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Neuromuscular Disorders 101: Living with Peripheral Neuropathy

Foreword


Neuromuscular disorders cause major changes in an individual's daily function and independence. Its broad term encompasses a large variety of diseases with different presentations. As healthcare evolves, so does clinical research updating disease diagnostic criteria and treatment options for neuromuscular disorders. This series will discuss neuromuscular disorders from a health science point of view concerning etiology, pathophysiology, and treatment of neuromuscular disorders. The series will also discuss in depth the types of disorders and their etiology, diagnosis criteria, and medical rehabilitation management.


The series is divided into the following eight chapters:

  1. Neuromuscular Disorders 101: Living with Peripheral Neuropathy

  2. Neuromuscular Disorders 101: The Progression of Muscular Dystrophy

  3. Neuromuscular Disorders 101: The Effects of Amyotrophic Lateral Sclerosis

  4. Neuromuscular Disorders 101: The Break Down of Polymyositis

  5. Neuromuscular Disorders 101: Charcot-Marie-Tooth Disease: Effects on Childhood to Adulthood

  6. Neuromuscular Disorders 101: The Dysfunction of Multiple Sclerosis

  7. Neuromuscular Disorders 101: In the Face of Myasthenia Gravis

  8. Neuromuscular Disorders 101: Infection to Impairment: Guillain-Barre Syndrome


Peripheral neuropathy (PN) is defined by damage to the peripheral nervous system (PNS), which is responsible for sending sensory information to the central nervous system (e.i. brain and spinal cord) and other parts of the body (NIH, n.d.). These peripheral nerves serve as communication poles from your body to your brain. For example, a person sitting by a fireplace realizes that their feet are getting too hot, so the peripheral nerves in their feet send signals to the brain indicating discomfort due to the increase in temperature. The brain then sends signals to the lower extremity muscles and feet to move away from the fire. A variety of conditions cause PN, which damage the connection line between your brain and body, creating increased risk of injury. In this series article we will look at peripheral neuropathy and its effects on neuromuscular impairment.


Peripheral nerves contain motor, sensory, and autonomic nerve fibers (Castelli, Desai, & Cantone, 2020). The National Institute of Neurological Disorders and Stroke further define each nerve fiber (NIH, n.d.):


  • Motor nerves control muscle movement under conscious thought (e.i. Walking, grasping things, or talking)

  • Sensory nerves carry information such as light touch, temperature, or pain.

  • Autonomic nerves control organs and regulate activity that is not consciously controlled (e.i. Breathing, digestion, heart function)


A majority of PN conditions affect all three categories, damaging nerve fibers causing lack of motor control and/or altered sensation, such as paraesthesia. Paraesthesia can cause feelings of discomfort such as tingling, pins and needles, or feelings of bugs crawling on one’s skin (Beran, 2015). Many terms are associated with PN that describe alterations in sensation and neuropathic pain. Nerve signaling and communication in PN is altered three ways: loss of nerve signals sent, nerve signaling when there should not be, errors that distort the messages being sent from the nerve signals (NIH, 2020).



Figure 1: Glossary of pain terms (Beran, 2015)



Causes of PN include diabetes mellitus, nerve injury, alcohol use, hereditary diseases, and nutrition deficiencies, however idiopathic causes make up for 25% to 46% of cases (Castelli, Desai, & Cantone, 2020). Diabetic neuropathy is a common type of PN, effecting 18-47% of diabetic cases (NIH, n.d.). Diabetic peripheral neuropathy (DNP) causes ulcers, amputations, and massive health care costs, expensing $10 billion in healthcare costs in the United States (NIH n.d.)


Symptoms of PN are dependent on the type of nerve fiber damaged (NIH,2020). Muscle weakness, uncontrolled muscle twitching and painful cramps are symptoms of motor nerve damage. Symptoms involving sensory nerve damage vary depending on damage to the large or small sensory fibers. Large fiber damage impairs the ability to feel vibrations and touch, markedly in the hands and feet. Small fiber damage causes inability to sense pain or temperature changes. Autonomic nerve damage affects unconscious activity in the human body, potentially causing gastrointestinal dysfunction, heat intolerance, and loss of control in blood vessels to expand/contract to regulate blood temperature.



Figure 2: Symptoms of peripheral neuropathy (Moawad, 2022)


Evaluation requires careful screening due to PN’s wide variety of symptoms. Most commonly used diagnostic test for PN is the examination of light touch with a 10-gram Semmes-Weinstein monofilament (SWME) (Watson, &. Dyck, 2015). SWME is a non-invasive and cost effective clinical test where monofilaments are pressed until bent for one second against multiple areas of the foot. Patients indicate to the clinician if they sense the monofilament pressed (Watson, & Dyck, 2015). General clinical guidelines suggest loss of protective sensation in a 10-gram monofilament (Feng, Schlösser, & Sumpio, 2009). Other diagnostic tests include vibration assessment with a 128-Hz tuning fork, and examination of ankle deep tendon reflexes. SWME and vibration have been shown to be both sensitive and specific for the diagnosis of PN versus superficial pain and ankle reflex testing (Watson, & Dyck, 2015). A common clinical pattern of PN is symmetric in the body and symptoms starting at the end-terminal of a nerve (e.i. Distal foot or hand) and sensory symptoms occurring before motor impairment (Watson, & Dyck, 2015). Proprioception impairments may display as motor ataxia and balance impairments. A common patient complaint is abnormal sensation feeling like one is wearing gloves or stockings (Beran, 2015). Nerve conduction studies and electromyography may be warranted to diagnose PN if the patient’s history is too vague or a complex case, requiring further imaging such as magnetic resonance imaging and ultrasonography, or nerve biopsy.




Figure 3: The 10-g monofilament test for diabetic neuropathy (Aring, Jones, & Falko, 2005)



Lifestyle modifications can assist in the prevention of PN. Maintaining a healthy diet, avoiding exposure to toxins, engaging in exercise, addressing nutrient/vitamin deficiencies are ways to prevent PN (NIH, 2020). Cessation from smoking is significantly beneficial due to its effect on blood vessel constriction, reducing the supply of nutrients peripheral nerves receive. Exercise increases blood flow and oxygen in the body, increasing the amount of nutrients given to nerve endings. Exercise also improves strength, reduces one’s risk of muscle weakness or atrophy. Those diagnosed with a PN-related condition, such as diabetes, self-monitoring skills are vital to avoid further impairment and illness. Such skills involve control of blood sugar levels and proper foot care to prevent further complications (Aring, Jones, & Falko, 2005). Routine foot assessments should be performed to look for callus formation, broken or dry skin, and signs of infection and treated as instructed by the provider. Proper footwear should distribute equal pressure around the whole foot and not specific areas to avoid ulcer formation. It is recommended for all patients with diabetes to have yearly foot examinations performed by a healthcare provider (Aring, Jones, & Falko, 2005).



Figure 4: The 4 essentials for preventing DFU* (Nhan, Strauss, & Miller, 2013)

*DFU: Diabetic foot ulcer



Peripheral neuropathy has a variety of symptoms and is associated with a multitude of health conditions (NIH, 2020). The medical screening process is extremely detailed, beginning with the clinician obtaining thorough subjective information followed by appropriate test screening. Once diagnosed, clinicians should facilitate a tailored treatment and disease management plan to avoid debility or severe health complications. Health prevention for PN includes adopting healthy lifestyle habits consisting of diet, exercises and the cessation of negative health behaviors (e.i. Smoking and excessive alcohol intake).



Bibliographical References

Aring, A. M., Jones, D. E., & Falko, J. M. (2005). Evaluation and prevention of diabetic neuropathy. American family physician, 71(11), 2123–2128.


Beran R. Paraesthesia and peripheral neuropathy. Aust Fam Physician. 2015; 44(3):92-95.


Castelli G, Desai KM, Cantone RE. Peripheral neuropathy: Evaluation and differential diagnosis. Am Fam Physician. 2020;102(12):732-739.


Feng, Y., Schlösser, F. J., & Sumpio, B. E. (2009). The Semmes Weinstein monofilament examination as a screening tool for diabetic peripheral neuropathy. Journal of vascular surgery, 50(3), 675–682.e1. https://doi.org/10.1016/j.jvs.2009.05.017


Kazamel, M., Stino, A. M., & Smith, A. G. (2021). Metabolic syndrome and peripheral neuropathy. Muscle & nerve, 63(3), 285–293. https://doi.org/10.1002/mus.27086


Nhan L., Strauss, M.B., Miller, S.S. (2013). Preventing diabetic foot ulcers: A 4-pronged approach. Consultant 360, 53(12).


National Institute of Neurological Disorders and Stroke. (n.d.) Peripheral neuropathy fact sheet. Retrieved December 15, 2020, from https://www.ninds.nih.gov/peripheral-neuropathy-fact-sheet#3208_1


Tofthagen, C., Visovsky, C., & Berry, D. L. (2012). Strength and balance training for adults with peripheral neuropathy and high risk of fall: current evidence and implications for future research. Oncology nursing forum, 39(5), E416–E424. https://doi.org/10.1188/12.ONF.E416-E424


Watson, J. C., & Dyck, P. J. (2015). Peripheral Neuropathy: A Practical Approach to Diagnosis and Symptom Management. Mayo Clinic proceedings, 90(7), 940–951. https://doi.org/10.1016/j.mayocp.2015.05.004

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Holly Bennett

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