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Diagnosing and Managing Peripheral Neuropathy

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Diagnosing and Managing Peripheral Neuropathy DIAGNOSING AND MANAGING PERIPHERAL NEUROPATHY By Rebecca Storment Garcia A manuscript submitted in partial fulfillment of The requirements for the degree of Master of Nursing Washington State University College of Nursing May 2003 11 To the Faculty of Washington State University: The members ofthe committee appointed to examine the dissertation/thesis of REBECCA STORMENT GARCIA find it satisfactory and recommend that it be accepted. Chair iii DIAGNOSING AND MANAGING PERIPHERAL NEUROPATHY Abstract By Rebecca Storment Garcia, Washington State University May 2003 Chair: Lorna Schumann The successful management of neuropathic pain is measured by the degree of relief and functional improvement experienced by the patient. Neuropathy can be divided into two major types: focal mononeuritis and diffuse polyneuropathy. Symptoms of neuropathy present in many different ways depending on the types of nerve fibers affected. Large nerve fiber neuropathies present with symptoms such as weakness, muscle wasting, deficits in proprioception, deep tendon reflexes and vibratory sense. Small nerve fiber neuropathies present with alterations to heat, cold and pain sensations. Neuropathic pain has been described as intolerable burning, crushing, searing, stabbing, stinging, pins and needles, aching, and electrical shocks. Peripheral neuropathy has a variety of causes such as entrapment, ischemia, hereditary disorders, systemic and metabolic disease, vitamin deficiency, and toxic exposure making an accurate diagnosis difficult. Therefore, a thorough detailed medical history combined with a physical and neurologic exam is the first step in reaching a definitive diagnosis leading to the effective management of neuropathic pain. IV TABLE OF CONTENTS Page SIGNATURE PAGE ii ABSTRACT iii LIST OF TABLES vi DEDICATION vii MANUSCRIPT Epidemiology 1 Pain theories 2 Neuropathic pain 4 Types of pain 5 Stages of neuropathy 5 Types of peripheral neuropathy 6 Ischemic neuropathies 6 Entrapment neuropathies 7 Diffuse polyneuropathies 8 Hereditary neuropathies 9 Neuropathy associated with systemic and metabolic disorders 10 Nutritional deficiencies 11 Toxic disorders 13 Idiopathic inflammatory polyneuropathy 13 Infection 14 Diagnosis 16 v Treatment options 19 Research 24 Ineffective Treatments 25 Summary 26 vi LIST OF TABLES Page 1. Various causes of peripheral neuropathy 29 2. Examples of Small and Large Nerve Fiber Function 30 3. Treatment Options for Dysthesia, Paresthesia, and Muscular Pain 31 4. Differentiate between Mononeuritis and Entrapment 32 5. Toxic Neuropathies: Clinical & Pathological Features 33 6. Occupations leading to Neuromuscular Disorders 34 7. Treatment options for Distal symmetrical Polyneuropathy 35 vii Dedication This paper is dedicated to my husband, Jose, and children, Joseph and Gabriel, with heartfelt gratitude for their support and forbearance during this endeavor. I would also like to thank Theresa, Libby and Francisco for their patience and support. 1 The successful management of neuropathic pain is measured by the degree of relief and functional improvement experienced by the patient. Successful management is achieved by first obtaining an accurate diagnosis, which may be difficult since neuropathic pain encompasses a diverse number of syndron1es. The first step to reaching a definitive diagnosis is to obtain a detailed medical history combined with a physical and neurologic exam (Talarico, Sudarshan, Marcus & Caudill, 1998). Epidemiology Approximately 1% of the population, or 2.5 million people in the United States suffer from moderate to severe neuropathic pain. More than 15 different mechanisms causing neuropathic pain have been identified by research. There are more than 30 drugs that are currently being developed for the treatment of neuropathic pain. (Novel compounds to drive the neuropathic pain market, 2003). "Neuropathic Pain", a report from Enhanced Perspective Publications, states that the current U.S. neuropathic pain market is worth an estimated 430 million dollars. The United States Food and Drug Administration has approved more products, some completely new in the treatment of neuropathic pain, are expected on the market by the end of 2003. It is predicted that the neuropathic pain market will double to $800 million by 2007 (Novel compounds to drive the neuropathic pain market, 2003). There are numerous causes of neuropathic pain. Toxic substances, various drugs, and many infectious diseases can cause neuropathy (Mosby, 1998). Other causes of neuropathic pain are infiltrating surgery, ischemia (thalamic syndrome) radiotherapy, chemotherapy, endocrine disorders, and vitamin deficiencies (Sykes, Johnson, & Hanks, 1997). Refer to Table 1 for various causes of peripheral neuropathy. 2 Pain Theories In the 16th century, a French philosopher and mathematician, Rene Descartes, proposed one of the earlier pain theories. He theorized that the intensity of pain is directly related to the amount of associated tissue injury. The Specificity Theory is generally accurate when applied to certain types of injuries such as a pinprick or cutting one's hand with a knife. However, during World War II, Beecher observed that one out of three soldiers wounded in combat required morphine. Upon returning to his practice after the war, Beecher noted that trauma patients with similar injuries required different amounts of morphine for pain from their wounds. He believed that the meaning attached to the injuries in the two groups explained the different levels of pain; for the soldier it meant going home, for the civilian patient it meant loss of income, activities and other negative consequences. Patients following limb amputation experience phantom pain. The patient may report sensations as though the limb is still there. The Specificity Theory does not account for pain experience when there is no ongoing tissue injury (Modem theories of chronic pain, 2003). The Gate Control theory proposes that "gates" located on nerve fibers in the spinal cord, between the peripheral nerves and the brain, control the flow of pain messages from the peripheral nerves to the brain. Factors that determine how the spinal nerve gates will manage the pain signal are intensity of the pain message, and competition from other incoming nerve messages (touch, vibration, heat, etc). Signals from the brain also tell the spinal cord to increase or decrease the priority of the pain signal. The message can be handled in the following ways, depending on how the gate processes the signal: allowed to 3 pass directly to the brain; altered prior to being forwarded to the brain; or prevented from reaching the brain (Modem theories of chronic pain, 2003). Endorphins produced by the brain stem, which acts as a morphine-like substances, can inhibit or blunt incoming pain signals. Vigorous exercise, stress and excitement may stimulate the production of endorphins. The inhibition of pain signals is why athletes may not notice pain of a fairly serious injury until after the competition is over or why exercise helps control chronic back pain (Modem theories of chronic pain, 2003). Stress and anxiety can amplify pain signals at the nerve gate as it moves up the spinal cord. Impulses from the brain can "close" the nerve gate, preventing the signal from reaching the brain. Events and conditions can cause pain gates to open, causing more suffering. Sensory factors that include injury, inactivity, long-term narcotic use, poor body mechanics, and poor pacing of activities intensify pain. Cognitive factors, such as focusing on the pain, having no outside interests or distractions, worrying about the pain, and other negative thoughts open pain gates intensifying pain. Factors such as depression, anger, anxiety, stress, frustration, hopelessness and helplessness also add to the pain level. Sensory factors, such as increasing activities, short-term use of pain medications, relaxation training and meditation can close the pain gates. Cognitive factors including outside interest, distraction and thoughts that help a patient cope, can close the pain gates. Having a positive attitude, overcoming depression, taking control of one's pain, and stress management can reduce suffering (Modem theories of chronic pain, 2003). 4 Neuropathic Pain Symptoms of neuropathy present in many different ways depending on the types of nerve fibers affected. An accurate diagnosis is made difficult, when more than one fiber type is involved. Large-fiber nerves are myelinated transmitting impulses quickly. Neuropathies present with symptoms such as weakness, muscle wasting, and deficits in proprioception, deep tendon reflexes and vibratory sense. When A-delta fibers are affected the patient will experience deep-seated pain, numbness, and impaired cold perception (Vinik, 2000). C fibers are unmyelinated nerves that transmit impulses more slowly. When C fibers are affected, spontaneous pain (often described as burning sensation), allodynia (nonpainful stimuli interpreted as painful), and hyperalgesia (minimally painful stimuli interpreted as excruciatingly painful) occur. Pain is poorly localized with a dull ache that lingers after the initial pain (Banasik, 2000, p. 1082). Decreased sensitivity to light touch, pinprick and heat are symptoms that follow with C fiber impairment. Snlall-fiber neuropathies usually precede large-nerve-fiber damage and are manifested initially in the lower peripheral nerves. Small-nerve fibers of the autonomic nervous system can be affected causing delayed gastric emptying, orthostatic hypotension,
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