Introduction to Foot Neuropathy: Difference between revisions

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== Introduction ==
== Introduction ==
diabetes is a global epidemic. It's been found to affect more than 537 million adults worldwide. 75% of those individuals have been found to come from low- to middle-income countries or low- to middle-income regions of more affluent countries. It is believed that 50% of individuals with diabetes are undiagnosed, and those that are diagnosed have been found to have diabetes for many years prior to their diagnosis. 6,7 million deaths have been attributed to diabetes, although the article did not mention the timeframe that involved that number. Diabetes accounts for 9% of total health care costs for adults, and the complications of foot and lower extremity issues related to diabetes affects 40 to 60 million people worldwide. The prevalence of neuropathy in one study was found to be anywhere from 10 to 85 percent, and the discrepancies found in the various studies were attributed to different definitions of when a diagnosis of neuropathy is made, which caused that huge variable in the prevalence study.
Diabetes is a global epidemic, affecting more than 537 million adults worldwide.<ref name=":7">Hicks CW, Wang D, Windham BG, Matsushita K, Selvin E. [https://www.nature.com/articles/s41598-021-98565-w Prevalence of peripheral neuropathy defined by monofilament insensitivity in middle-aged and older adults in two US cohorts]. Scientific reports. 2021 Sep 27;11(1):19159.</ref>  Of those, 40 to 60 million people have diabetic-related foot and lower extremity complications. Diabetes accounts for 9% of total adult health care costs.<ref name=":2" /> 


Another startling finding is that less than 33% of physicians surveyed will recognise the signs of a neuropathy when they're evaluating their patient. The lifetime risk of an individual developing a diabetic foot ulcer after they have diabetes is anywhere from 19 to 34 percent. Or put another way, one in four people with diabetes will develop a diabetic foot ulcer at some point in time. A person with diabetes who develops a diabetic foot ulcer is at 2,5 times greater risk of mortality than a person with diabetes who doesn't develop a diabetic foot ulcer. To put that more seriously, a person with a diabetic foot ulcer has a 5% mortality rate within one year. Their mortality rate increases to 42% within 5 years of developing a diabetic foot ulcer. After 5 years of a minor amputation, the mortality rate is 46%. And with a major amputation, after 5 years, the mortality rate increases to 57%. After 1 year, 20% of diabetic foot ulcers remain unhealed. And the recurrence rate after they do heal is 40% within one year and 65% within five years, which is a huge problem for diabetic patients. Once they have a foot ulcer, their risk of developing another one is significantly high.  
Peripheral neuropathy is a common consequence of diabetes, with a prevalence of anywhere from 10 to 85%.<ref name=":2" />. The outcomes of peripheral neuropathy can be devastating to include (1) foot ulcers, (2) major amputation, (3) falls, (4) intracranial injuries, and (5) decreased quality of life.<ref name=":7" />  Approximately one in four people with diabetes will develop a diabetic foot ulcer, which puts them on a medical slippery slope:
 
* They have a 2.5 times greater mortality risk than people with diabetes who did not develop a foot ulcer.
* Their mortality rate increases to 42% within 5 years of developing a diabetic foot ulcer.  
* After 1 year, 20% of diabetic foot ulcers remain unhealed.  
* The recurrence rate for healed diabetic foot ulcers within one year is 40%, and with five years in 65%.<ref name=":2" />
 
This article will provide an introduction to the causes and types of peripheral neuropathy, exploring aetiology beyond diabetes.


== Neuroanatomy Review ==
== Neuroanatomy Review ==
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== Peripheral Neuropathy ==
== Peripheral Neuropathy ==
Peripheral neuropathy (PN) describes the many conditions which involve damage to the peripheral nervous system.  Initially, that presents as nerve malfunction due to cellular and chemical changes. Eventually, that malfunction becomes true nerve or structural damage, resulting in atrophy and demyelination<ref name=":2">Merwarth, D. Understanding the Foot Programme. Introduction to Foot Neuropathy. Physioplus. 2023.</ref>. There are more than 100 known types of peripheral neuropathy, each with unique symptoms and prognosis. PN symptoms are dependent on the category of nerves involved, motor, sensory, or autonomic<ref name=":0" />.   
The term peripheral neuropathy (PN) describes many conditions which involve damage to the peripheral nervous system.  Initially, this damage presents as nerve malfunction due to cellular and chemical changes. However, over time the nerve malfunction becomes true nerve or structural damage, resulting in atrophy and demyelination<ref name=":2">Merwarth, D. Understanding the Foot Programme. Introduction to Foot Neuropathy. Physioplus. 2023.</ref>. There are more than 100 known types of peripheral neuropathy, each with unique symptoms and prognosis. PN symptoms are dependent on the category of nerves involved, motor, sensory, or autonomic<ref name=":0" />.   


The exact pathophysiology of PN is contingent upon the underlying disease processes, however the mechanisms of peripheral nerve injury exhibit similar patterns.  These reactions include (1) segmental demyelination, (2) [https://www.physio-pedia.com/Wallerian_Degeneration?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Wallerian degeneration], and (3) axonal degeneration<ref name=":1" />.   
The exact pathophysiology of PN is contingent upon the underlying disease processes, however the mechanisms of peripheral nerve injury exhibit similar patterns.  These reactions include (1) segmental demyelination, (2) [https://www.physio-pedia.com/Wallerian_Degeneration?utm_source=physiopedia&utm_medium=search&utm_campaign=ongoing_internal Wallerian degeneration], and (3) axonal degeneration<ref name=":1" />.   
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The [https://www.nih.gov National Institute of Health] (NIH) states that PN aetiology can involve many causes, to include metabolic, systemic, and toxicity<ref name=":1" />:
The [https://www.nih.gov National Institute of Health] (NIH) states that PN aetiology can involve many causes, to include metabolic, systemic, and toxicity<ref name=":1" />:


* [[Diabetes|Diabetes mellitus]]<ref name=":2" /><ref name=":1" />
* [[Diabetes|Diabetes mellitus]]<ref name=":2" /><ref name=":1" />(most common cause of PN)
* Chronic [[alcoholism]]<ref name=":2" /><ref name=":1" />
* Chronic [[alcoholism]]<ref name=":2" /><ref name=":1" />
* Nutritional deficiencies (e.g., B1, B6, B12, and vitamin E)<ref name=":2" /><ref name=":1" />
* Nutritional deficiencies (e.g., B1, B6, B12, and vitamin E)<ref name=":2" /><ref name=":1" />

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Introduction[edit | edit source]

Diabetes is a global epidemic, affecting more than 537 million adults worldwide.[1] Of those, 40 to 60 million people have diabetic-related foot and lower extremity complications. Diabetes accounts for 9% of total adult health care costs.[2]

Peripheral neuropathy is a common consequence of diabetes, with a prevalence of anywhere from 10 to 85%.[2]. The outcomes of peripheral neuropathy can be devastating to include (1) foot ulcers, (2) major amputation, (3) falls, (4) intracranial injuries, and (5) decreased quality of life.[1] Approximately one in four people with diabetes will develop a diabetic foot ulcer, which puts them on a medical slippery slope:

  • They have a 2.5 times greater mortality risk than people with diabetes who did not develop a foot ulcer.
  • Their mortality rate increases to 42% within 5 years of developing a diabetic foot ulcer.
  • After 1 year, 20% of diabetic foot ulcers remain unhealed.
  • The recurrence rate for healed diabetic foot ulcers within one year is 40%, and with five years in 65%.[2]

This article will provide an introduction to the causes and types of peripheral neuropathy, exploring aetiology beyond diabetes.

Neuroanatomy Review[edit | edit source]

  • Nervous system division, shutterstock ID- 2187989357.jpg
    Central Nervous System: includes the brain and spinal cord. The central nervous system (CNS) is the body's processing centre. In general terms, the three functions of the CNS are to (1) take in sensory information, (2) process that information, and (3) send out motor signals. Through these mechanisms, the CNS controls most of the body's functions, to include: movement, sensation through our five senses, and higher level functions such as cognition, awareness, and speech. The spinal cord is an extension of the brain and serves as a neural pathway for information exchange with the rest of the body.
  • Peripheral Nervous System: a complex network of nerves which convey sensory information in from the body to the CNS via the spinal cord, and transmit information out from the CNS via the spinal cord to the body. Examples of outgoing signals transmitted along the peripheral nervous system (PNS) include (1) motor information for muscle activity and(2) autonomic functioning (heart rate, blood pressure, respiration, digestion, sexual arousal)[3].
    • Motor Nerves: relay information to skeletal muscles and somatic tissue, which creates voluntary movement
    • Sensory Nerves: conveys sensory information about the environment in from sensory receptors in the body to the CNS
    • Autonomic Nervous System: relay motor information to the visceral organs to innervate smooth muscle, cardiac muscle, and glands and functions to maintain the body's homeostasis. The autonomic nervous system has two parts: the sympathetic and parasympathetic divisions which innervate visceral organs. The sympathetic stimulates ("fight or flight") while the parasympathetic inhibits ("rest and digest") their functions.

Peripheral Neuropathy[edit | edit source]

The term peripheral neuropathy (PN) describes many conditions which involve damage to the peripheral nervous system. Initially, this damage presents as nerve malfunction due to cellular and chemical changes. However, over time the nerve malfunction becomes true nerve or structural damage, resulting in atrophy and demyelination[2]. There are more than 100 known types of peripheral neuropathy, each with unique symptoms and prognosis. PN symptoms are dependent on the category of nerves involved, motor, sensory, or autonomic[3].

The exact pathophysiology of PN is contingent upon the underlying disease processes, however the mechanisms of peripheral nerve injury exhibit similar patterns. These reactions include (1) segmental demyelination, (2) Wallerian degeneration, and (3) axonal degeneration[4].

Classification methods of PN include:

  1. Categorisation as mono-neuropathies, multifocal neuropathies, poly-neuropathies and radiculopathies[5][4].
  2. Further sub-classification by separating PN as axonal, demyelinating, or mixed[4].

Common symptoms of PN include:

  • Numbness and paresthesias
  • Pain
  • Muscle weakness
  • Loss of deep tendon reflexes [4]

To learn more about neuropathy, please read this optional article.

Aetiology of Peripheral Neuropathies[edit | edit source]

The National Institute of Health (NIH) states that PN aetiology can involve many causes, to include metabolic, systemic, and toxicity[4]:

Types of Peripheral Neuropathies[edit | edit source]

Sensory Neuropathy[edit | edit source]

"Sensory neuropathies refer to a host of diseases that result in loss of sensation throughout the body ... [sensory neuropathy conditions] may further sub-divide into small fiber (pain-dominant) and large fiber (ataxia-predominant) pathologies."[8]

To classify a sensory neuropathy, it is important to identify the size of the nerve fiber and the degree of myelination involved. Some diseases, such Diabetes, can involve sensory polyneuropathy.[8]

  • Small fiber neuropathies (Aδ and small unmyelinated C fibers)
    • transmit noxious stimuli and thermal signals
    • Aδ fibers regulate preganglionic sympathetic and parasympathetic function
    • C fibers regulate postganglionic autonomic function
    • Symptoms: burning, shooting pain with paresthesia[8], impairment of pain, temperature and autonomic functions[9]
  • Large fiber neuropathies (Aβ fibers)
    • Aβ fibers regulate proprioceptive sensory input of vibration and touch.
    • May be involved in the development of ataxia[8]
    • Symptoms: loss of joint position and vibrational sense and sensory ataxia[9]with resulting gait impairments[2]

Special Topic: Loss of Protect Sensation[edit | edit source]

Loss of Protective Sensation (LOPS) is a complication common to patients with diabetic neuropathy. PN related to diabetes is an "anatomically diffuse process" which affects sensory and autonomic nerve fibers and, in more advanced cases, distal motor fibers. Symptoms tend to develop distally in the toes, then advance by moving proximal. This disease process leads to LOPS meaning the person is unable to sense minor trauma and injury from mechanical, thermal, or chemical causes.[10]

LOPS is an important symptom used in the classification of diabetic foot wounds[11] because the foot is more vulnerable to physical and thermal trauma and predisposes it to deformity.[12]

Common mechanisms of injury related to LOPS:

  1. Exposure to constant, prolonged pressure such as wearing shoes that are too tight
  1. Exposure to moderate to high repetitive pressure which causes the development of a callus which in turn acts as a source of pressure
  2. Exposure to brief high pressure such as stepping on a sharp object which causes a wound or other injury[2]

For more information on testing for LOPS, please read this article.

Motor Neuropathy[edit | edit source]

Motor neuropathy is the result of damage to the motor nerves.[2]

Signs of motor neuropathy include:

  • Foot deformities resulting from muscle imbalances within the foot[2] and the non-enzymatic glycation of proteins.
    • Common deformities include (1) hammer toe, (2) claw toe, and (3) pes equinu[2]
  • Changes in gait pattern due to tendon shortening
    • Tendons commonly effected include (1) Achilles tendon and the (2) flexor hallucis tendons[2]
  • Loss of deep tendon reflexes (DTR's)[2]
  • Other symptoms can include:
    • muscle twitching and cramps
    • muscle weakness or paralysis
    • muscle wasting[13]

Add images from Diane's lecture

Autonomic Neuropathy[edit | edit source]

"Autonomic neuropathies are a collection of syndromes and diseases affecting the autonomic neurons, either parasympathetic or sympathetic, or both. Autonomic neuropathies can be hereditary or acquired in nature."[14]

Signs and symptoms of autonomic neuropathy can present across a wide variety of body systems. Many of these impairments can affect a patient's gait pattern putting them at greater risk for foot dysfunction and wound formation. Impairments such as changes in the frequency and urgency to get to the bathroom, and their ability to effectively scan the environment and see for safety awareness can increase their fall risk.

  • Cardiovascular system.
    • The body may respond more slowly to changes in body position, stress, physical activity, sleep, and breathing patterns. Examples include: light-headedness with positional changes or exercise.[15]
    • Impaired chest pain sensation to recognise a cardiac event such as a heart attack.[2][15]
  • Digestive system. Digestive difficulties can include:[15]
    • feelings of bloating, fullness, and nausea
    • vomiting
    • constipation
    • diarrhea
    • fecal incontinence
    • gastroparesis
    • swallowing impairments
  • Urogenital system.
    • Bladder impairments[15]
      • impaired ability to sense need to void
      • urinary incontinence
      • bladder infections stemming urinary retention
  • Integumentary system.
    • Non-enzymatic glycation of protein[2][16]
      • Causes thickened, taut, inflexible skin on the foot. These skin changes present additional pressures against bony prominences which can put the patient at risk of developing an ischaemic ulcer over those areas.[2]
      • Predisposes skin for formation of skin fissures.[2] [16]
      • Causes contracture of the fascial structures, which can lead to joint deformity of the foot[16]
      • Impaired wound healing[16]
    • Sweat glands.
      • Can experience difficulty regulating perspiration, or changes in sweating patterns. For example: increased night sweats or sweating while eating. This can greatly affect the body's ability to regulate body temperature.[2][15]
      • Can also experience anhidrosis (dry skin).[2]
  • Eyes. Can experience difficulty with pupil adaptation to changes in light, and night blindness when driving.[15]
  • Can develop hypoglycemia unawareness.[15]

Resources[edit | edit source]

  • bulleted list
  • x

or

  1. numbered list
  2. x

References[edit | edit source]

  1. 1.0 1.1 Hicks CW, Wang D, Windham BG, Matsushita K, Selvin E. Prevalence of peripheral neuropathy defined by monofilament insensitivity in middle-aged and older adults in two US cohorts. Scientific reports. 2021 Sep 27;11(1):19159.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 Merwarth, D. Understanding the Foot Programme. Introduction to Foot Neuropathy. Physioplus. 2023.
  3. 3.0 3.1 National Institute of Health. Peripheral Neuropathy. Available from: https://www.ninds.nih.gov/health-information/disorders/peripheral-neuropathy#toc-what-is-peripheral-neuropathy- (accessed 3/August/2023).
  4. 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 4.20 Hammi C, Yeung B. Neuropathy. 2022 Available from;https://www.ncbi.nlm.nih.gov/books/NBK542220/(last accessed 5/August/2023)
  5. Martyn CN, Hughes R. Epidemiology of peripheral neuropathy. Journal of neurology, neurosurgery, and psychiatry. 1997 Apr;62(4):310.
  6. Oaklander AL, Mills AJ, Kelley M, Toran LS, Smith B, Dalakas MC, Nath A. Peripheral neuropathy evaluations of patients with prolonged long COVID. Neurology-Neuroimmunology Neuroinflammation. 2022 May 1;9(3).
  7. Rögnvaldsson S, Steingrímsson V, Turesson I, Björkholm M, Landgren O, Kristinsson SY. Peripheral neuropathy and monoclonal gammopathy of undetermined significance: a population-based study including 15,351 cases and 58,619 matched controls. haematologica. 2020 Nov 11;105(11):2679.
  8. 8.0 8.1 8.2 8.3 National Institute of Health. Sensory Neuropathy. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559020/ (accessed 6/August/2023).
  9. 9.0 9.1 Misra UK, Kalita J, Nair PP. Diagnostic approach to peripheral neuropathy. Annals of Indian Academy of Neurology. 2008 Apr;11(2):89.
  10. Centers for Medicare & Medicaid Services. Diabetic Peripheral Neuropathy with Loss of Protective Sensation (LOPS). Available from: https://www.cms.gov/medicare-coverage-database/view/ncacal-decision-memo.aspx?proposed=N&NCAId=22&amp%3Bfromdb=true#:~:text=Long%20nerves%20are%20affected%20first,%2C%20thermal%2C%20or%20chemical%20sources. (accessed 6/August/2023).
  11. Swanson T, Ousey K, Haesler E, Bjarnsholt T, Carville K, Idensohn P, Kalan L, Keast DH, Larsen D, Percival S, Schultz G. IWII Wound Infection in Clinical Practice consensus document: 2022 update. Journal of wound care. 2022 Dec 1;31(Sup12):S10-21.
  12. Adams OP, Herbert JR, Howitt C, Unwin N. The prevalence of peripheral neuropathy severe enough to cause a loss of protective sensation in a population‐based sample of people with known and newly detected diabetes in Barbados: a cross‐sectional study. Diabetic Medicine. 2019 Dec;36(12):1629-36.
  13. NHS. Peripheral neuropathy symptoms. Available from: https://www.nhs.uk/conditions/peripheral-neuropathy/symptoms/ (accessed 6/August/2023).
  14. Medscape. Autonomic Neuropathy. Available from: https://emedicine.medscape.com/article/1173756-overview?form=fpf (accessed 6/August/2023).
  15. 15.0 15.1 15.2 15.3 15.4 15.5 15.6 National Institute of Health. Autonomic Neuropathy. Available from: https://www.niddk.nih.gov/health-information/diabetes/overview/preventing-problems/nerve-damage-diabetic-neuropathies/autonomic-neuropathy (accessed 15/August/2023).
  16. 16.0 16.1 16.2 16.3 Mooney J. Illustrated Dictionary of Podiatry and Foot Science E-Book. Elsevier Health Sciences; 2009 Jul 30.