostic testing.
By the end of this session, learners will be able to:
Develop and refine a differential diagnosis for peripheral neuropathy
Discuss the workup for common & typical cases
Perform a comprehensive diabetic foot exam
by ADA/NDEP standards
Treat painful peripheral neuropathy
(1) This document discusses neuroinflammatory disorders like multiple sclerosis and neuromyelitis optica. MS most commonly affects women aged 15-45 and has a relapsing-remitting clinical course. (2) It also summarizes evaluation, treatment including immunotherapies, and guidelines for vaccination in MS patients. (3) Autoimmune encephalitis can be paraneoplastic or associated with antibodies like NMDA receptor antibodies, and may respond to immunotherapy and tumor treatment.
This document discusses two cases of neurocysticercosis in children. In both cases, the children presented with seizures and were found to have cystic lesions in their brains consistent with neurocysticercosis based on MRI findings. They were both treated with anti-seizure medications, albendazole, and steroids. Their seizures resolved with treatment and follow-up MRIs showed improvement in the brain lesions. Neurocysticercosis is caused by the larval form of the pork tapeworm infecting the brain and is most commonly seen in areas where pork consumption and poor sanitation allow the tapeworm to spread between humans.
Ccf neuro res rapidly progressive dementia 2013 03-27applebyb
Rapidly progressive dementia can be caused by many conditions, not just prion diseases. Prion diseases should not be the default diagnosis, as there are treatable and reversible causes that could be missed. While diagnostic tests like CSF 14-3-3, EEG, and brain MRI findings can support a prion disease diagnosis, they are not specific and can be present in other non-prion conditions as well. A thorough evaluation is needed to avoid misdiagnosis, and symptomatic treatment should still be considered even for prion diseases.
This document provides an overview of multiple sclerosis (MS), including its epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment. Some key points:
1. MS typically affects people between the ages of 15-45 and is more common in women. It has a variable geographic distribution and prevalence of around 0.1% in the US.
2. The pathophysiology involves chronic inflammation and demyelination in the central nervous system resulting in neurological deficits. MRI is an important tool for diagnosis and monitoring disease progression.
3. Clinical symptoms can include visual disturbances, motor and sensory problems, fatigue, and cognitive issues. Relapsing-remitting is the most common disease course.
This document discusses neuromodulation techniques for psychiatric disorders, including deep brain stimulation (DBS) and vagus nerve stimulation (VNS). It provides an overview of DBS and VNS indications for various psychiatric conditions such as OCD, depression, Tourette's syndrome, and more. The document also describes specific DBS and VNS cases from Italy for conditions like OCD, depression, and chronic pain. It discusses the state of the field and guidelines for ethical surgery for psychiatric disorders.
This document provides information about acoustic neuromas (vestibular schwannomas). It defines acoustic neuromas as benign tumors of vestibular nerve schwann cells that arise from the schwann cells within the internal auditory canal. The document discusses the pathogenesis, clinical presentation in different stages, diagnostic evaluations including audiological and radiological tests, differential diagnosis, and treatment options including surgery, observation, and radiotherapy.
This document provides an overview of neuromyelitis optica (NMO), including its clinical presentation, pathogenesis, diagnostic criteria, treatment, and biomarkers. Some key points:
- NMO predominantly targets the optic nerve and spinal cord, often causing severe vision loss or paralysis. It was previously considered a variant of multiple sclerosis but is now recognized as a distinct condition.
- The discovery of antibodies against aquaporin-4 helped establish NMO as a separate autoimmune disease, with these antibodies detected in around 70-80% of cases.
- In addition to optic neuritis and transverse myelitis, NMO can involve other areas of the CNS and cause a range of neurological and non-
This document provides an overview of key information for assessing and managing seizures and epilepsy in the emergency department setting. It includes learning objectives, a sample case study, guidelines on taking a seizure history and differential diagnosis, acute seizure management and status epilepticus protocols. It also summarizes epilepsy epidemiology, classification, pathophysiology, syndromes and diagnostic evaluation.
This document discusses multiple sclerosis (MS), including:
1) Epidemiology shows it is most common in young white women at northern latitudes and those with Scandinavian ancestry or vitamin D deficiency.
2) Diagnosis relies on clinical patterns and exclusion of other causes, supported by MRI, CSF, and evoked potential studies showing lesions in white matter tracts.
3) The 2010 McDonald criteria provide guidelines for diagnosing MS based on demonstrations of dissemination of lesions in space and time through clinical attacks and imaging/laboratory results.
Neuro-ophthalmic Diagnoses You Don't Want To Miss !neurophq8
The presentation will discuss common life-threatening of vision-threatening neuro-ophthalmic emergencies.
Target: Ophthalmologists/Neurologists/Family Physicians/Internists/Emergency Physicians.
This document discusses trigeminal neuralgia (TGN), including its definition, diagnosis, management, and surgical treatment. It begins by defining TGN as recurrent episodes of sharp, electric shock-like pain in the trigeminal nerve distribution triggered by innocuous stimuli. It then discusses diagnostic criteria and classical vs. atypical TGN. Management involves pharmacotherapy with carbamazepine or oxcarbazepine as first-line options, with second-line drugs including lamotrigine and baclofen for refractory cases. For refractory TGN with neurovascular compression seen on MRI, microvascular decompression surgery is the treatment of choice for younger patients; other options for refractory or older patients include
This document discusses several common neurological disorders seen in patients with HIV/AIDS, including toxoplasmosis, herpes simplex virus encephalitis, cytomegalovirus encephalitis, cryptococcal meningitis, dementia, primary CNS lymphoma, and progressive multifocal leukoencephalopathy. For each disorder, it covers causes, frequency, presentation, diagnosis, and treatment approaches. The overall purpose is to educate participants on identifying, diagnosing, and managing neurological complications in HIV/AIDS patients.
This document provides an overview of seizures and epilepsy. It defines seizures and epilepsy, discusses epidemiology, classification of seizures, causes, pathogenesis, clinical evaluation, and management. Seizures are caused by abnormal neuronal activity in the brain, while epilepsy is defined as two or more unprovoked seizures. Evaluation involves a detailed history, physical exam, EEG, and imaging tests. Management depends on seizure type and underlying cause, and may involve lifestyle changes and antiepileptic medications.
Prion diseases are rapidly progressive neurodegenerative disorders caused by abnormal prion proteins. There are several types including sporadic, familial, variant, and acquired from animals. Prion diseases are untreatable and fatal due to prion protein conversion and deposition in the brain leading to neurodegeneration. Diagnosis involves tests of brain imaging, EEG, CSF and genetic analysis while treatment is largely supportive due to lack of effective disease-modifying therapies.
Lab diagnosis of ctd By Dr Arif Iqbal MD Dermatology UCMS & GTBH7867878678
This document discusses laboratory diagnosis of connective tissue diseases through detection of antinuclear antibodies. It provides details on the sensitivity and specificity of various antinuclear antibody tests for different diseases. Indirect immunofluorescence is the standard technique for antinuclear antibody detection while ELISA is also commonly used. The document outlines the clinical significance and interpretation of several specific antinuclear antibodies including anti-DNA, anti-histone, anti-RNP, anti-Ro, and anti-La antibodies.
Motor neuron diseases affect motor neurons, leading to muscle weakness and atrophy. Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in adults, characterized by both upper and lower motor neuron signs that spread to multiple body regions. While there is no cure for ALS, a multidisciplinary approach including symptomatic treatments can help manage the disease.
This document provides an overview of neuromyelitis optica spectrum disorders (NMOSD). It discusses the epidemiology, clinical features, diagnostic criteria, investigations, neuroimaging findings, and treatments for NMOSD. Key points include that NMOSD predominantly affects the optic nerves and spinal cord, is strongly associated with antibodies against the aquaporin-4 protein, and treatments involve high-dose steroids, plasma exchange, or intravenous immunoglobulins for acute exacerbations. The diagnostic criteria were revised in 2015 to incorporate aquaporin-4 antibody testing and distinguish NMOSD from multiple sclerosis.
This document provides an overview of seizure disorders including basics, epidemiology, risk factors, pathophysiology, diagnosis, treatment, and prognosis. Some key points:
- Seizures are caused by excessive firing of neurons resulting in impaired brain function. Common causes include brain tumors, head injuries, infections, genetic factors.
- Around 200,000 new cases of epilepsy are diagnosed in the US each year, most commonly in children under 15 and older adults over 65.
- Diagnosis involves differentiating epileptic from non-epileptic seizures based on eyewitness accounts and EEG/MRI testing. Initial lab work checks for metabolic causes.
- Treatment primarily involves anti-epileptic medications chosen based
Serious skin signs in sick patients fitzpatrickClinton Pong
This document discusses the approach to dermatologic diagnosis. There are two main clinical situations - incidental findings like asymptomatic lesions that are medically inconsequential, and important lesions that should not be overlooked like melanomas. The other situation is the chief complaint of the patient, which can be minor problems like localized rashes or more serious skin signs in sick patients. It then lists examples of serious skin signs in sick patients such as generalized rashes with fever, blisters, pustules or scaling that could indicate conditions such as viral exanthems, pustular psoriasis, or exfoliative erythroderma.
Potency & $ ratings of topical corticosteroidsClinton Pong
This document provides a table summarizing the potency and generic/brand names of various topical corticosteroids. It divides them into 7 groups based on their potency from ultra-high to least potent. For each corticosteroid, it lists the generic name, common brand name(s), available dosages, vehicle/formulation, and typical cost for the lowest strength on LowestMed as of May 2014. The table acts as a reference for comparing the relative strengths and formulations of different topical corticosteroid medications.
Most common derm lesions ddx sx-to-dx sternClinton Pong
The document discusses organizing the differential diagnosis of rashes based on the morphology of the primary lesion. The primary lesion must first be identified before categorizing the eruption's morphology. Common primary lesions include macules, papules, plaques, nodules, vesicles, and bullae. Differential diagnoses are then suggested based on the morphology and distribution of the primary lesion, such as papulosquamous eruptions including eczematous dermatitis, psoriasis, and tinea infections. Folliculopapular eruptions may be caused by acne, rosacea, or folliculitis. Dermal reaction patterns can result from conditions like urticaria, sarcoidosis,
Advanced dermatology jeopardy orientation for family medicine residents (with gameshow in other slides)
Identify the most common lesions seen in primary care practice
Identify the 4S’s: Serious Skin Signs in Sick Patients
Apply metacognitive principles to dermatologic diagnosis
System I pattern recognition
System II hypothetical-deductive reasoning
Advanced dermatology jeopardy orientation for family medicine residents (with gameshow in other slides)
Identify the most common lesions seen in primary care practice
Identify the 4S’s: Serious Skin Signs in Sick Patients
Apply metacognitive principles to dermatologic diagnosis
System I pattern recognition
System II hypothetical-deductive reasoning
This document discusses the detection, evaluation, and treatment of hypertension. It begins by covering methods for detecting hypertension, including through ambulatory blood pressure monitoring. Next, it addresses recommendations for evaluating patients diagnosed with hypertension. Finally, the document outlines lifestyle modifications and medications that can be used to treat hypertension through therapeutic lifestyle changes and references several studies on sodium and potassium regulation in the kidneys and the use of diuretics and antihypertensive drugs.
Adolescent social media -- Medical perspectiveClinton Pong
Discussion for medical students' consideration
The Internet and its context
-- For teens
-- For adults
Erikson’s Stages of Development
Social Media
-- Benefits
-- Risks
Recommendations
Aims: to give clinicians tools they can use to improve their ability to reflect on a differential dx and aid in correct diagnosis
Objectives:
-- define a dual process cognitive model used when making a diagnosis
-- recognize common heuristics and their related cognitive errors and biases
-- apply a systematic, routine method for differential diagnosis generation.
The document outlines an upcoming presentation on diabetes management. It will review guidelines from major organizations for treating diabetes, discuss treatment goals and hemoglobin A1c levels, and compare the most effective, common, and economical medication options. It will also touch on alternative/complementary therapies and emphasize smoking cessation, blood pressure control, and other lifestyle factors important in diabetes care. Key treatment algorithms and medications to be covered include metformin, sulfonylureas, thiazolidinediones, DPP-4 inhibitors, GLP-1 agonists, and insulin. References from guidelines, reviews, and textbooks will be used.
1) The document defines differential diagnosis and discusses common errors made in developing a differential diagnosis.
2) It introduces the BALM framework for generating a systematic differential diagnosis, which involves considering the condition's location, acuteness, ability to cause systemic effects, and relative probability.
3) The BALM approach involves considering various systems and disciplines that may be involved, such as metabolic, endocrine, infectious, etc. to develop a list of potential diagnoses in a structured manner.
The document summarizes a clinical trial that compared the blood pressure medication amlodipine to atenolol. The trial found that amlodipine was superior to atenolol in preventing cardiovascular events and reducing the risk of new-onset diabetes. Patients taking atenolol had a higher rate of developing diabetes compared to those taking amlodipine. Therefore, the author recommends switching patients from atenolol to amlodipine to better manage cardiovascular risks and reduce the risk of diabetes.
This document provides guidelines for cervical cancer screening and management of abnormal findings according to the 2007 ASCCP guidelines. Key points include: initiating screening at age 21 or 3 years after first sexual intercourse; transitioning to every 3 year screening after age 30 with 3 normal annual pap smears; diagnostic excisional procedure is recommended for CIN II or III in adults but observation is preferred for adolescents; and endometrial biopsy is recommended for women over 35 with atypical glandular cells to evaluate for endometrial cancer.
- Leiomyomas (uterine fibroids) are benign smooth muscle tumors that arise in the myometrium of the uterus and affect 20-75% of women of reproductive age.
- Risk factors include being Black, nulliparity, obesity, and nonsmoking. Symptoms can include heavy menstrual bleeding, pelvic pain, infertility, and pressure symptoms.
- Lei Moma, a 33-year-old obese African American woman, presents with heavy periods, pelvic pain, and fertility problems. Exam reveals an enlarged, irregular, and tender uterus consistent with multiple fibroids.
This document summarizes key points about multiple gestations including twins and triplets. It notes that the incidence is increasing due to assisted reproductive technologies and discusses the higher risks of preterm delivery, low birth weight, and maternal complications. Management may include selective fetal reduction in early pregnancy or delivery planning based on gestational age and fetal well-being monitoring. Close surveillance is important due to risks of conditions like preeclampsia, growth restriction, and twin-twin transfusion syndrome.
2. Objectives
• By the end of this session, learners will be able to:
• Develop and refine a differential diagnosis for
peripheral neuropathy
• Discuss the workup for common & typical cases
• Perform a comprehensive diabetic foot exam
o by ADA/NDEP standards
• Treat painful peripheral neuropathy
3. Definition
Pain initiated or caused by a primary lesion
or dysfunction in the peripheral nervous
system
(“Dysfunction” includes nociceptive and psychogenic
conditions)
Nociceptive = Response to tissue injury
Neuropathic = Pathologic or maladaptive pain
• International Association for the Study of Pain
• [Classification of Chronic Pain: Descriptions of chronic pain syndromes and
definitions of pain terms. 2nd ed. 2002. ]
4. Symptoms
Neuralgias Neuropathies
• Can be • Motor nerves may also
spontaneous, episodic or cause painful cramps
continuous
• Abnormal tactile and
thermal sensations Nociceptive aberrancy
• Numbness • Dysesthesia, hyperalges
• Tingling ia and allodynia
• Pins and Needles • Painful percept evoked
• Burning by stimuli below
nociceptor threshold
• Shooting
• Electric shock-like
sensation
5. Classifications
• Location • Timing
o Acute
o Axonal vs Myelin o Sub-acute
o Large vs Short-diameter fibers o Chronic
• Large = vib/prop • Nerve Injury
• Small = pain/temp o Neuropraxia
• Both = light touch o Axonotmesis
o Neuronotmesis
o Nerve Trunk vs Nerve Root
o Wallerian degeneration
o Sensory vs Motor Nerves
• Focal • Acquired
o Metabolic
o Mononeuropathy
o Infectious
• Multifocal o Inflammatory
o Toxic
o Mononeuropathy multiplex o Mechanical
• Generalized o Traumatic
o Polyneuropathy • Hereditary
6. Epidemiology
• Only 3 prevalence studies on peripheral neuropathy
o Italy: ~8% of Italians 55+ y/o with a PCP going for surgery have peripheral
neuropathy
o Bombay India: 2.4% of Indians surveyed door-to-door met criteria
• Carpal tunnel syndrome and DM most common
o Sicily: 7% of Sicilians surveyed door-to-door met criteria
• DM neuropathy dx’ed in 0.3%
• My best numbers are seen on the next slide
o (x% of cases = overall percentage gathered from small studies on
incidence for underlying dx of peripheral neuropathy)
o (x% of [diagnosis] = overall percentage of patients with dx that have
peripheral neuropathy)
o Best study was in Oklahoma on elderly
• n=795 Peripheral
neuropathy
Diagnosis
• JABFP Sept-Oct 2004
7. Differential dx
Common Other interesting ones
• Diabetes (30% of cases) • Infectious
o Hep B/C (1.3% of OK elderly)
o 2/3 of DM o Lyme disease, HIV, CMV, Leprosy, Chagas
• Idiopathic (30% of cases) • Drugs/Toxins/Chemotx
o Isoniazid, Hydralazine, Lithium, Flagyl, Amit
• Post herpetic neuralgia o
riptyline, statins, retroviral, Dapsone
Taxol, Vincristine
• Mechanical o EtOH, arsenic, cyanide, Pb, Hg, thallium
o Disc compression • Immune-mediated (6.3% of OK elderly)
o Guillain-Barré
o OA [(+) in 19.9% of OK elderly] o MGUS/MM, Sjogrens, Lupus, Vasculitic
o Inflammation • Inflammatory
o Carpal tunnel (5.8% of ♀, 0.6% of ♂) o Parsonage-Turner
• GI/Malnutrition • Cancer-related
o Paraproteinemic (discovered in 10% of (-)
o Alcoholic (1/3 of Spanish alcoholics) workup cases)
o B12 (5% of OK elderly) o Paraneoplastic syndrome
o B6 • Hereditary (0.6% of OK elderly)
o Charcot Marie Tooth, Fabry’s, famillial
amyloid neuropathy, porphyria
10. Diagnosis (DynaMed)
• Highest yield (AAN level C) • Other tests
o Blood glucose o CBC, Lytes, BUN/Cr, BG, LFTs, Ca,
• A1c (26% yield*) Mag Phos
o Serum B12 with metabolities o HIV
(methymalonic acid +/- o Lyme
homocysteine) o CXR
• 2% yield* o Heavy metals, lead, coproporphyrin
o Serum protein immunofixation
electrophoresis • If (+)Family history
• 3% yield* o Initial genetic testing to consider
(AAN level A)
• If (-)diabetes (AAN level C) • CMT1A dupllication/HNPP
o Consider test for impaired glucose deletion
tolerance • Cx32 (GJB1)
o 2hr GTT (61-62% yield*) • MFN2
• 0% yield* • Specialist tests
o TSH, ESR, Folate o Autonomic testing (AAN level B)
• EMG/NCS (level 3[lacking-direct]) o Nerve biopsy (AAN level U)
o Confirmed dx in 59% • Sural nerve bx may be useful but
cause persistent pain
o Changed dx in 14% o Affected management in 60%
o Expanded dx in 18% o 33% reported increased pain
at biopsy site 6 mo later
*yield from a small study from a tertiary referral center in Utah
o Skin biopsy (AAN level C)
Arch Intern Med 2004 May 10;164(9):1021
11. Case 1
• 85 year old Caucasian male veteran who • (these are all
complains of restless legs and progressive risk factors for
trouble with balance and walking bilateral
sensory
• PMH of HLD deficits)
• Meds: statin, fibrate o 65-74 yo: 26%
o 75-84 yo: 36%
o 85+ yo: 54%
• Routine CPEX notable for: • In addition to
o Hx of DM
• Increasing BMI from 30 to 35 o B12 deficiency
• Absence of Achilles reflex and loss of fine o Rheumatoid
arthritis
touch o Absence of hx
of HTN
• Gait: normal, timed get-up-and-go is 10 o Income
seconds <$15,000
J Am Fam Pract 2004 Sep-Oct;17(5):309 n=795
12. Idiopathic
• ?age-related?
• Clinical research focusing on impaired glucose
tolerance as a culprit
o Fasting >110 & <125 or 2hr GTT >140 &<199 (75g load)
• 35-50% of pt with idiopathic sensory neuropathy
have IGT
• Painful sensory neuropathy of small caliber afferent
fibers in the lower limbs
• In early stages, DTR, muscle strength and EMG/NCS
are spared
13. Case 2
• 48 yo Italian-American male with PMH of diabetes
comes in for routine diabetes exam
o Lives in the North End and works as a bank teller; walks to work every day for
~20 min/day. His 75 yo mother cooks ―pastas and calzones‖ for him but he has
been trying to have smaller portions.
o He saw the podiatrist once last year and was told he had ―elephantiasis.‖
• Meds: metformin, ACEi, BB
• PE significant for:
o Morbid obesity (BMI 45)
o Markedly swollen 3+ non-weeping lower extremities with leathery alligator like
hyperkeratotic plaques by the heels and lower legs; unable to examine the
entire leg. Onychomycosis, Xerosis. Nails are all long and dystrophic with
discoloration and absent hair growth from the shins inferiorly. Left great toenail
bleeding
o Monofilament sensation absent bilaterally on 0/5 points detected
• Labs:
o A1c 6.5%, LDL 108, BUN/Cr 23/0.9, Albumin 3.9, Urine Alb/Cr 6,
14. Diabetes
• 2/3 of all diabetes patients have a peripheral nervous disorder
o (also includes dysautonomia, painless foot neuropathy)
o Progressive
• 5 years after diagnosis: 4%
• 20 years after dx: 15%
• Etiology (proposed pathways)
o Persistent hyperglycemia activates polyol pathway for neural accumulation of
fructose & sorbitol
o Autoimmune damage
o Endoneural vascular ischemic damage
• Intensive treatment lowers incidence by 60%
o Diabetes Control and Complications Trial (DCCT)
• a ten-year clinical study that concluded in 1993
• ANY sustained lowering of the blood glucose helps, even if the person has a
history of poor control
• follow-up study shows reduction in microvascular changes persist for at least four
years after, despite increasing blood glucose levels
o United Kingdom Prospective Diabetes Study (UKPDS)
• significantly lower prevalence of neuropathy at 9 and 15 years than patients
randomized to conventional therapy
15. Diabetes syndromes
• Painful diabetic • Diabetic neuropathic
cachexia
neuropathy o Acute onset: Severe diffuse
o 11% of insulin-treated neuropathic pain in lower
extremities
population
o Spreads to all the lower limbs/trunk
o 25% of hospital diabetic clinic and hands, typically worsening at
population night
o Small fiber distal symmetric o Severe weight loss (up to 60%!)
o Depression
polyneuropathy
o Lasts for several months and slowly
• Long-lasting/unremitting, subsides over 8-12 months
burning, shooting o Tx: aggressive insulin infusion
• often with • Painful lumbosacral
allodynia/hyperalgesia, radiculoplexus neuropathy
alteration of thermal o Acute onset: severe asymmetric
perception and autonomic deep aching pain localized
dysfunction proximally in the lower limb
• Cold/warm/painful o May have associated proximal
weakness and wasting in the same
hypesthesia area
16. Uremic neuropathy
• 80% of pt with advanced renal failure have a
sensory motor axonal polyneuropathy
• Characterized by cramps and restlessness in
legs, dysesthesia
• Concomitant DM may cause a severe motor
polyneuropathy with intense cramps
22. Case 3 pt 1
• 53 yo Caucasian male with PMH of Bipolar
disorder, EtOH abuse and seizure disorder (s/p
trigeminal neuralgia ―surgery decompression)
presents with shoulder pain
o Two years ago, he broke his arm after a seizure + fall at home with
progressively worse right neck, shoulder and arm pain
o 8/10 Burning debilitating pain radiating down the right shoulder and arm
to the elbow and encompasses the upper arm bicep/tricep
o Denies clumsiness/dropping things in the right hand
o Currently tried lidocaine patch, tylenol, tramadol and neurontin and
flexeril without relief
23. Case 3 pt 2
• CPEX:
o CN II-XII intact
o Tone: normal without cogwheeling/spasticity
o Normal 2+ reflexes in biceps/triceps/brachioradialis bilaterally
o Strength: 5/5 except right deltoid 4+/5, biceps 4+/5, due to pain
o No atrophy, no tremor
o Psych exam normal
• MRI:
o Cervical degenerative disc disease, uncoverterbral joint and facet
arthritis, post operative changes at C5-6 with an anterior fusion
o Cg-7 disc herniation and focal spinal stenosis with cord deformity
o Mild cord atrophy and myelomalacia at C6-7
24. Case 3 pt 3
• EMG/NCS:
o Motor conduction studies of both ulnar and right median nerves are
nromal. Sensory conduction studies of both ulnar and radial nervers
demonstrate very reduced amplitudes. The right ulnar latency is mildly
reduced. The right Median sensory response is moderately reduced
o Concentric needle EMG studies of the right upper extremity demonstrate
mild chronic denervative changes in the APB and FDI. The C5-7
paraspinal muscles are normal.
• Impression:
o Consistent with the presence of an axonal, predominantly
sensory, peripheral neuropathy in the upper extremities.
o There is no evidence for a right cervical radiculopathy
25. Cervical radiculopathy
• Annual incidence 83 per 100,000
o in Rochester NY (1976-1990) n=561
o Higher in men than women
o Highest in 50-54 years of age
o C6-C7 affected in 64% of cases
o Recurrence common 32% within 5 years
o Luckily, 90% had few or no symptoms at follow up
• (mild cases likely to be underrepresented)
26. Alcohol
• Spanish study of Incidence: 1/3 of alcoholics in a
hospital clinic fulfilled EP criteria
• Mainly the consequence of nutritional deficiency
o Thiamine
o B6
o B12
• Sensory motor axonal neuropathy affecting all fiber
types
• Severe burning/stabbing, associated w/
hyperalgesia/allodynia
• Sensory ataxia
27. Case 4 pt 1
• L.R. 76 yo PMH of DM, COPD, chronic back pain presents
to the ED with leg weakness, numbness and gait
instability.
• 2 months ago, she had facial numbness around her lips
with weakness with swallowing and an inability to tell if
food was inside or outside her mouth. She also had
numbness of her right hand.
• 1 month ago, she had a whole body pain. Within two
weeks, she developed numbness in her hands and feet
and had difficulty walking with weakness in both legs.
• She reports that this all started when she got ―bunch of
shots.‖
28. Case 4 pt 2
• ―Bilateral Bell’s Palsy‖ resolved with a five-day
course of steroids
• LP showed cytoalbuminologic dissociation with
protein of 90 and 0 WBCs
• EMG/NCS impression: mild chronic generalized
sensory motor polyneuropathy, axonal in nature.
• Diagnosed with Guillain-Barre and was given a
course of IVIG that improved her gait mobility
• She was not diagnosed with CIDP
• 2 years later, she is able to stand up, but still has
chronic pain in her lower legs and can only
ambulate for about 10-20 steps.
29. Guillain-Barré Syndrome (GBS)
• Epidemiology
o Annual incidence of 1-2 per 100,000 population
o 40-66% due to C. jejuni, also linked to Shigella, CMV
o Very rarely linked to vaccines (except for vaccinia old-rabies w/ myelin
and 1976 US Swine flu vaccine)
• England: n=200+ cases, imm vs nonimm, OR of 1.8 [95% CI 0.7-4.4]
• HPI
o Preceding URI or GI infection
o 85% of pts repots moderate/severe pain at onset
• S/sx:
o 1) stabbing, deep dorsal LBP radiating into the limbs
o 2) Dysesthetic extremity pain with burning/tingling
o 3) Joint/muscle pain
o Characteristic: Weakness of limb and respiratory muscles
• Mortality previously ~1/3 of pts; down to 5-10% with vent support
30. Case 5 pt 1
• RI is a 84 yo male with PMH of HTN/zoster, home visit
• A couple of years ago, he had a shingles outbreak
on his leg and the pain was so bad that he lost
nearly fifty pounds (down to 170#) and feels that
the loss of appetite was secondary to the pain.
• His kidneys were ―blocked up‖ around the same
time and was on HD for a few months and was
given a ―bladder bag‖ and has Q6 week visits at SH
for foley changes after declining suprapubic surgery
• He still has some residual pain from the zoster and
lives independently. Otherwise well, no back pain
31. Case 5 pt 2
• Old vesicular patch scar pattern on the left-medial
anterior thigh
• Large inguinal hernia easily reducible, foley draining
clear yellow urine
• Neuro exam intact. No sensory changes to light
touch or sensitivity over the zoster scar
• BUN/Cr 38/2.1, Alk phos 1301, SPEP/UPEP negative
except total protein high at 59.6
• PSA: 88.3
• MRI chest: multiple bone through the thoracic and
lumbar spine concerning for ossesous neoplastic
disease
32. VZV-Postherpetic neuralgia
• Ganglionopathy
• Acute phase
o Acute neuralgia at site of inflammation
o Lasts for several weeks
• Long-lasting neuropathic pain
o 3+ months after healing of the skin lesion
o Major or complete sensory loss
o Hyperalgesia/allodynia (light stroking or warming)
33. Cancer
Drugs
(Large fiber neuropathy)
• Paclitaxel • Paraneoplastic
o Ascending distal polyneuropathies
paraesthesiae/dysesthesia with
burning pain/allodynia to cold or • Acute sensory
mechanical stimulation ganglionopathy
o Vibration/pin/cold sensation are
o 90% of the time, it precedes other
impaired
symptoms of cancer
o Stocking-glove distribution
o Anti-Hu neuronal antibody (+)
• Cisplatin o Most commonly SCLC
o Painless ataxia o More rarely: ovarian, breast or
lymphoma
• Vincristine
o Large fiber sensory/motor • Paraproteinemic
neuropathy neuropathy
o Muscle aches o SPEP(+) in 10% of unexplained
neuropathies
34. Treatment (1)
• Opioids (level 2[mid-level])
o ―Timely and fearless use‖ for acute
ganglionopathy and plexopathy
• Tramadol
o 50-100mg Q6hr prn pain, max dose 400mg/day
o Antagonize nociceptive nerve trunk injury
• Steroids
o In cases of acute inflammatory component to nerve injury
• Capsaicin (Zostrix) 0.025% (A-1)
o Up to 3-4x/day x 4-6 weeks, apply with gloves and don’t rub eyes
o Chili pepper extract depleting substance P/VIP/CCK/somatostatin stores
• TCAs (Amitrip/Nortrip/Desip) (level 2[mid-level], A-2)
o Start at 10mg Qhs and increased up to 25mg Qhs and by 25mg increments as
tolerated
o May experience relief in 2 weeks
35. Treatment (2)
• Anticonvulsants: unknown MOA
• Gabapentin (Neurontin) (A-2)
o 300mg Qhs x2 nights, then 300mg BID x2 days, increase to 300mg TID and
additional 300mg doses as tolerated
o ADR: leukopenia, somnolence/dizziness/ataxia/fatigue
• Pregabalin (Lyrica) (A-2)
o 100mg Qhs
o Titrated over 2 weeks to max of 600mg Qhs
o ADR: somnolence/dizziness, headache, dry mouth, peripheral edem
• Botulinum toxin (Botox) (Level 2[mid-level])
• Clonazepam (no RCTs)
• Phenytoin (no RCTs)
36. CAM treatment (evidence-harm)
• 43% of pt with peripheral neuropathy use CAM
• Megavitamins (35%)
o Vitamin B complex (B-100) (B-2) one tab BID
• for deficiency syndromes
• Caution: High dose B6 (1000mg/d) can cause toxic neuropathy!
o Acetyl-L-carnitine 500 BID-1000TID (A-1)
• For chemo-induced and DM neuropathy
o Alpha-lipoic acid 600-1800 PO Daily (A-1)
o Benfotiamine-B1 50-100 TID (B-1)
• For DM neuropathy
o Vitamin E 400-800 IU Daily (B-2)
• Magnets (30%)
o Magnetic insoles (A-1)
• Acupuncture (30%) (B-1)
o Beta-endorphin release
• Herbals (22%)
o Geranium oil (Neutragen PN) topically several times a day (level 1[likely-reliable])C-1)
• Reduces neuropathic foot pain for up to 4 hours
o Evening Primrose Oil 360mg PO daily of GLA from EPO (A-1)
• Chiropractor (21%)
37. Objectives
• By the end of this session, learners will be able to:
• Develop and refine a differential diagnosis for
peripheral neuropathy
• Discuss the workup for common & typical cases
• Perform a comprehensive diabetic foot exam
o by ADA/NDEP standards
• Treat painful peripheral neuropathy
38. Take Home Points
• Think systematically
• High-yield actions:
o Drug review:
chemotx, INH, B6, Hydralazine, Metronidazole, Lithium, Amitriptyline
o Labs: fasting glucose, A1c, BUN/Cr, CBC, ESR, UA, B12 and TSH
o Order for EMG/NCS
o Refer to Neuro (if considering: autonomic eval, LP, CXR, EKG, PFT: FVC)
• By prevalence, think about:
o Diabetes (30% of cases)
o Idiopathic (30% of cases)
o Consider
• Post herpetic neuralgia, Mechanical (Disc
compression, OA, Inflammation, Carpal tunnel), Alcoholic, B12
39. References
• DynaMed: Peripheral Neuropathy (Accessed December, 2012)
• AAN/AANEM National Guideline Clearinghouse 2009 Jun1:13615
• Arch Intern Med 2004 May 10;164(9):1021
• Boulton et al. Comprehensive Foot Examination and Risk Assessment. Diabetes Care August
2008 vol. 31 no. 8 1679-1685
o http://care.diabetesjournals.org/content/31/8/1679.long
• Martyn C et al. Epidemiology of peripheral neuropathies. Neuroepidemiology. J.
Neuro/Neurosurg/Psych. 1997; 62:310-318
• Marchettini, P. et al., Painful Peripheral Neuropathies. Current Neuropharmacology. 2006. 4 175-
181.
o http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430688/pdf/CN-4-3-175.pdf
• Mold J et al. Prevalence, Predictors and Consequences of Peripheral Sensory Neuropathy in
Older Patients. JABFP Sept-Oct 2004. 17;5: 309-318
• PONCELET, AN. An Algorithm for the Evaluation of Peripheral Neuropathy. Am Fam Physician.
1998 Feb 15;57(4):755-764.
o http://www.aafp.org/afp/1998/0215/p755.html
• Schaumberg H., et al. Sensory Neuropathy from Pyridoxine Abuse — A New Megavitamin
Syndrome. N Engl J Med 1983; 309:445–8.
o http://www.nejm.org/doi/pdf/10.1056/NEJM198308253090801
• Rakel. Integrative Medicine. 2nd edition. Chapter 15: Peripheral Neuropathy pp 157-168
• Feet Can Last a Lifetime – A Health Care Provider’s Guide to Preventing Diabetes Foot Problems
o http://ndep.nih.gov/publications/PublicationDetail.aspx?PubId=116
o http://ndep.nih.gov/media/FootExamForm.pdf
40. Questions?
• Please comment on:
• 1. What was the most important thing you learned
today?
• 2. What question remains uppermost in your mind
afterward?
• 3. What is the muddiest point in today's lecture?