Wednesday, 1 April 2015

Neuropathy Affects Balance

Today's post from (see link below) is all over the internet in various forms at the moment but to my mind is pretty much another 'duh!' moment as far as neuropathy news is concerned. Almost every experienced neuropathy patient will be able to tell you that their neuropathy has compromised their balance in some way and it doesn't take a great deal of imagination to understand why (given the other symptoms we experience). However, these things all have to be proved in one way or another via studies and research and this article does go into the science behind balance issues. Worth a read but you knew it didn't you?

Diabetic Peripheral Neuropathy Compromises Balance During Daily Activities
Published online before print March 12, 2015, doi: 10.2337/dc14-1982 Diabetes Care March 12, 2015

Steven J. Brown1,
Joseph C. Handsaker1,
Frank L. Bowling2,
Andrew J.M. Boulton2 and
Neil D. Reeves1

+ Author Affiliations

1School of Healthcare Science, Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, U.K.
2Faculty of Medical and Human Sciences, University of Manchester, U.K.
Corresponding author: Steven J. Brown,



Patients with diabetes with peripheral neuropathy have a well-recognized increased risk of falls that may result in hospitalization. Therefore this study aimed to assess balance during the dynamic daily activities of walking on level ground and stair negotiation, where falls are most likely to occur.


Gait analysis during level walking and stair negotiation was performed in 22 patients with diabetic neuropathy (DPN), 39 patients with diabetes without neuropathy (D), and 28 nondiabetic control subjects (C) using a motion analysis system and embedded force plates in a staircase and level walkway. Balance was assessed by measuring the separation between the body center of mass and center of pressure during level walking, stair ascent, and stair descent.


DPN patients demonstrated greater (P < 0.05) maximum and range of separations of their center of mass from their center of pressure in the medial-lateral plane during stair descent, stair ascent, and level walking compared with the C group, as well as increased (P < 0.05) mean separation during level walking and stair ascent. The same group also demonstrated greater (P < 0.05) maximum anterior separations (toward the staircase) during stair ascent. No differences were observed in D patients.


Greater separations of the center of mass from the center of pressure present a greater challenge to balance. Therefore, the higher medial-lateral separations found in patients with DPN will require greater muscular demands to control upright posture. This may contribute to explaining why patients with DPN are more likely to fall, with the higher separations placing them at a higher risk of experiencing a sideways fall than nondiabetic control subjects.
Received August 18, 2014.
Accepted February 17, 2015. 

© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

Tuesday, 31 March 2015

The Vocabulary Of Neuropathy

Today's post from (see link below) is a thorough look at peripheral neuropathy using a range of neuropathy terms which we may meet in the course of our treatment but rarely get to find out what they mean. Neuropathy could have its own dictionary! and many patients are left confused by the plethora of words that are thrown at them, either by their doctors or in the texts they read. It's worthwhile knowing what these terms mean because that leads to a better understanding of how our disease is being treated and why. This article is more directed at medical professionals than patients but that shouldn't stop us looking it through and seeing what applies to our own individual cases. Don't worry if much of it passes you by; every little helps and inside knowledge is always useful!

Paraesthesia and peripheral neuropathy
Volume 44, No.3, 2015 Pages 92-95

Roy G Beran MBBS, MD, FRCP, FRACGP, FACLM, B LegS, Consultant Neurologist, Conjoint Associate Professor of Medicine, Department of Medicine, University of New South Wales, Sydney, NSW; Professor, School of Medicine, Griffith University, Gold Coast, QLD.


Paraesthesia reflects an abnormality affecting the sensory pathways anywhere between the peripheral sensory nervous system and the sensory cortex. As with all neurology, the fundamental diagnostic tool is a concise history, devoid of potentially ambigu-ous jargon, which properly reflects the true nature of what the patient is experiencing, provocateurs, precipitating and relieving factors, concomitant illnesses, such as diabetes, and any treatments that could evoke neuropathies.


Some localised neuropathies, such as carpal tunnel syndrome (CTS) or ulnar neuropathy, produce classical features, such as weakness of the ‘LOAF’ (lateral two lumbricals, opponens pollicis, abductor pollicis brevis and flexor pollicis brevis) median in-nervated muscles, thereby obviating need for further neurophysiology. Nerve conduction studies may be necessary to diagnose peripheral neuropathy, but they may also be normal with small fibre neuropathy. Even with a diagnosis of peripheral neuropathy, definition of the underlying cause may remain elusive in a significant proportion of cases, despite involvement of consultants. 


Treatment is based on the relevant diagnosis and mechanism to address the cause. This includes better glycaemic control for diabetes, night splint for CTS or elbow padding for ulnar neuropathy, modifying lifestyle with reduced alcohol consumption or replacing dietary deficiencies or changing medications where appropriate and practical. Should such intervention fail to relieve symptoms, consideration of intervention to relieve symptoms of neuropathic pain may be required.

Peripheral neuropathy is such a broad subject that it is impossible to do it justice in a brief overview such as this. The topic, for the preparation of this review, was to explore ‘paraesthesia and peripheral neuropathy’ with a focus on the needs of the general practitioner 9GP). It follows that this paper will, of necessity, be somewhat superficial, the goal being to assist GPs in their approach to patients with pareasthesia. Some of the investigations and management will be touched on but further consideration is reserved for the consultant. To offer maximal value and focus, the style adopted will be pragmatic, trying to offer some pearls, rather than offer a comprehensive treatise as is available in any standard text. 


As is the case with all neurology, the most important diagnostic tool is a detailed comprehensive history that reflects what the patient is trying to convey. Patients will often volunteer vague terms, such as ‘numb’, and need help to tease out what they are describing. The term ‘numb’ may mean abnormal sensation, including loss of feeling, tingling, pins and needles, electric shock-like sensations, a feeling of heaviness or loss of function, a loss of dexterity, or a host of other possibilities, depending on the individual patient. Patients do not present with the complaint of ‘paraesthesia’ but will often complain of ‘numbness’ and it is imperative to determine if this means paraesthesia, before embarking on a diagnostic paradigm.1

Paraesthesia is a technical term used to reflect a perception of abnormal sensation, including feelings of pins and needles, tingling, pricking or a feeling as if ants are crawling over/under the skin and patients should be encouraged to fully describe what they are feeling. Patients should be encouraged to use their own language, rather than trying to inject jargon, which may be ambiguous and fail to really convey what the patient is trying to describe. Paresthesia suggests abnormality affecting the sensory nervous system and may arise anywhere from the peripheral nerve to the sensory cortex. It is one of the terms attached to peripheral neuropathy for which there is a lexicon (Table 1). Patients should describe what they are feeling and the distribution of the abnormal sensation, what provokes it, when it started, what, if anything, they can do to relieve it and any associated features.1

When taking a history from the patient, it is important to explore other features, such as concomitant illnesses, medications and/or drugs used, other treatments provided, past medical history and family history, system review and exposure to chemicals. Perhaps the most common diagnosis associated with peripheral neuropathy is diabetes2 and paraesthesia is often accepted as the hallmark symptom for neuropathic pain.1 It is important to differentiate the discomfort of paraesthesia from other sources of pain, such as musculoskeletal pain, as may occur with osteoarthritis.

Table 1. Glossary of pain terms


Pain perceived following non-noxious, innocuous stimulus (eg light touch causes burning pain)

Antalgia (antalgic)

Pain perception (noun), pain provoked action (adjective) (eg antalgic gait – altered gait due to the influence of pain)


An altered perception of sensation with abnormal (often unpleasant) feeling associated with stimulation, such as touching over the affected area causes ‘strange feeling’


Reduced perception of stimulus (both words are interchangeable)
Decreased sensation


Increased perception of pain


Increased perception of stimulus (need not be pain)


Decreased sensation to one or more modalities while concurrently having increased perception of pain (hyperalgia) or pain with innocuous stimulation (allodynia)


Reduced perception of pain


Abnormal sensations, such as ‘pins and needles’, tingling, prickling, reduced or even loss of sensation. It implies abnormality anywhere along the sensory pathway from peripheral nerve to sensory cortex – the epitome of ‘neuropathic pain’

Reproduced with permission from Beran R. Neurology for General Practitioners. Sydney: Elsevier Australia, 2012

Focus on aetiology

Clinicians will often overlook the potential for iatrogenically induced peripheral neuropathy, as may occur with frequently used medications, including amiodarone, statins, antiretrovirals, tacrolimus or even agents not often considereed to be associated with peripheral neuropathy, such as levodopa, which is commonly used to treat Parkinson’s disease.3 It is widely accepted that various chemotherapies for malignancy can cause peripheral neuropathy, including taxanes, platinum compounds, vinca alkaloids, proteasome inhibitors and antiangiogenic/immunomodulatory agents.4 Deficiencies of vitamins, such as B6 or B12, may evoke peripheral neuropathies and may be associated with therapies, including levodopa.3 This may necessitate special consideration, especially in vegans.

Other dietary deficiencies may be associated with peripheral neuropathy. For example, toxic levels of homocysteine are associated with vitamin B6 and B12 deficiencies.2 Medications such as metformin cause B12 deficiency5 as do other medications, such as phenytoin, which reduces folate needed for B12.6 There has been a push to offer dietary supplements, including vitamins B6, B12, D and E, and magnesium to address problems with peripheral neuropathy.2,7 Patients who are alcohol-dependent often have a variety of causes for peripheral neuropathy, which include both direct toxic effects of excess alcohol as well as poor diet, particularly deficient in thiamine (vitamin B1).8 It follows that the history obtained should include the usual causes of nerve damage being explored but doctors often ignore taking an adequate dietary history and nutritional neuropathies may be overlooked.9


If a detailed history is taken, the diagnosis of peripheral neuropathy should be straightforward. The suspicion should have been established and features such as a ‘glove and stocking’ abnormal sensation should be a giveaway to suggest peripheral neuropathy.

What has not been addressed, thus far, are some of the very localised peripheral neuropathies that may present with very localised paraesthesia. These include carpal tunnel syndrome10 or ulnar neuropathy,11 which relate to direct pressure or vascular supply to the nerve.11

Focal neuropathies

A proper history and examination may be all that is required to diagnose carpal tunnel neuropathy or ulnar neuropathy. The median nerve supplies only four muscles in the hand, represented by the mnemonic ‘LOAF’: lateral two lumbricals; opponens pollicis, abductor pollicis brevis and flexor pollicis brevis.1 Patients will complain of paraesthesia in the hand but the history may be very vague, although it usually includes being woken from sleep because of the dysaesthesia.1 Weakness, restricted to these four muscles of the hands, is pathognomonic of median nerve impairment, as is found with carpal tunnel syndrome. Similarly, sparing of the LOAF muscles of the hand through involvement of the abductor digiti minimi and medial two lumbricals is indicative of ulnar neuropathy, usually traumatised by turning over in bed and focusing the full body weight on the elbow, where the ulnar nerve traverses the medial humeral epicondyle.1

If the above has been found then the diagnosis has been made, thereby negating a need for nerve conduction studies unless the patient fails to respond to conservative intervention with either a night splint for carpal tunnel or padding of the medial epicondyle of the elbow for ulnar neuropathy.1 In addition to diagnosing these focal neuropathies and instituting local conservative intervention, it is imperative to exclude contributory diagnoses, such as vitamin deficiencies, thyroid disease, vasculitities, diabetes and various medications, such as those already described, together with other agents, such as amiodarone, nitrofurantoin or statins.1 It follows that other investigations are warranted, particularly blood tests to look for these associated diagnoses.

Proper physical examination should have defined the distribution of the dysaesthesia reflective of the paraesthesia, which was the presenting symptom. Impairment of deep tendon reflexes, especially at the periphery (such as ankle jerks) provides additional confirmatory evidence of a possible sensory–motor neuropathy. When testing sensation, movement from impaired sensation to retained sensation is favoured, thus moving from the periphery, passing distal-to-proximal (foot, ankle, calf to knee), is preferable as it is easier for a patient to appreciate increased perception, especially pin prick and light touch, than is the reverse. This will help demarcate the ‘glove and stocking’ impaired sensation that accompanies peripheral neuropathy.


Neurophysiology, using nerve conduction studies and electromyography, may be required, especially for the patient who proves to be a very poor historian or in whom confirmation of a diagnosis may dictate altered therapy. This may be the case in a poorly compliant patient whose diabetes is uncontrolled and in whom such confirmation may encourage better compliance, as well as the possible addition of insulin to the regimen. It must be acknowledged that nerve conduction studies may not be abnormal in small fibre neuropathy yet the patient may still present with neuropathic symptoms. A perfect example of this is the painful diabetic neuropathy, which requires insulin and improved glycaemic control.

For more complex cases of peripheral neuropathy, there may be a need for more detailed investigation including evoked studies, imaging (possibly with magnetic resonance imaging or ultrasonography) and nerve biopsy. In these cases it seems appropriate to involve a consultant neurologist, which implies further consideration that is beyond the scope of this paper. Even with the involvement of consultant colleagues and comprehensive evaluation, the underlying mechanism of a significant proportion of neuropathies remains indeterminate.

Treatment is determined by the relevant diagnosis. By far the most common cause of peripheral neuropathy, heralded by paraesthesia, is diabetes mellitus. Once diagnosed and confirmed, patients should be more closely monitored, encouraged to be more compliant with the prescribed treatment and, in many cases, insulin should be added to the treatment regimen,1 together with nutritional approaches.2

Nutritional neuropathies are addressed by correcting the nutritional deficiencies that have been identified.79 Those neuropathies caused by exposure to medications are addressed by reconsidering treatment options, when possible, and close monitoring of the consequences complemented by conservative supportive symptomatic relief.

Carpal tunnel syndrome may be provoked by direct trauma to the median nerve, as may occur with exposure to vibrating machinery or direct impact from repeated use of tools, such as a screwdriver pushing into the palm of the hand, but by far the most common cause is sleeping with the wrist hyperflexed, thereby impeding vascular supply to the median nerve. Treatment with a night splint, specifically prepared for the individual patient (not a generic splint) designed to be in the ‘natural’ position (mildly dorsiflexed rather than the flat, ‘neutral’ position) is usually all that is needed. Padding of the elbow to protect the ulnar nerve as it passes over the humeral epicondyle when turning over in bed at night is often sufficient to relieve ulnar neuropraxia. The response to therapy is predicated by the severity of the problem at the time of presentation and hence early detection and intervention are invaluable.

Addressing the underlying cause of the peripheral neuropathy, which presents with paraesthesia, is the initial approach to intervention. There may be a need to consider lifestyle issues and the involvement of other health practitioners, such as occupational therapists, physiotherapists or podiatrists, and review of fundamental factors such as diet, alcohol consumption and medications. Should the paraesthesia persist, even after treating the cause of neuropathy, the question of neuropathic pain assumes greater significance.

Treatment of neuropathic pain is beyond the scope of this paper, which has focused specifically on paraesthesia and peripheral neuropathy. There is a host of agents available to treat neuropathic pain, including antidepressants (tricyclic antidepressants and serotonin and noradrenaline reuptake inhibitors), antiepileptic medications (such as carbamazepine or pregabalin), antispasmodics (such as baclofen) and a variety of other treatments (including topical analgesics). 


As with all neurological conditions, the most important diagnostic tool is a good history, complemented by physical examination – usually to confirm the diagnosis, already considered, based on the history obtained. Paraesthesia is the usual presentation for a sensory neuropathy, which may affect the sensory pathway from peripheral nerve to sensory cortex. Having made the diagnosis, many of the conditions, but particularly carpal tunnel syndrome and ulnar neuropathy, can be effectively managed by the GP without requiring consultant involvement. Addressing the underlying problem is often all that is required but, in complex cases, referral to a specialist may be necessary.

Competing interests: None.
Provenance and peer review: Commissioned, externally peer reviewed. 

Beran RG. Neurology for General Practitioners. Sydney: Elsevier, 2012. Search PubMed
Curtis L. Nutritional approaches to treat diabetic neuropathy: a systematic review. Int J Diab Research 2013;2:56–60. Search PubMed
Muller T, van Laar T, Comblath DR, et al. Peripheral neuropathy in Parkinson’s disease: levodopa exposure and implications for duodenal delivery. Parkinsonism Relat Disord 2013;19:501–07. Search PubMed
Argyriou AA, Kyritsis AP, Makatsoris T, Kalofonos HP. Chemotherapy-induced peripheral neuropathy in adults: A comprehensive update of the literature. Cancer Manag Res 2014;6:135–47. Search PubMed
Singh AK, Kumar A, Karmakar D, Jha RK. Association of B12 deficiency and clinical neuropathy with metformin use in type 2 diabetes patients. J Postgrad Med 2013;59:253–57. Search PubMed
Shorvon SD, Reynolds EH. Anticonvulsant peripheral neuropathy: A clinical and electrophysiological study of patients on single drug treatment with phenytoin, carbamazepine or barbiturates. J Neurol Neurosurg Psychiatry 1982;45:620– 26 Search PubMed
Reynolds E. Vitamin B12, folic acid and the nervous system. Lancet Neurol 2006;5:949–60. Search PubMed
Koike H, Sobue G. Alcoholic Neuropathy. Curr Opin Neurol 2006;19:481–86. Search PubMed
Kumar N. Nutritional Neuropathies. Neurol Clin 2007;25:209–55. Search PubMed
Bland JD. Carpal Tunnel Syndrome. BMJ 2007;335:343–46. Search PubMed
Werner CO, Ohlin P, Elmqvist D. Pressures recorded in ulnar neuropathy. Acta Orthopod Scand 1985;56:404–06. Search PubMed

Monday, 30 March 2015

The Fallacy Of Neuropathy Cures

Today's post from (see link below) is written by a doctor who is as clearly irritated as this blog is, by claims that neuropathy can be cured thanks to one expensive treatment or another. He makes it quite clear that although certain treatments may reduce the effects of the symptoms, neuropathy can not be cured and as of March 2015 (date of this article) that remains the only truth that you can be certain of. Please don't buy into lurid advertisements that claim to be able to 'cure' your neuropathic condition - they can't and the best they may be able to offer is a reduction in the severity of your symptoms.

Confusion regarding neuropathy ‘cures’
By Dr. David Raynor Tuesday, March 10, 2015

Peripheral polyneuropathy is a condition that adversely affects nerves in the peripheral nervous system, which are all the nerves outside the brain and spinal cord. Podiatrists often see patients with peripheral neuropathy in the lower extremities.

The peripheral nervous system has two components. The sensory nerves transmit impulses from sensory receptors to the brain for processing. The motor nerves take impulses from the brain to create an action. Simply stated, sensory nerves are used to feel and motor nerves are used for movement. Peripheral neuropathy can affect motor nerves, but changes are mainly recognized by patients in the sensory nerves because they can feel that their sensation has changed and something “doesn’t feel right.” Patients may not readily notice weakness due to motor-nerve affects, as they may compensate to overcome slight deficits.

Sensory neuropathy symptoms can include exaggeration or diminished sensation of any type due to nerve damage. Common complaints are degrees of numbness or loss of sensation, burning, itching, stiffness and tightness. Pain from neuropathy can be annoying, severe or even debilitating in advanced cases. No one knows exactly what causes neuropathy, but diabetes is the most commonly associated cause, though many other causes exist.

Treating neuropathy symptoms can be difficult, as there is no cure. Unless the causative agent responsible for the neuropathy is cured, you cannot cure neuropathy. Neuropathy can be managed in certain cases, but not cured — regardless of claims made otherwise. Pain and annoying sensation from neuropathy can be managed in many cases with pharmaceutical agents, but no treatment exists to restore “lost” sensation. Pharmaceuticals do not cure or restore sensation, either. Oral or topical methods can effectively be used to reduce neuropathy symptoms to improve quality of life, but these need to be maintained and can have side-effects. Reduction to exposure damaging the nerves may temporarily improve symptoms, such as reeling in uncontrolled diabetes, but in truth the damage is done and symptoms will invariably return.

Neuropathy is unpleasant at minimum and can be debilitating in severe cases. Claims are made regarding surgery, therapy and medicinal options to cure or restore nerves. I know of no cure for neuropathy. Medicinal treatments to reduce symptoms from sensory peripheral polyneuropathy are the most potent or advanced treatments I know of to date.

David B. Raynor. DPM, is a podiatrist in Inverness and can be reached at 352-726-3668 or at with questions or suggestions for future columns.

Sunday, 29 March 2015

Restless Leg Syndrome Or Neuropathy?

Today's post from (see link below) looks at a question that confuses both patients and doctors alike and that is whether you have restless leg syndrome, or neuropathy, or both! Because the symptoms seem to be similar, it's sometimes difficult to distinguish between the two, although people with restless leg syndrom may argue that their symptoms are even more unique than those of neuropathy patients. Also, it may be technically true that RLS is a form of neuropathy in itself. Either way, it's a very annoying complaint and may be treated somewhat differently than 'normal' neuropathy. Your doctor should be able to help and refer you to a specialist if necessary. Useful article.

Is it restless leg syndrome or neuropathy?
Sharon M. O'Brien, MPAS, PA-C March 11, 2015 

Take the time to make the distinction between restless leg syndrome and neuropathy.

This week, a third patient came with a diagnosis of restless leg syndrome (RLS) when a more accurate diagnosis should have been neuropathy. Consequently, I thought I should try to clarify the difference between the two.

RLS is loosely defined as having pain in the extremities, especially during relaxation, that is eased by movement or walking. The symptoms are often characterized as "creepy crawling" or "jumpy legs" but are described as painful at times. However, there are more specific criteria that need to be met in order to make a diagnosis. (See below.)

Restless leg syndrome occurs in about 10% of the population and tends to run in families, so ask patients if anyone else in the family has similar symptoms or has been previously diagnosed with RLS.

The diagnostic criteria for RLS is defined in the International Classification of Sleep Disorders as follows: 

"The patient reports an urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs.
The urge to move or the unpleasant sensations begin or worsen during periods of rest or worsen during periods of rest or inactivity such as lying or sitting.
The urge to move or the unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity
The urge to move or the unpleasant sensations are worse, or only occur, in the evening or night.
The disorder is not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder."1

Neuropathy is described as burning, shooting, electrical, pins-and-needles type of pain in the extremities. This pain is usually not eased by walking, and many patients complain that movement makes the pain worse. This pain is generally present most of the time and does not change during particular times of the day.

What can make a diagnosis difficult is when a patient has neuropathy and RLS, as the two can occur together. RLS can also be seen in patients with kidney disease, Parkinson's disease, and iron deficiency. It is often seen in pregnancy and can be seen in patients taking antidepressants or antipsychotic drugs.

Besides the patient complaints, check a ferritin level in patients suspected of having RLS. Iron levels should be kept above 50 ng/mL in patients who have symptoms. Add iron if levels fall below. If this does not control symptoms, medications that can be helpful include ropinirole and pramipexole. I often try gabapentin for RLS, especially if there is a neuropathic component as this can help both.

The most important questions to ask your patients are:

When does the pain occur?
Does movement make the pain go away or feel better?

These questions will most likely help you with the diagnosis. In most cases, if the pain is occurring with inactivity, in the evening, and walking makes the pain feel better, then you are safe to assume it is RLS. If not, look for something else.

Have you had a difficult time distinguishing between RLS and neuropathy?

Sharon M. O'Brien, MPAS, PA-C, is a practicing clinician with an interest is helping patients understand the importance of sleep hygiene and the impact of sleep on health.


American Academy of Sleep Medicine. International Classification of Sleep Disorders, 2nd edition, pocket version: Diagnostic and Coding Manual. Westchester, Illinois: American Academy of Sleep Medicine, 2006.

Saturday, 28 March 2015

Autonomic Neuropathy: An Overview

Today's post from (see link below) is another overview of autonomic neuropathy. If your doctor has told you you may have autonomic neuropathy, you are probably experiencing symptoms in various parts of your body. These symptoms can affect the functions you normally take for granted and don't even think about and are very frustrating because many aspects of your daily life may be affected. These symptoms may also appear alongside the more easily recognised neuropathic symptoms involving your feet and hands. Getting as much information as possible is very important in helping you understand what's happening to you and you can find more articles about autonomic neuropathy by using the search facility to the right of the blog.

March 1, 2015 by Douglas Vansant Website:

Autonomic Neuropathy is a group of symptoms that occur when there is damage to the nerves that manage every day body functions such as blood pressure, heart rate, sweating, bowel and bladder emptying, and digestion.

Because Autonomic Neuropathy is a group of symptoms, not a specific disease. There are many causes.

Autonomic neuropathy involves damage to the nerves that carry information from the brain and spinal cord to the heart, bladder, intestines, sweat glands, pupils, and blood vessels.

Autonomic neuropathy may be seen with:
Alcohol abuse
Diabetes (diabetic neuropathy)
Disorders involving scarring of tissues around the nerves
Guillain Barre syndrome or other diseases that inflame nerves
Inherited nerve disorders
Multiple sclerosis
Parkinson’s disease
Spinal cord injury
Surgery or injury involving the nerves

Symptoms vary depending on the nerves affected. They usually develop gradually over years. Symptoms may include:

Stomach and intestines
Constipation (hard stools)
Diarrhea (loose stools)
Feeling full after only a few bites (early satiety)
Nausea after eating
Problems controlling bowel movements
Swallowing problems
Swollen abdomen
Vomiting of undigested food


Abnormal heart rate or rhythm
Blood pressure changes with position and causes dizziness when standing
High blood pressure
Shortness of breath with activity or exercise

Difficulty beginning to urinate
Feeling of incomplete bladder emptying
Leaking urine


Sweating too much or not enough
Heat intolerance brought on with activity and exercise
Sexual problems including erection problems in men and vaginal dryness and orgasm difficulties in women
Small pupil in one eye
Weight loss without trying


Signs of autonomic nerve damage are not always seen when your doctor or nurse examines you. Your blood pressure or heart rate may change when lying down, sitting, and standing.

Special tests to measure sweating and heart rate may be done. This is called “autonomic testing.”

Other tests depend on what type of symptoms you have.


Treatment to reverse nerve damage is most often not possible. As a result, treatment and self-care are focused on managing your symptoms and preventing further problems.

Your doctor or nurse may recommend:

Extra salt in the diet or taking salt tablets to increase fluid volume in blood vessels
Fludrocortisone or similar medications to help your body retain salt and fluid
Medicines to treat irregular heart rhythms
Sleeping with the head raised
Wearing elastic stockings
The following may help your intestines and stomach work better:
Daily bowel care program
Medications that increase gastric motility (such as Reglan)
Sleeping with the head raised
Small, frequent meals
Medicines and self-care programs can help you if you have:
Urinary incontinence
Neurogenic bladder
Erection problems


How well you do depends on the cause of the problem and if it can be treated.


Fluid or electrolyte imbalance such as low blood potassium (if excessive vomiting or diarrhea)
Injuries from falls (with postural dizziness)
Kidney failure (from urine backup)
Psychological/social effects of impotence

When to Contact a Medical Professional

Call for an appointment with your health care provider if you have symptoms of autonomic neuropathy. Early symptoms might include:
Becoming faint or lightheaded when standing
Changes in bowel, bladder, or sexual function
Unexplained nausea and vomiting when eating
Early diagnosis and treatment increases the likelihood of controlling symptoms.
Autonomic neuropathy may hide the warning signs of a heart attack. They are sudden fatigue, sweating, shortness of breath, nausea, and vomiting.


Preventing or controlling disorders associated with autonomic neuropathy may reduce the risk. For example, people with diabetes should closely control blood sugar levels.

Alternative Names

Neuropathy – autonomic; Autonomic nerve disease

Friday, 27 March 2015

How Spinal Cord Neurons Control Pain

Today's post from (see link below) is a very interesting look at a study which has identified nerve cells in the spine that regulate pain signals and determine whether they should be forwarded to the brain - like a sort of central sorting office for mail. It's called a 'gate control theory'. It's a fascinating read but it will take some considerable time before scientists will be able to manipulate these neurons by use of specifically delivered viruses and actively control pain in humans. Even itching may be able to be controlled by manipulating these nerve cells in the spine. Fascinating read.
Spinal cord neurons that control pain and itch
Date: March 19, 2015 Source:University of Zurich


The spinal cord transmits pain signals to the brain, where they are consciously perceived. But not all the impulses arrive at their destination: Certain neurons act as checkpoints and determine whether a pain signal is relayed or not. Researchers from UZH identified these neurons and their connections. Moreover, they developed means to specifically activate these neurons, which reduces not only pain -- but astonishingly also alleviates itch.

Sensing pain is extremely unpleasant and sometimes hard to bear -- and pain can even become chronic. The perception of pain varies a lot depending on the context in which it is experienced. 50 years ago, neurobiologist Patrick Wall and psychologist Ronald Melzack formulated the so-called "Gate Control Theory" of pain. The two researchers proposed that inhibitory nerve cells in the spinal cord determine whether a pain impulse coming from the periphery, such as the foot, is relayed to the brain or not. A team headed by Hanns Ulrich Zeilhofer from the Institute of Pharmacology and Toxicology at the University of Zurich did now reveal which inhibitory neurons in the spinal cord are responsible for this control function: As the study published in the science journal Neuron shows, the control cells are located in the spinal dorsal horn and use the amino acid glycine as an inhibitory messenger.

The pain gate can be manipulated with viruses

With the aid of genetically modified viruses, the research group from UZH managed to specifically interfere with the function of these neurons in mice. They discovered that disabling the glycine-releasing neurons leads to an increased sensitivity to pain and signs of spontaneous pain. Moreover, Zeilhofer's team developed viruses that enable these specific pain-control cells to be activated pharmacologically. Mice treated with these viruses were less sensitive to painful stimuli than their untreated counterparts. Activating these nerve cells also alleviated chronic pain. And the surprising additional result: "Evidently, the neurons don't just control pain, but also various forms of itch," explains Zeilhofer.

How light touch controls pain

One key aspect of the Gate Control Theory is that various influences can modulate the pain-controlling neurons' activity. Based on our experience from everyday life, for instance, we know that gently rubbing or holding an injured extremity can alleviate pain in this area. According to the theory, non-painful contact with the skin is supposed to activate the inhibitory cells. Sure enough, the UZH researchers were able to verify this hypothesis and confirm that the inhibitory, glycine-releasing neurons are innervated by such touch-sensitive skin nerves.

Moreover, the pharmacologists were able to demonstrate that neurons on the superficial layers of the spinal cord, where the relay of the pain signals takes place, are primarily inhibited by glycine signals. "These three findings identify for the first the neurons and connections that underlie the Gate Control Theory of pain," sums up Zeilhofer.

Targeted therapy in humans not yet possible

Can these findings be used to treat pain? "The targeted stimulation or inhibition of particular types of neurons in humans is still a long way off and might only be possible in a few decades' time," says Zeilhofer. Another way may well reach the target sooner -- namely via the receptors that are activated by the inhibitory neurons: "As these receptors are located on the neurons that relay pain signals to the brain, their specific pharmacological activation should also block pain," says Hanns Ulrich Zeilhofer. His group has already achieved promising initial results in this field, too.

Story Source:

The above story is based on materials provided by University of Zurich. Note: Materials may be edited for content and length.

Journal Reference:
Edmund Foster, Hendrik Wildner, Laetitia Tudeau, Sabine Haueter, William T. Ralvenius, Monika Jegen, Helge Johannssen, Ladina Hösli, Karen Haenraets, Alexander Ghanem, Karl-Klaus Conzelmann, Michael Bösl, Hanns Ulrich Zeilhofer. Targeted Ablation, Silencing, and Activation Establish Glycinergic Dorsal Horn Neurons as Key Components of a Spinal Gate for Pain and Itch. Neuron, 2015; 85 (6): 1289 DOI: 10.1016/j.neuron.2015.02.028

Thursday, 26 March 2015

ED Drugs To Treat Neuropathy

Today's post from (see link below) is the second article in two days about the potential benefits of Sildenafil for people living with nerve pain. It backs up yesterday's post with more information, presented in an easily understood manner. An interesting point is that many trial studies fail, or produce unsatisfactory results because the test subjects (frequently rodents) are mainly juvenile, when in fact in humans, neuropathy is often at its worst in later years. In the case of the sildenafil investigation, they used older mice to confirm results that had been seen in humans using viagra. It seems that sildenafil (main ingredient of viagra) may well improve neuropathic symptoms, possibly because of a better blood supply to the sciatic and other nerves.

Erectile Dysfunction Drug Relieves Nerve Damage in Diabetic Mice 
Released: 17-Mar-2015 Source Newsroom: Henry Ford Health System

Newswise — DETROIT – New animal studies at Henry Ford Hospital found that sildenafil, a drug commonly used to treat erectile dysfunction, may be effective in relieving painful and potentially life-threatening nerve damage in men with long-term diabetes.

The research targeted diabetic peripheral neuropathy, the most common complication of diabetes, affecting as many as 70 percent of patients.

The study was recently published online in PLOS ONE.

Lei Wang, M.D., the Henry Ford neuroscientist who led the research, said that although numerous drugs have been shown to be effective in earlier animal experiments, most have not provided benefits in clinical trials.

“Generally, young diabetic animals with an early stage of peripheral neuropathy are used to investigate various drug treatments,” Dr. Wang explains. “But patients with diabetes who are enrolled in clinical trials often are older and have advanced peripheral neuropathy.

“Failure to develop and properly evaluate treatments in the laboratory that properly reflect the target clinical population with diabetic peripheral neuropathy may contribute to the failure of clinical trials.”

To mimic clinical trials in which diabetes patients have advanced peripheral neuropathy, the Henry Ford researchers chose male mice with type II diabetes that were 36 weeks old, roughly equivalent to middle age in humans.

Earlier animal experiments from the Henry Ford group showed that sildenafil, commonly known by the brand name Viagra, improved blood supply to the sciatic nerve.

In addition, it was noted that diabetes patients who took Viagra for erectile dysfunction had fewer symptoms of peripheral neuropathy.

However, it was not known if this therapeutic effect held true for long-term peripheral neuropathy because the diabetic mice used in the previous experiments were relatively young – 16 weeks old.

So the Henry Ford researchers chose diabetic mice that were more than twice as old.

In one group, 15 such mice were treated with an oral dose of sildenafil/Viagra every day for eight weeks. A control group of 15 age-matched diabetic mice were treated daily with the same amount of saline.

After a battery of nerve and function tests were performed on both the drug-treated and control groups, results “revealed that sildenafil markedly improved sensory function starting at six weeks after treatment compared with saline-treated diabetic mice,” Dr. Wang says.

“These data indicate that sildenafil improves neurological function even in middle-aged mice with long-term diabetic peripheral neuropathy.”

While stressing that the findings remain experimental, Dr. Wang says they provide new insights into the underlying mechanisms of long-term diabetic nerve damage and may lead to the development of a sildenafil treatment for long-term diabetic peripheral neuropathy.

Diabetic peripheral neuropathy is particularly insidious because, as it progresses and damages nerves in extremities and other parts of the body, many patients are unaware of it because pain sensors are numbed.

As a result, a cut or sore on the bottom of a foot, for instance, may not be noticed until an infection sets in and spreads, possibly leading to amputation or even death.

Because diabetic neuropathy results from chronically high blood sugar levels, diabetes patients are strongly encouraged to closely monitor those levels and control them through diet.

Over-the-counter and prescription drugs – including antidepressants and opiates – are available to treat neuropathy pain, but often have undesirable side effects.

Wednesday, 25 March 2015

Erection Drugs Help Neuropathy!

Today's post from (see link below) is a rare neuropathy hot topic on the internet at the moment and one you may welcome as being something capable of killing two birds with one stone - if you're a man that is (for women, the benefits may only apply to their neuropathic problems). Basically, the theory is that sildenafil will improve blood flow to the nerves and by testing it on mature mice, it has been found that their neuropathic symptoms improved considerably. More information tomorrow.

ED Medicine Reduces Diabetic Nerve Damage in Animal Study
March 20, 2015 by Diane Fennell

The erectile dysfunction drug sildenafil (brand name Viagra) may be effective at relieving painful neuropathy, or nerve damage, in men with long-term diabetes, according to preliminary animal research recently published in the journal PLOS ONE. Approximately 60% to 70% of people with diabetes have some form of neuropathy, according to the National Institutes of Health.

In previous animal studies, sildenafil has been shown to improve blood supply to the sciatic nerve, which extends from the lower end of the spinal cord into the legs, and it has also been noted that people with diabetes taking the medicine have fewer symptoms of peripheral neuropathy (a type of nerve damage in the arms, legs, hands, and feet).

Many other drugs have been shown to be effective at relieving neuropathy in animal studies but have not demonstrated benefits in human trials. According to scientists at Henry Ford Hospital, this may be because these trials use young animals with an early stage of peripheral neuropathy, while most people used in studies of the condition are older and have an advanced form of peripheral neuropathy.

To better simulate the condition of participants in human trials, the researchers used 30 male mice with Type 2 diabetes that were 36 weeks old, which is roughly equivalent to middle age in people. Fifteen of the mice were given an oral dose of sildenafil every day for eight weeks, while the other fifteen mice served as a control group and were given the same amount of saline daily.

After performing a variety of nerve and function tests on both groups of mice, the researchers found that mice given sildenafil experienced noticeably improved neuropathy symptoms starting at six weeks after treatment compared with the mice that were given saline.

“Generally, young diabetic animals with an early stage of peripheral neuropathy are used to investigate various drug treatments. But patients with diabetes who are enrolled in clinical trials often are older and have advanced peripheral neuropathy,” notes lead study author Lei Wang, MD. “These data indicate that sildenafil improves neurological function even in middle-aged mice with long-term diabetic peripheral neuropathy.”

Although this line of research is still in the early stages, it has the potential to eventually lead to the development of a sildenafil-based treatment for long-term diabetic peripheral neuropathy, Dr. Wang added.

For more information, read the Henry Ford Health System press release “Erectile Dysfunction Drug Relieves Nerve Damage in Diabetic Mice” or see the study in PLOS ONE. And for more information about coping with painful neuropathy, see the article “Controlling Neuropathic Pain: Tips From an Occupational Therapist,” by Erica K. Jacques.

Tuesday, 24 March 2015

8-Gly Carb To Help Reduce Neuropathic Pain

Today's post from (see link below) talks about microglia, which are cells in the spinal cord that are responsible for releasing nitrous oxide when there's nerve damage. This nitrous oxide is partly responsible for the extent of your neuropathic pain at a later stage. Scientists have found a compound which (simply put) can inhibit nitrous oxide release and thus theoretically, reduce pain and other symptoms. The compound is called 6-chloro-8-(glycinyl)-amino-β-carbolin, or 8-Gly carb which hardly rolls off the tongue for patients but the name isn't important, its potential is. As usual, the end product is still somewhere in the future but every little snippet of news increases our general understanding of our condition and puts pressure on the relevant authorities to work as fast as they can to improve our lives with neuropathy.

UC Davis team finds a prime drug candidate for neuropathic pain  
February 10, 2015 | By John Carroll

Neuropathic pain has been linked closely to microglia, immune cells in the spinal cord which are known to release cytokines and other chemicals including nitrous oxide in the wake of peripheral nerve damage. A team of UC Davis researchers says that inhibiting nitrous oxide at the time that nerve damage is done could prevent neuropathic pain from occurring later. And they've found a compound that they say is very effective at doing just that.

The compound is 6-chloro-8-(glycinyl)-amino-β-carbolin, or 8-Gly carb, which belongs to a class of compounds known to blunt nitrous oxide. The
team says that this compound is significantly better at that task than any other known compound. And it appears to do its work without blocking cytokine expression.

Neuropathic pain often doesn't begin until well after physical trauma. And once it does begin it can linger for years as the brain is believed to be misinterpreting nerve signals from the site of the damage.

"A compound like 8-Gly carb that selectively targets nitrous oxide production and does not block cytokine expression makes a promising candidate for drug development aimed at preventing a neuropathic pain syndrome without interfering with recovery," said Fredric Gorin, professor and chair of the UC Davis Department of Neurology and co-principal investigator for the study.

Now new preclinical work is being planned that could set the stage for clinical studies.

- here's the release