DOCSLIB.ORG

General Approach to Peripheral Nerve Disorders

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
General Approach to Peripheral Nerve Disorders Review Article Address correspondence to Dr James A. Russell, General Approach to Lahey Hospital and Medical Center, Department of Neurology, 41 Mall Rd, Peripheral Nerve Burlington, MA 01805, [email protected]. Relationship Disclosure: Disorders Dr Russell has served as a consultant for W2O Group, receives publishing royalties James A. Russell, DO, FAAN from McGraw-Hill Education, and has received personal compensation for medicolegal ABSTRACT record review. Unlabeled Use of Purpose of Review: This article provides a conceptual framework for the Products/Investigational evaluation of patients with suspected polyneuropathy to enhance the clinician’s Use Disclosure: ability to localize and confirm peripheral nervous system pathology and, when Dr Russell reports no disclosure. possible, identify an etiologic diagnosis through use of rational clinical and judicious * 2017 American Academy testing strategies. of Neurology. Recent Findings: Although these strategies are largely time-honored, recent insights pertaining to the pathophysiology of certain immune-mediated neuropa- thies and to evolving genetic testing strategies may modify the way that select causes of neuropathy are conceptualized, evaluated, and managed. Summary: The strategies suggested in this article are intended to facilitate accurate bedside diagnosis in patients with suspected polyneuropathy and allow efficient and judicious use of supplementary testing and application of rational treatment when indicated. Continuum (Minneap Minn) 2017;23(5):1241–1262. INTRODUCTION incidence and prevalence of neuropathy Peripheral neuropathy is a very com- in general, and chronic idiopathic axonal mon problem in neurology practice. neuropathy in particular, increase with Estimates of its incidence and preva- age.1,3 The prevalence of probable or lence are variable, undoubtedly based definite polyneuropathy in those who on the population studied, the defini- are older than 80 years of age was tion of neuropathy used, and the estimated to exceed 30% in one large intensity of the evaluation employed.1Y6 population study.3 In the Netherlands, neuropathy inci- Lack of consensus in diagnostic dence in an adult population approxi- criteria and variable terminology add mates 77 per 100,000 person-years.1 to uncertainty regarding the epide- Also in the Netherlands, the prevalence miology of peripheral neuropathy,8 of definite neuropathy is estimated at and variable opinions exist regarding 5.5%, and the prevalence of probable the role of electrodiagnosis in neu- and definite neuropathy combined is ropathy determination.6,9 However, it estimated at 13.1%, but these are likely is generally accepted that the minimal underestimated.3 Sensory loss in the standards for diagnosing neuropathy feet often goes unrecognized, particu- include at least two of the follow- larly in those with diabetes mellitus or ing features: distal symmetric sensory Supplemental digital content: who are elderly; only 10% to 15% of symptoms, distal symmetric sen- Direct URL citations appear in the printed text and are included patients with diabetes mellitus reported sory loss, and diminished or absent in the HTML, PDF, and app 1,7 6 to be aware of their neuropathy. The ankle reflexes. The commonly used versions of this article. Continuum (Minneap Minn) 2017;23(5):1241–1262 ContinuumJournal.com 1241 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. Approach to Peripheral Nerve Disorders KEY POINTS h Peripheral neuropathy is designations of distal symmetric inflammatory demyelinating poly- a common neurologic polyneuropathy, chronic axonal poly- radiculoneuropathy [CIDP], the neu- problem, affecting neuropathy, or chronic idiopathic ropathy of monoclonal gammopathy 12 approximately 5% of axonal polyneuropathy, which have of undetermined significance). adults and as many as subtle conceptual differences, are gen- Patients should be informed that 30% of patients who erally used synonymously. good treatment options do not neces- are elderly. The etiologies of peripheral neu- sarily follow from a diagnosis, such as h Although they have ropathy are legion, exceeding 200 hereditary neuropathy, estimated to 2 minor conceptual depending on the classification system include as many as one-third of cases. differences, used.2,5,9 Identification and assign- However, informed diagnostic pursuit distal symmetric ment of an etiology are influenced by provides the opportunity for diag- polyneuropathy, chronic variables that include the population nostic closure, education regarding axonal polyneuropathy, studied, the nature and intensity of the disorder’s natural history, and and chronic idiopathic the evaluation, and the willingness to counseling germane to the preven- axonal polyneuropathy assign causation to a laboratory abnor- tion and management of potential may be considered Y mality that may be coincidental.1 3,7,10 future morbidity. In the case of distal as essentially synonymous terms. One study reporting a 58% prevalence sensory polyneuropathy, the patient of test abnormalities in patients with can be reassured that progression h Although the primary peripheral neuropathy considered only to nonambulation or amputation is goal in the evaluation 9% of these abnormalities to be diag- uncommon.7,13 of a patient with 11 peripheral neuropathy nostically significant. To be confi- ANATOMIC, PHYSIOLOGIC, is to identify the cause dent of a causal relationship between whenever possible, a a test abnormality and peripheral AND PATHOPHYSIOLOGIC common category of neuropathy, the clinician should con- CONSIDERATIONS IN polyneuropathy is sider the neuropathy pattern and the PERIPHERAL NEUROPATHY chronic idiopathic contextual features in each case, Understanding peripheral nerve anat- axonal polyneuropathy, allowing generation of a relevant dif- omy and physiology is required for which may represent ferential diagnosis aligned with these adequate clinical assessment and close to a half of features. Judicious testing in the proper electrodiagnostic study design. Under- patients with neuropathy clinical context reduces the risk of false- standing the pathophysiology of the in some populations. positive testing. disorder allows for rational therapeu- h Accurate diagnosis of As with any diagnostic assessment, tic strategy and prognostication. In polyneuropathy directs the patient should be advised of the view of their unique anatomic and treatment in a limited risks and benefits involved in the physiologic properties, peripheral number of cases but diagnostic workup. Ideally, a treatable nerves are vulnerable to multiple also provides the benefit disorder is identified; however, diag- potential insults.14 of diagnostic closure, opportunities for nosis may be elusive. Following eval- Axonal Polyneuropathies education regarding the uation, 20% to 50% of patients are natural history of the designated as chronic idiopathic axo- The viability of peripheral nerves disease, and a means nal polyneuropathy or chronic axonal depends on the metabolic capabilities 1,3,4,7,11 by which to prevent polyneuropathy. Although a of anterior horn cells and dorsal root and address potential 2016 study reported that a diagnosis ganglia and effective axon transport. future morbidities. could be achieved in two-thirds of The latter is bidirectional and essential 284 patients with chronic idiopathic for axonal nutrition and support for axonal neuropathy when reevaluated, the normal turnover of organelles over half of these individuals were (particularly mitochondria) and pro- assigned a diagnosis that should have teins (such as microtubules and been apparent on initial evaluation neurofilaments).15 Anterograde trans- (eg, diabetic neuropathy, chronic port from cell body to neuromuscular 1242 ContinuumJournal.com October 2017 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. KEY POINT junction along axons is dependent on myelin sheath. Peripheral nerve myelin h Disordered axonal the kinesin family of molecular mo- of Schwann cell origin is compacted transport is thought tors; retrograde transport depends on along the internode, noncompacted at to be the mechanism the dynein/dynactin complex. Animal the paranode (allowing for increased underlying the models using nerve toxins have surface area of potential pathogenic pathophysiology of shown disruption of critical axon significance), and absent at the nodes most toxic and transport proteins resulting in distal of Ranvier (where ion channels are metabolic neuropathies axonal degeneration. This can be read- concentrated). Predominantly demye- and some hereditary ily extrapolated to the pathophysio- linating peripheral neuropathies neuropathies. logic basis for toxic or metabolic affecting myelin or Schwann cells length-dependent neuropathies in may be either acquired or heritable humans.1,16Y20 The same neuropathy (Table 1-1).19,22,23 Demyelinating neu- pattern can be also be attributable to ropathies impair nerve conduction gene mutations involved in cell migra- by allowing current leakage through tion, anterograde and retrograde trans- exposed axons where a paucity of ion port, folding of cytoskeletal proteins, channels exists, thus impeding action and neurofilament organization.19,21 potential propagation.24 Acquired demyelinating neuropa- Demyelinating thies are thought to be immune Polyneuropathies mediated through either cellular or Optimal peripheral nerve function is humoral mechanisms. Antigenic targets
Load more

Recommended publications
  • Neuropathy, Radiculopathy & Myelopathy
    Neuropathy, Radiculopathy & Myelopathy Jean D. Francois, MD Neurology & Neurophysiology Purpose and Objectives PURPOSE Avoid Confusing Certain Key Neurologic Concepts OBJECTIVES • Objective 1: Define & Identify certain types of Neuropathies • Objective 2: Define & Identify Radiculopathy & its causes • Objective 3: Define & Identify Myelopathy FINANCIAL NONE DISCLOSURE Basics What is Neuropathy? • The term 'neuropathy' is used to describe a problem with the nerves, usually the 'peripheral nerves' as opposed to the 'central nervous system' (the brain and spinal cord). It refers to Peripheral neuropathy • It covers a wide area and many nerves, but the problem it causes depends on the type of nerves that are affected: • Sensory nerves (the nerves that control sensation>skin) causing cause tingling, pain, numbness, or weakness in the feet and hands • Motor nerves (the nerves that allow power and movement>muscles) causing weakness in the feet and hands • Autonomic nerves (the nerves that control the systems of the body eg gut, bladder>internal organs) causing changes in the heart rate and blood pressure or sweating • It May produce Numbness, tingling,(loss of sensation) along with weakness. It can also cause pain. • It can affect a single nerve (mononeuropathy) or multiple nerves (polyneuropathy) Neuropathy • Symptoms usually start in the longest nerves in the body: Feet & later on the hands (“Stocking-glove” pattern) • Symptoms usually spread slowly and evenly up the legs and arms. Other body parts may also be affected. • Peripheral Neuropathy can affect people of any age. But mostly people over age 55 • CAUSES: Neuropathy has a variety of forms and causes. (an injury systemic illness, an infection, an inherited disorder) some of the causes are still unknown.
    [Show full text]
  • Hereditary Spastic Paraparesis: a Review of New Developments
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.69.2.150 on 1 August 2000. Downloaded from 150 J Neurol Neurosurg Psychiatry 2000;69:150–160 REVIEW Hereditary spastic paraparesis: a review of new developments CJ McDermott, K White, K Bushby, PJ Shaw Hereditary spastic paraparesis (HSP) or the reditary spastic paraparesis will no doubt Strümpell-Lorrain syndrome is the name given provide a more useful and relevant classifi- to a heterogeneous group of inherited disorders cation. in which the main clinical feature is progressive lower limb spasticity. Before the advent of Epidemiology molecular genetic studies into these disorders, The prevalence of HSP varies in diVerent several classifications had been proposed, studies. Such variation is probably due to a based on the mode of inheritance, the age of combination of diVering diagnostic criteria, onset of symptoms, and the presence or other- variable epidemiological methodology, and wise of additional clinical features. Families geographical factors. Some studies in which with autosomal dominant, autosomal recessive, similar criteria and methods were employed and X-linked inheritance have been described. found the prevalance of HSP/100 000 to be 2.7 in Molise Italy, 4.3 in Valle d’Aosta Italy, and 10–12 Historical aspects 2.0 in Portugal. These studies employed the In 1880 Strümpell published what is consid- diagnostic criteria suggested by Harding and ered to be the first clear description of HSP.He utilised all health institutions and various reported a family in which two brothers were health care professionals in ascertaining cases aVected by spastic paraplegia. The father was from the specific region.
    [Show full text]
  • Hereditary Spastic Paraplegia
    8 Hereditary Spastic Paraplegia Notes and questions Hereditary Spastic Paraplegia What is Hereditary Spastic Paraplegia? Hereditary Spastic Paraplegia (HSP) is a medical term for a condition that affects muscle function. The terms spastic and paraplegia comes from several words in Greek: • ‘spastic’ means afflicted with spasms (an alteration in muscle tone that results in affected movements) • ‘paraplegia’ meaning an impairment in motor or sensory function of the lower extremities (from the hips down) What are the signs and symptoms of HSP? Muscular spasticity • Individuals with HSP commonly will have lower extremity weakness, spasticity, and muscle stiffness. • This can cause difficulty with walking or a “scissoring” gait. We are grateful to an anonymous donor for making a kind and Other common signs or symptoms include: generous donation to the Neuromuscular and Neurometabolic Centre. • urinary urgency • overactive or over responsive “brisk” reflexes © Hamilton Health Sciences, 2019 PD 9983 – 01/2019 Dpc/pted/HereditarySpasticParaplegia-trh.docx dt/January 15, 2019 ____________________________________________________________________________ 2 7 Hereditary Spastic Paraplegia Hereditary Spastic Paraplegia HSP is usually a chronic or life-long disease that affects If you have any questions about DM1, please speak with your people in different ways. doctor, genetic counsellor, or nurse at the Neuromuscular and Neurometabolic Centre. HSP can be classified as either “Uncomplicated HSP” or “Complicated HSP”. Notes and questions Types of Hereditary Spastic Paraplegia 1. Uncomplicated HSP: • Individuals often experience difficulty walking as the first symptom. • Onset of symptoms can begin at any age, from early childhood through late adulthood. • Symptoms may be non-progressive, or they may worsen slowly over many years.
    [Show full text]
  • Peripheral Neuropathy
    Peripheral Neuropathy U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health Peripheral Neuropathy What is peripheral neuropathy? n estimated 20 million people in A the United States have some form of peripheral neuropathy, a condition that develops as a result of damage to the peripheral nervous system — the vast communications network that transmits information between the central nervous system (the brain and spinal cord) and every other part of the body. (Neuropathy means nerve disease or damage.) Symptoms can range from numbness or tingling, to pricking sensations (paresthesia), or muscle weakness. Areas of the body may become abnormally sensitive leading to an exaggeratedly intense or distorted experience of touch (allodynia). In such cases, pain may occur in response to a stimulus that does not normally provoke pain. Severe symptoms may include burning pain (especially at night), muscle wasting, paralysis, or organ or gland dysfunction. Damage to nerves that supply internal organs may impair digestion, sweating, sexual function, and urination. In the most extreme cases, breathing may become difficult, or organ failure may occur. Peripheral nerves send sensory information back to the brain and spinal cord, such as a message that the feet are cold. Peripheral 1 nerves also carry signals from the brain and spinal cord to the muscles to generate movement. Damage to the peripheral nervous system interferes with these vital connections. Like static on a telephone line, peripheral neuropathy distorts and sometimes interrupts messages between the brain and spinal cord and the rest of the body. Peripheral neuropathies can present in a variety of forms and follow different patterns.
    [Show full text]
  • Small Fiber Neuropathy in Patients Meeting Diagnostic Criteria For
    olog eur ica N l D f i o s l o a r n d r e u r s o J Levine, et al., J Neurol Disord 2016, 4:7 Journal of Neurological Disorders DOI: 10.4172/2329-6895.1000305 ISSN: 2329-6895 Research Article Open Access Small Fiber Neuropathy in Patients Meeting Diagnostic Criteria for Fibromyalgia Todd D Levine1*, David S Saperstein1, Aidan Levine1, Kevin Hackshaw2 and Victoria Lawson2 1Phoenix Neurological Associates, 5090 N, 40th Street, Suite 250, Phoenix, AZ 85018, USA 2Division of Neuromuscular Diseases, Department of Neurology, The Ohio State Wexner Medical Center, 395 W. 12th Ave, 7th Floor, Columbus, OH 43210, USA *Corresponding author: Todd D Levine, Phoenix Neurological Associates, LTD. 5090 N 40th Street, Suite # 250, Phoenix, AZ 85018, USA, Tel: 6022583354; Fax: 6022583368; E-mail: [email protected] Rec date: Sep 21, 2016; Acc date: Oct 06, 2016; Pub date: Oct 11, 2016 Copyright: © 2016 Levine TD. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Introduction: The cause for fibromyalgia (FM) is unknown and diagnostic criteria can be nonspecific. Many patients with FM have nonspecific sensory symptoms consistent with a neuropathic process. Previous studies have shown that a significant percentage of patients diagnosed with FM have small fiber neuropathy (SFN) based on decreased intraepidermal nerve fiber density (IENFD) on according to punch skin biopsy testing. The purpose of this study was to demonstrate that punch skin biopsy testing is an effective way to identify SFN and its underlying causes in patients previously diagnosed with FM.
    [Show full text]
  • Pharmacologic Management of Chronic Neuropathic Pain Review of the Canadian Pain Society Consensus Statement
    Clinical Review Pharmacologic management of chronic neuropathic pain Review of the Canadian Pain Society consensus statement Alex Mu MD FRCPC Erica Weinberg MD Dwight E. Moulin MD PhD Hance Clarke MD PhD FRCPC Abstract Objective To provide family physicians with EDITOR’S KEY POINTS a practical clinical summary of the Canadian • Gabapentinoids and tricyclic antidepressants play an important role in Pain Society (CPS) revised consensus first-line management of neuropathic pain (NeP). Evidence published statement on the pharmacologic management since the 2007 Canadian Pain Society consensus statement on treatment of neuropathic pain. of NeP shows that serotonin-norepinephrine reuptake inhibitors should now also be among the first-line agents. Quality of evidence A multidisciplinary • Tramadol and opioids are considered second-line treatments owing to their interest group within the CPS conducted a increased complexity of follow-up and monitoring, plus their potential for systematic review of the literature on the adverse side effects, medical complications, and abuse. Cannabinoids are current treatments of neuropathic pain in currently recommended as third-line agents, as sufficient-quality studies are drafting the revised consensus statement. currently lacking. Recommended fourth-line treatments include methadone, anticonvulsants with lesser evidence of efficacy (eg, lamotrigine, lacosamide), tapentadol, and botulinum toxin. There is some support for analgesic Main message Gabapentinoids, tricyclic combinations in selected NeP conditions. antidepressants, and serotonin-norepinephrine reuptake inhibitors are the first-line agents • Many of these pharmacologic treatments are off-label for pain or for treating neuropathic pain. Tramadol and on-label for specific pain conditions, and these issues should be clearly other opioids are recommended as second- conveyed and documented.
    [Show full text]
  • Peripheral Neuropathy Is a Common Neurological Disorder Resulting from Damage/Degeneration of the Peripheral Nerves (I.E
    What is Peripheral Neuropathy? Peripheral Neuropathy is a common neurological disorder resulting from damage/degeneration of the peripheral nerves (i.e. the nerves that leave the spinal cord and brain and travel to the limbs, trunk, and organs). Neuropathy can affect one (mononeuropathy) or multiple (polyneuropathy) nerves. It may be caused by diseases of the nerves or as the result of systemic illnesses. Many neuropathies have well-defined causes such as diabetes, uremia/kidney disease, AIDS, thyroid disease, or nutritional deficiencies. In fact, diabetes is one of the most common causes of peripheral neuropathy. Some neuropathies are hereditary while others can result from exposure to toxins such as heavy metals, drugs, or alcohol. Other forms of neuropathy can result from direct pressure on nerves due to entrapment, trauma, penetrating injuries, contusions, fracture, or dislocated bones. Pressure involving the superficial nerves can result from prolonged use of crutches or staying in one position for too long. Pressure from a tumor can occasionally cause loss of function in a nerve. One common example of entrapment neuropathy is carpal tunnel syndrome. Although the causes of peripheral neuropathy are diverse, they produce common symptoms including weakness, numbness, paresthesias (abnormal sensations such as burning, pins/needles sensations, or tingling) and pain in the arms, hands, legs and/or feet. The most common form of neuropathy tends to involve the toes, feet, and/or lower legs and usually is symmetrical. About 85% of “garden-variety” neuropathies have no specific identifiable (i.e. reversible) cause. However, 15% of cases have an identifiable cause. It is these cases which can be treated, halted, or reversed.
    [Show full text]
  • Distinguishing Radiculopathies from Mononeuropathies
    CURRICULUM, INSTRUCTION, AND PEDAGOGY published: 13 July 2016 doi: 10.3389/fneur.2016.00111 Distinguishing Radiculopathies from mononeuropathies Jennifer Robblee and Hans Katzberg* Division of Neurology, University Health Network (UHN), University of Toronto, Toronto, ON, Canada Identifying “where is the lesion” is particularly important in the approach to the patient with focal dysfunction where a peripheral localization is suspected. This article outlines a methodical approach to the neuromuscular patient in distinguishing focal neuropathies versus radiculopathies, both of which are common presentations to the neurology clinic. This approach begins with evaluation of the sensory examination to determine whether there are irritative or negative sensory signs in a peripheral nerve or dermatomal distri- bution. This is followed by evaluation of deep tendon reflexes to evaluate if differential hyporeflexia can assist in the two localizations. Finally, identification of weak muscle groups unique to a nerve or myotomal pattern in the proximal and distal extremities can most reliably assist in a precise localization. The article concludes with an application of the described method to the common scenario of distinguishing radial neuropathy versus C7 radiculopathy in the setting of a wrist drop and provides additional examples for self-evaluation and reference. Edited by: Keywords: radiculopathy, focal neuropathy, mononeuropathy, neuromuscular, nerve root Adolfo Ramirez-Zamora, Albany Medical College, USA Reviewed by: INTRODUCTION Ignacio Jose Previgliano, Maimonides University Although nerve conduction studies (NCS) and electromyography (EMG) are standard tests in the School of Medicine, Argentina evaluation of focal peripheral neuropathies (1), newer techniques, including peripheral nerve ultra- Robert Jerome Frysztak, sound and MRI neurography, have started to gain acceptance (2).
    [Show full text]
  • Neuropathic Pain a Management Update Milana Votrubec Ian Thong
    Pain Neuropathic pain A management update Milana Votrubec Ian Thong Background Neuropathic pain is defined as ‘pain arising as a Neuropathic pain is described as burning, painful, cold or direct consequence of a lesion or disease affecting the electric shocks and may be associated with tingling, pins and somatosensory system’.1 This article will focus on the needles, numbness or itching. detection and management of diabetic polyneuropathy, Objective postherpetic neuralgia, trigeminal neuralgia and chronic This article summaries the diagnosis and management of four regional pain syndrome (CRPS). Importantly, disc disease common neuropathic pain presentations. and trauma can cause neuropathic pain, however these are Discussion beyond the scope of this article. A validated diagnostic screening tool can help identify patients with neuropathic pain. A systematic approach to A high index of suspicion is required for the diagnosis of neuropathic clinical assessment and investigation will clarify the diagnosis. pain as it can develop slowly over time. If neuropathic pain is suspected, Good glycaemic control is important in the prevention and a validated diagnostic screening tool such as the Leeds Assessment of management of diabetic polyneuropathy; management options Neuropathic Symptoms and Signs (LANSS), the Self reported LANSS include antidepressants, gabapentinoids and controlled release (S-LANSS), the Neuropathic Pain Questionnaire (NPQ), the Douleur opioids. Pain that lasts for more than 3 months after the onset Neuropathique en 4 (DN 4)
    [Show full text]
  • The Voice of the Patient: Neuropathic Pain Associated with Peripheral
    The Voice of the Patient A series of reports from the U.S. Food and Drug Administration’s (FDA’s) Patient-Focused Drug Development Initiative Neuropathic Pain Associated with Peripheral Neuropathy Public Meeting: June 10, 2016 Report Date: February 2017 Center for Drug Evaluation and Research (CDER) U.S. Food and Drug Administration (FDA) Table of Contents Introduction .............................................................................................................................. 3 Meeting overview ......................................................................................................................................... 3 Report overview and key themes ................................................................................................................. 4 Topic 1: Disease Symptoms and Daily Impacts That Matter Most to Patients .............................. 5 Perspectives on most significant symptoms ................................................................................................. 6 Overall impact of neuropathic pain associated with peripheral neuropathy on daily life ........................... 8 Topic 2: Patient Perspectives on Treatments for Neuropathic Pain Associated with Peripheral Neuropathy ............................................................................................................................... 9 Perspectives on current treatments ............................................................................................................. 9 Perspectives
    [Show full text]
  • Use of Methadone for the Treatment of Diabetic Neuropathy
    Reviews/Commentaries/ADA Statements COMMENTARY Use of Methadone for the Treatment of Diabetic Neuropathy LEWIS HAYS, MD, MPH MICHELLE DORAN, APRN, BC-PCM property, methadone, in theory, appears COLEEN REID, MD KARYN GEARY, APRN, BC-PCM to be the ideal opioid for neuropathic pain and may account for the demonstration that the need for opioid escalation was significantly less in patients treated for pain with methadone than in those Editor’s comment: This is the second Commentary of those that will appear from time to time describing treated with morphine (7,9). treatments that may not have been validated by appropriate clinical trials but seem to be effective in 2). Inhibition of the reuptake of nor- diabetic patients based on small studies and/or extensive clinical experience. This one describes effective epinephrine and serotonin. Facilitates im- opioid treatment for those diabetic patients failing nonopioid therapies for painful neuropathy. proved analgesia in neuropathic pain. Diabetes Care 28:485–487, 2005 Tricyclic antidepressants have traditionally been used to accomplish this task (2,10). 3). Trimodal metabolism/excretion. Metabolism in the liver via the cyto- ethadone, a schedule II opioid, to be more opioid responsive than those chrome P-450 system, fecal, and, to a was developed in Germany in the with pain from central nervous system le- lesser extent, renal excretion (other opi- M 1940s as a spasmolytic and was sions (5). Of the more than 2 million oids are excreted renally) (1). not used as an analgesic agent until many Americans affected by chronic neuro- 4). No active metabolites. This de- years later.
    [Show full text]
  • Peripheral Neuropathies by Dr.Mohammad Al Nazy
    Peripheral Neuropathies by Dr.Mohammad Al nazy Done by: Faisal Alzahrani Revised by: Sarah Almubrik & Mohanad Alsuhaim Special Thanks to: Malak alqahtani Objectives: ● Weren’t given References: Optional: Slides - Black “Team 433” Doctor’s notes - Red Step up / davidson - Blue Extra explanation - Grey 1 Editing file Chapter 5 Anatomy ● Peripheral Nervous System: There are two types of cells in the peripheral nervous system. These cells carry information to (sensory nervous cells) and from (motor nervous cells) the central nervous system (CNS). Cells of the sensory nervous system send information to the CNS from internal organs or from external stimuli. Motor nervous system cells carry information from the CNS to organs, muscles, and glands. The motor nervous system is divided into the somatic nervous system and the autonomic nervous system. The somatic nervous system controls skeletal muscle as well as external sensory organs such as the skin. This system is said to be voluntary because the responses can be controlled consciously. Reflex reactions of skeletal muscle however are an exception. These are involuntary reactions to external stimuli. The autonomic nervous system controls involuntary muscles, such as smooth and cardiac muscle. This system is also called the involuntary nervous system. The autonomic nervous system can further be divided into the parasympathetic and sympathetic divisions. 2 Motor Starts as the axons of anterior horn cells (in the spinal Pathway cord) come out through the ventral root. It’s divided into somatic and autonomic nervous system) Sensory Starts from periphery where sensory cells receive stimuli Pathway and send it to the CNS. It enters the spinal cord through the dorsal root (passing through dorsal root ganglia) ❖ Sensory tracts Dorsal Column (Gracile (inferior to t6) & Cuneate Fasciculi (superior to t6)) 1.
    [Show full text]