Lifestyle and Neuropathy interview with an expert in the field

Okay, most HIV patients who also have neuropathy, try to change their lifestyle in some way, to try reduce some of the worst effects of the disease. That's normal; it's not obligatory, it's just a normal reaction to try something out if someone advises you that it will help...so how does a bad diet, drinking and recreational drug use affect people's neuropathy? These are just some of the questions in this interview for Aidsmap.com files (see link below) with Dr Hadi Manji, one of only a handful of neurologists in the UK with extensive clinical experience of HIV-related neuropathy.

ATU: How can you tell whether the neuropathy is caused by HIV or by the medicines used to treat it?

Dr Hadi Manji:The presentation of HIV neuropathy is very similar to drug-related neuropathy, but there are some clues to tell whether it is the drugs or not. Sometimes the drug-related neuropathies come on very rapidly, almost explosively.My impression is that drug-related neuropathies may also be more painful. And if there's involvement of the fingers, that, to my mind, would be more drug – than HIV-related.

ATU: How many people have both HIV and drug-related neuropathy together?

HM: In my experience, a lot of people – up to 60% – who develop neuropathy that is attributed to the drugs are still left with neuropathy when they stop the offending drug, despite some improvement. My feeling is that these individuals probably had asymptomatic HIV related neuropathy that was unmasked by the drugs.

ATU:What other factors can make neuropathy worse?

HM:The bottom line is, if you've got nerve -related problems for whatever reason – HIV or antiretrovirals – and you add another factor that damages nerves, you are more likely to cause further damage. For example, when I see patients, I ask about alcohol intake, because alcohol damages nerves, making you more vulnerable to neuropathy.

ATU: How much alcohol is too much?

HM: It would seem reasonable that anyone who drinks more than the recommended 21 units a week for men [14 for women] may be more vulnerable. It's impossible to be categorical about these things because the other factor in alcohol-related neuropathy is vitamin B deficiency due to poor diet.

ATU: Does that also mean that people who use recreational drugs, and have a poor diet, could get neuropathy?

HM:There's no evidence that recreational drugs themselves cause neuropathy. However, the poor nutrition that can accompany drug-taking could certainly be a factor, since it is deficiency of the B vitamins which is important for nerve function.The cause of neuropathy in people who eat badly for any reason is usually thiamine (vitamin B1) deficiency.

ATU:Would you suggest that people whose diet is likely to be poor, for whatever reason, supplement with a vitamin B-complex tablet?

HM: I think that's reasonable, but with a caveat. One of the B-complex vitamins, B6, if taken in excess, causes neuropathy. At one stage in New York, B6 overdose was a common cause of neuropathy, because people were taking too much in their supplements. It's also worth checking B12 levels if you're a vegetarian, or if you have chronic diarrhoea.

ATU:What else do you check for when you see your patients for the first time?

HM: Diabetes is a cause of neuropathy, so I always check my patients' blood sugar. I also check to see if there are any other drugs that could cause neuropathy. For example, isoniazid, which is used to treat TB, can cause neuropathy.

ATU: What about co-infection with hepatitis C?

HM: Although there is a mechanism by which hepatitis C can cause neuropathy, it is very rare. I haven't seen more neuropathy in coinfected patients.

ATU: Are all the d-drugs equally likely to cause neuropathy, and of all the HAART medications, is it only d-drugs that can cause neuropathy?

HM: Of the antiretrovirals, only ddC, ddI and d4T are associated with neuropathy.The others aren't. ddC used to be the worst offender, but use of that drug has reduced significantly. In fact, compared with the early studies, incidence of neuropathy from all of these drugs is reducing for two reasons. First, lower drug doses are being used. Secondly, people aren't quite so immunosuppressed when they start the drugs, so they don't run the risk of this asymptomatic HIV-related neuropathy, as it is less likely to occur in people with higher CD4 counts.

ATU: How do you treat people with neuropathy who have no option but to
remain on d-drugs?

HM: Often, if the person is doing well as far as CD4 count and viral load are concerned, both the patient and HIV doctor are not that keen on stopping the d-drug.You could consider reducing the dose of the offending drug, but then there are concerns about resistance. Otherwise, all we can do then is to control the symptoms by using other drugs to make life a bit more bearable.

ATU: Do you prescribe antidepressants?

HM: I think they have a role to play, so I wouldn't write them off completely. I tend to use one of the tricyclics, amitryptyline.The crucial
thing is to start at the lowest possible dose (10mg), since it causes drowsiness. However,this does work in the patients' favour,particularly if they take it at night, because they can get a decent night's sleep.

ATU: Given the promising pain-reducing qualities of smoked marijuana presented at the recent Retroviruses Conference, would you support its use in the UK?

HM: In terms of other neuropathies, I have had patients who have said that smoking cannabis may be helpful.These results from San Francisco are preliminary, and it's never been trialled in a formal setting. Since there is no definite evidence to its benefit, I currently wouldn't be able to recommend it.

ATU: Before HAART, about one third of people reported HIV-related neuropathy. Why hasn't the incidence of neuropathy decreased in the HAART era?


HM: It's a combination of people living longer, and use of the d-drugs.We may see even more neuropathies appear as people with HIV are living longer.This is because there may well be increased risks for other causes of neuropathy that we currently see in non-HIV peripheral nerve clinics – diabetes, for example. So, when doctors see patients who are ageing with HIV, they will have to consider not just HIV or the drugs they take, but the other causes, too.

http://www.aidsmap.com/files/file1000724.pdf

Neuropathy Images And Text To Make You Think

Today's post from recent posts on the Neuropathy Association's Facebook page (see link below) is nothing more than a series of images which may teach you something you didn't know about neuropathy. They are loosely based on the rarer neuropathies. Remember, there are over 100 different types of neuropathy although most people suffer from very similar symptoms, irrespective of the cause. These images may open your eyes to the variety of suffering that neuropathy can bring and you may have to Google a few terms to get an explanation but that's surely not too hard to widen your knowledge! Millions across the world suffer from debilitating nerve damage and we're nowhere nearer any sort of cure than we were 50 years ago!

Selected Neuropathy Association Facebook page Images
2014




Catching up on the Facebook chat is possible via the neuropathy association home page






















 https://www.facebook.com/NeuropathyAssociation

What Can Actually Happen To You If You Have Neuropathy

Today's post from neuropathytreatmentgroup.com (see link below) is actually an article attached to an advertisement for a neuropathy treatment and this blog does not support the treatment offered, nor any other form of advertising for so-called curative neuropathy products. Neuropathy is with you for life I'm afraid and all you can do is reduce the severity of the symptoms using chemical drugs or various alternative treatments and supplements. It can't be cured (at the moment), so please don't believe any website that tells you it can. HOWEVER, this article is packed with such useful and accurate information, I can only applaud the author and recommend the content to readers of this blog. It explains simply and clearly what can happen to you if you have neuropathy. Worth a read.

What No One Tells You About Neuropathy and Muscle Control
2016
 
Have you noticed your muscles acting a little strange since developing neuropathy? Perhaps they affect your ability to walk? Or maybe you find it difficult to use your fingers to pick something up? While we normally associated peripheral neuropathy with symptoms like pain, numbness and tingling – there are other symptoms as well.

The peripheral nervous system is made up of three different kinds of nerves: motor, sensory and autonomic. Each type of nerve controls different functions. Motor nerves send signals from the brain and spinal cord to your muscles – controlling motor functions like walking, dexterity and more. Sensory nerves do the opposite – relaying signals like temperature, pain, etc. from the muscles back to the brain and spinal cord. Finally, the autonomic nerves control involuntary or semi-voluntary functions like heart rate, digestion, blood pressure and more.

Peripheral neuropathy can affect some or all of these nerves. The symptoms you experience will depend entirely upon the type of nerve(s)that have been damaged as a result of your neuropathy. If your sensory nerves have been damaged you will experience symptoms such as pain, numbness, tingling or burning. Damage to the autonomic nerves can lead to problems with dizziness, sweating (either too much or too little), nausea, vomiting, diarrhea, constipation, difficulty urinating and more.

If your motor nerves fall victim to nerve damage – various motor functions can be affected. Lets take a look at five possible symptoms you might experience if your neuropathy has damaged your motor nerves:

Loss of balance and difficulty walking

Damage to the motor nerves can make walking difficulty. Your legs may feel heavy and difficult to move or you may feel constantly off balance. Since damage to the motor nerves disrupts the signals from your brain and spinal cord to the muscles – telling them what to do – even something as simple as walking can become a difficult task.

Damage to the sensory nerves can exacerbate this problem. The pain or numbness usually associated with damage to these nerves often affect the feet – making walking even more problematic.

For those suffering from symptoms related to motor nerve damage – extra caution should be used when walking on stairs or other areas where a fall risk is greater. Allowing extra time and avoiding rushing to perform tasks can also help limit your risk of falling.

Loss of Dexterity

Do you find it difficult to pick things up or use your hands to perform certain tasks? If so, that’s a sign your neuropathy has affected your motor nerves. Damage to the motor nerves can affect the ability of your brain to send signals properly to the muscles in your hands. You may notice somewhat delayed reactions in your hands or the muscles in your hands may feel weak – inhibiting your ability to perform even normal tasks like picking something up or moving your fingers.

Some common difficulties associated with loss of dexterity are inability to grip objects, loss of hand strength, difficulty writing or typing, difficulty performing tasks that require small movements, decreased reflexes and more. While you may not be able to restore complete control or strength to the hands – doing regular hand exercises can help you rebuild and maintain muscle strength and improve dexterity control.

Muscle Weakness; Deterioration

As damage to your motor nerves inhibits the ability of your brain and spinal cord to transmit messages to your muscles – you may find yourself limiting the use of your arms, legs, hands and feet. For many, this decrease in physical activity results in muscle deterioration and weakness. As the muscles deteriorate, you lose muscle mass and tone (this is often referred to as muscle atrophy).

Muscle weakness further contributes to the loss of dexterity, balance and difficulty walking previously mentioned. While exercise is often difficult and pain for those with neuropathy – there are low-impact exercises that will help you retain muscle mass and prevent muscle deterioration.

Try these 5 Low Impact Exercises for Neuropathy if you’re experiencing muscle weakness or deterioration!

Cramps; Spasms

The deterioration of muscle mass and the disruption of signals from the brain to the muscles can also lead to painful cramps, muscles spasms and twitches. For many, the cramping strikes at night and can range in severity from mild to extremely painful. In addition to cramping, many experience uncontrollable spasms or muscle twitching – which is visible just below the skin. While not as painful as cramps, they can be quite bothersome.

Loss of Muscle Control

As we’ve already touched on with the sections on loss of balance and dexterity – damage to the motor nerves affects your ability to control your muscles properly. The motor nerves carry messages from the brain and spinal cord to the muscles – telling them what actions to perform. As this line of communication is disrupted – the ability to control muscles is diminished. This is made manifest in loss of reflexes, inability to move hands or feet quickly, difficulty with fine motor tasks (i.e. buttoning a shirt, writing, etc) and more.

While the most common symptoms associated with peripheral neuropathy are pain, numbness, burning or tingling in the hands or feet – they are not the only symptoms. When the motor nerves fall victim to neuropathy the symptoms can go far beyond pain or numbness. They can affect your ability to control muscles and perform otherwise simple physical tasks. Though you may not be able to completely reverse these negative effects, alternative approaches like exercise can help you build and maintain muscle mass – thus helping to minimize the impact of motor nerve damage.

http://www.neuropathytreatmentgroup.com/what-no-one-tells-you-about-neuropathy-muscle-control/

Why Neuropathy Means Your Brain Cant Avoid Falls

Today's post from sciencedaily.com (see link below) is an interesting one for many people living with neuropathy, irrespective of their age. If you have nerve damage problems in your feet and legs, balance becomes an issue, not only with normal walking but also if you happen to trip and fall. The article suggests that the younger you are, the better your chances of recovering from the stumble and avoiding a bone-breaking fall but the older you are increases the risk of a serious injury from loss of balance. The science shows that it has to do with the brain's reaction times to threatening situations. When you're young, your brain identifies the risk and takes measures to avoid it and correct your stance before you fall, whereas older people have slower reaction times and often can't correct the situation in time. What isn't completely clear is if the nerve damage has anything to do with the 'slowing down' of the brain's reactions, or whether, like with other bodily functions, age simply means a reduction of all optimal functioning. Whatever the exact reasons are, the facts are obvious:- the older we are, the more likely we are to fall and break something after a neuropathy induced stumble. Can we do anything about it? Well, neuropathy patients are well-practiced in training their brain to concentrate at all times when walking but occasionally, the wrong signals the brain is receiving mean that an accident is almost inevitable. Whatever our age, with nerve damage you always have to be as alert as humanly possible. Lack of feeling, numbness, foot pain, burning and tingling and critically, misinterpreting signals we've grown up getting used to, make life with neuropathy a bit of a lottery. Avoiding broken bones is a daily objective for neuropathy sufferers and I don't think you have to be elderly to be aware of that!

For geriatric falls, 'brain speed' may matter more than lower limb strength 
Date:December 21, 2016Source:University of Michigan Health System 

Summary: It's not only risk factors like lower limb strength and precise perception of the limb's position that determine if a geriatric patient will recover from a perturbation, but also complex and simple reaction times, say researchers.

"Why does a 30-year-old hit their foot against the curb in the parking lot and take a half step and recover, whereas a 71-year-old falls and an 82-year-old falls awkwardly and fractures their hip?" asks James Richardson, M.D., professor of physical medicine and rehabilitation at the University of Michigan Comprehensive Musculoskeletal Center.

For the last several years, Richardson and his team set out to answer these questions, attempting to find which specific factors determine whether, and why, an older person successfully recovers from a trip or stumble. All this in an effort to help prevent the serious injuries, disability, and even death, that too often follow accidental falls.

"Falls research has been sort of stuck, with investigators re-massaging over 100 identified fall 'risk factors,' many of which are repetitive and circular," Richardson explains. "For example, a 2014 review lists the following three leading risk factors for falls: poor gait/balance, taking a large number of prescription medications and having a history of a fall in the prior year."

Richardson continues, "If engineers were asked why a specific class of boat sank frequently and the answer came back: poor flotation and navigational ability, history of sinking in the prior year and the captain took drugs, we would fire the engineers! Our goal has been to develop an understanding of the specific, discrete characteristics that are responsible for success after a trip or stumble while walking, and to make those characteristics measurable in the clinic."

Richardson's latest research finds that it's not only risk factors like lower limb strength and precise perception of the limb's position that determine if a geriatric patient will recover from a perturbation, but also complex and simple reaction times, or as he prefers to refer to it, a person's "brain speed." The work is published in the January 2017 edition of the American Journal of Physical Medicine & Rehabilitation.

"Our study wanted to identify relationships between complex and simple clinical measures of reaction time and indicators of balance in elderly subjects with diabetic peripheral neuropathy, nerve damage that can occur in those with diabetes," Richardson says.

"These patients fall twice as often as people their age typically do, so we wanted to examine each person's ability to make a decision in less than half a second, or around 400 milliseconds. Importantly, this is also about the length of time the foot is in the air before landing while walking, and about the time available to recover from a stumble or trip."

He realized they needed a new, easy way to measure that rapid decision-making ability.

Measuring simple and complex reaction time

Using a device developed with U-M co-inventors James T. Eckner, Hogene Kim and James A. Ashton-Miller, simple reaction time is measured much like a drop-ruler test used in many school science classes, but is a bit more standardized.

"The clinical reaction time assessment device consists of a long, lightweight stick attached to a rectangular box at one end. The box serves as a finger spacer to standardize initial hand position and finger closure distance, as well as a housing for the electronic components of the device," Richardson says.

To measure simple reaction time, the patient or subject sits with the forearm resting on a desk with the hand off the edge of the surface. The examiner stands and suspends the device with the box hanging between the subject's thumb and other fingers and lets the device drop at varying intervals. The subject catches it as quickly as possible and the device provides a display of the elapsed time between drop and catch, which serves as a measurement of simple reaction time.

Although measuring simple reaction time is useful, Richardson says that the complex reaction time accuracy has been more revealing. The initial set up of the device and subject is the same. However, in this instance, the subject's task is to catch the falling device only during the random 50 percent of trials where lights attached to the box illuminate at the moment the device is dropped, and to resist catching it when the lights do not illuminate.

"Resisting catching when the lights don't go off is the hard part," Richardson says. "We all want to catch something that is falling. The subject must perceive light illumination status and then act very quickly to withhold the natural tendency to catch a falling object."

In the study, Richardson and team used the device with a sample of 42 subjects, 26 with diabetic neuropathy and 16 without, with an average age of 69.1 years old, to examine their complex reaction time accuracy and their simple reaction time latency, in addition to the usual measures of leg strength and perception of motion.

They then looked to see how well these measures predicted one-legged balance time, the ability to control step width when walking on a hazardous uneven surface in the research lab and major fall-related injuries over the next 12 months.

Examining the results

In the subjects with diabetic peripheral neuropathy, good complex reaction time accuracy and quick simple reaction time were strongly associated with a longer one-legged balance time, and were the only predictors of good control of step width on the uneven surface. In addition, they appeared to identify those who sustained major fall-related injury during the one-year follow up. Surprisingly, the measures of leg strength and motion perception had no influence on step width control on the hazardous surface and did not appear to predict major injury.

"Essentially we found that those who were able to grab the device quickly, or quickly make the decision to let it drop, had quick brains that were somehow helping them stay balanced and avoid aberrant steps on the uneven surface," Richardson says.

He explains that the ability to avoid aberrant steps after hitting a bump while walking, and stay balanced while performing the trials, were likely based on the participant's brain processing speed. In particular, the ability to quickly withhold, or inhibit, a planned movement is required for good complex reaction accuracy and responding to a perturbation while walking. In both cases, the original plan of action must be aborted and a new one substituted within approximately a 400 milliseconds time interval.

"With this in mind, it makes perfect sense that brains fast enough to have good complex reaction time accuracy were also fast enough to quickly pay attention to the perturbation while walking, inhibit the step that was planned and quickly execute a safer alternative," Richardson says. "The faster your brain can oscillate between various external stimuli, or events, and your own internal thinking clutter, the better off you are. When an elderly person falls, it seems likely that their brain is not keeping up with what is happening and so it is not able to quickly, and selectively, attend to a particular stimulus, such as hitting a curb."

Richardson says this assessment, which cannot be produced from a computer or pen/pencil tests, could be valuable to other health care providers, such as primary care physicians, neurologists, geriatricians and a variety of rehabilitation professionals.

Story Source:

Materials provided by University of Michigan Health System. Note: Content may be edited for style and length.

Journal Reference:
James K. Richardson, James T. Eckner, Lara Allet, Hogene Kim, James A. Ashton-Miller. Complex and Simple Clinical Reaction Times Are Associated with Gait, Balance, and Major Fall Injury in Older Subjects with Diabetic Peripheral Neuropathy. American Journal of Physical Medicine & Rehabilitation, 2017; 96 (1): 8 DOI: 10.1097/PHM.0000000000000604

https://www.sciencedaily.com/releases/2016/12/161221090359.htm

Peripheral Neuropathy A Doctors Analysis

Ever wondered how the doctors or neurologists assess you and come to their conclusions? Today's post from medical-illness.blogspot.com (see link below) is a doctor's summary of a patient's condition after examination. His conclusion is neuropathy, probably caused by diabetes. It's interesting to look at this particular case study and see the bigger picture and maybe see similarities with our own general health. There may be a few warning pointers to look out for!
 

Diabetic Peripheral Neuropathy Personal history

Tuesday, November 4, 2014

 A known diabetic patient male patient, 46 years old, from ……….…., ………..……, married and has 3 off spring, the youngest is 16 years old, heavy smoker with no other special habits of medical importance, he is Rt. handed.

4 c/o
Loss of sensation in both hands and feet of 15 years duration.

4 HPI
The condition started 15 years ago by nocturnal burning painassociated with tingling, numbness started in both feet then progressed, one year later , to involve both hands then the patient developed gradual loss of sensation in both hands and feet, and he felt as if he walkedon cotton.
4 years later, the patient experienced weakness associated with flaccidity, falling of hair, brittle nails with no wasting or twitches. This weakness started in L.Ls then progressed, one year later, to involve both ULs. It's more in distal than proximal muscles, in extensor more than flexor muscles, in adductor more than abductor muscles. The patient also suffers from unsteadiness during eye closure with no involuntary movements.

The condition was associated with diminutionof vision, visual field defects, disturbance of color vision, ptosis in both eyes for which the patient was investigated and treated by laser photocoagulation more than once. The patient can't close his eyes firmly, with accumulation of the food behind both cheeks, no symptoms of other cranial nerve affection.
The patient has organic impotence with lost morning erection with no history of drugs known to cause erectile dysfunction.

The patient developed unsteadiness during standing with palpitation, nocturnal diarrhea, gustatory sweating and dyspepsia.

No symptoms of increased I.C.T.
No speech disturbance.
No symptoms suggesting other system affection.

4 Past history
- There is past history of D.M started 20 years ago manifested by polyuria, polydypsia, polyphagia. The patient is on insulin treatment and his blood sugar is out of control.

- There is past history of HPN started 15 years ago manifested by headache, blurred vision. The patient is on capoten and his hypertension is not controlled.
- Appendectomy operation was done at the age of 20 years.
- No history of other drug intake.
4 Family history
- No similar condition in family.
- No consanguinity.
- No common disease in family.

4 General exam
- Temperature: 37.2o c.
- Bl. Pressure: 140/80 (Recumbent position), 100/60 (standing position).
- Pulse: regular, 110 beat/minute, average volume, no special character, vessel wall not felt, equal in both sides with absent dorsalis pedis, anterior and posterior tibial and popliteal pulsation with intact femoral, radial, brachial and axillary pulsation.
- Mentality: The patient is fully conscious, well oriented for time, place and person. Average mood and memory. The patient is co-operative with average intelligence.
- Head: Examine for Retinopathy, teeth (Artificial teeth).
- L.L: Trophic ulcer, diabetic dermopathy.

4 Sensory:
- Superficial sensations: above knee and elbow level stock and glove anesthesia. Circumferential comparison must be done to exclude diabetic radiculopathy.
- Deep sensation:
§ Joint sense lost on both sides.
§ Vibration sense lost at level of peripheral nerve (medial malleolus, radial styloid process) with intact vibration sense at the level of posterior column (ASIS, clavicle).
§ Muscle sense lost (Calf muscles).
§ Lost nerve sense (Ulnar and lateral popliteal nerves).
§ +Ve Romberg's test.
- Cortical sensation : can't be examined due to loss of superficial sensation.

4 Examination of Speech: Normal.


4 Examination of Cranial Nerves:
- Optic Nerve is affected in the form of: diminution of visual acuity (Rt. eye : can count fingers at one meter, Lt. eye :blind), Tubular visual field defect .
- Ocular nerves
§ Inspection: bilateral ptosis (thumb test >> can't elevate his eye lids),pupils are dilated and irreactive to light or accommodation with no squint.
§ Power: loss of eyeball movements in all direction denoting paralysis of recti and oblique muscles of the eye.
N.B: nystagmus and conjugate eye movements can't be examined b because of loss of eye movements on examining each eye separately .
§ Reflexes: absent light and accommodation reflexes.
- Facial nerve
§ Inspection: symmetrical forehead, obliterated nasolabial folds on both sides with no tearing, no drippling of salive, no mouth deviation
§ Power: patient can't close his eyes firmly, can't elevate his eye brows , can't whistle, can't show his teeth, can't blow his cheeks
§ Reflexes: absent glabellar reflex à (bilateral LMNL).

4 Examination of Motor System :
4Inspection__
- There is wrist and ankle drop, trophic ulcer in L.L, loss of hair and brittle nail in U.L,L.L.
- No muscle wasting, no skeletal deformities, no involuntary movement.

4 Examination of Tone__
- Bilateral symmetrical hypotonia in both upper and lower limbs.

4 Percussion__
No fasciculation or myotonia.

4 Examination of Muscle Power
- Bilateral symmetrical Weakness in both upper and lower limbs. It is distal more than proximal, abductors more than abductors, extensors more than flexors.
- Abdominal muscles: weakness may be attributed to trunkal neuropathy or related to myopathy as the patient gives history of thyrotoxicosis.

4 Coordination
Coordination cannot be examined on both upper and lower limbs because of weakness.

4 Reflexes

- Deep reflexes: Areflexia in both upper and lower limbs.
- Superficial reflexes: lost plantar reflex in both L.L., lost abdominal reflex (trunkal neuropathy).
N.B: lost planter reflex may be due to loss on sensation on the sole of the foot, LMNL at S1, weakness in muscles of the big toe or skeletal deformities in big toe).

4 Back: No deformity, no swelling, no scars .
4 Gait: stamping (may be high steppage).
4 other system examination (search for autonomic neuropathy):

1- Cardiovascular system:
- Absent respiratory sinus arrhythmias.
- Persistent sinus tachycardia (already examined with pulse, and ask for palpitation).
- Painless myocardial infarction.
- Postural hypotension (already examined with pulse).

2- Genitourinary:
- Bladder disturbances (incontinence à ask for it)
- Impotence (psychic and organic à ask for it)

3- Marked sweating specially with meals (gustatory sweating à ask for it )


4- Gastrointestinal:
- Gastroparesis diabeticorum (ask for dyspepsia).
- Diabetic enteropathy (ask for nocturnal watery diarrhea and constipation).

4 pathogenesis
Sorbitol pathway.

4Investigation
- For diabetes: Bl. Sugar level with HBA1C, ECG, RFTs, blood lipid profile (cholesterol, HDL, LDL, TG)
- For P.N: Nerve Conduction velocity.

4 Treatment
- For diabetes: tight control.
- For the P.N.: Tegretol, gabapentin, vitamins, aldose reductase inhibitor
(disappointing results).


4 Diagnosis :
Diabetic Peripheral Neuropathy

4 N.B.

Lost abdominal reflex in this case may be due to trunkal neuropathy.
Abdominal muscles power can't be examined by resistance because of proximal myopathy à the patient has history of Thyrotoxicosis.
Lost knee reflex à not related to high stock level as lost superficial sensation has nothing to do with deep reflexes but is related to lost deep sensation at the level of the knee (evidenced by lost vibration sense at the knee and may be due to amyotrophy due to femoral neuropathy).
No muscle wasting à mainly sensory.

http://medical-illness.blogspot.com/2014/11/diabetic-peripheral-neuropathy.html

Neuropathy Management

Today's post from healthylifestyleplus.com (see link below) is a very simplistic introduction to neuropathy for those entirely new to the disease. It begs more questions than answers but that can be an encouragement to go on and do further research yourself, or have a list of questions ready for your doctor. Skimming through the alphabetical list to the right of this blog, will give you almost all the information you need until you are better acquainted with your own neuropathy situation.

Peripheral Neuropathy Treatment
Article by John Willhelm | March 7, 2013 |

A body can encounter trauma resulting in peripheral neuropathy which, simply stated, means significant damage to the nervous system.

When damage or trauma has been had to the nerve cells the body undergoes a lack of feeling and sensations where the trauma has occurred.

This disease is a heartbreaking one that can leave a person struggling to control the obsessive tingling in their feet and numbness in their hands.

Steps to Overcoming

Once thought to be a life changing and crippling disease, research regarding peripheral neuropathy has shown there are steps to overcoming the painful symptoms that comes with this painful diagnosis.

A Healthy Lifestyle

A healthy diet and lifestyle not only promotes good health but for those who have been diagnosed with diabetes maintain a healthy weight and regular exercise can prevent the onset of diabetic neuropathy. Selecting a healthy diet that is rich in antioxidants, low in fat and high in protein will help a diabetic reduce his or her chances of developing neuropathy in feet.

Avoiding Hazards

Peripheral neuropathy can be developed due to hazards that could have been avoided to some degree. Poisonous toxins such as alcohol, drugs and over usage of the vitamin B6 can lead to neuropathy when it could have been avoided.

Manage the Pain

Pain relief for tingling feet and numb feet is possible with some neuropathy treatment. Topical creams are available to help lessen the pain for a period of time as well as taking some form of prescribed medication has proven to be somewhat effective for short term relief.

Recent research has shown that a combination of vitamins, herbs, and Alpha-Lipoic can actually help restore the nerve damage and give longer lasting pain relief.

Peripheral neuropathy treatments are available you just need to explore your options and discover which treatment works best for you.

Getting Back to an Active Life

Just because you have been diagnosed with peripheral neuropathy does not mean your life is over and must end with this horrible bit of news. You can choose to embrace the diagnosis research treatment options and then get back to the active life you enjoyed before the pain took its toll.

Getting out and being active will only promote good health as you use your muscles and regain your movement.

http://www.healthylifestyleplus.com/body/peripheral-neuropathy-treatment/

Can Acupuncture Help with Neuropathy

Acupuncture is one of those treatments that divides opinion. Most people reason that if it has worked for thousands of years in Chinese medicine, it must be good. That may well be so and we've all seen the TV clips of operations undertaken with acupuncture needles but without anaesthetics but like any other treatment, alternative or otherwise, evidence-based proof is needed that it works when applied to nerve disease. Neuropathy is such a difficult affliction that even experienced Chinese doctor/acupuncturists admit that acupuncture is very much a hit and miss method as regards effectiveness in controlling neuropathic symptoms. Nevertheless, many people have found relief from acupuncture sessions. Today's enlightening post from Natural News.com (see link below) explains how Chinese medicine sees neuropathy and its potential treatment with acupuncture.
Although not normally done on this blog; the footnotes and references are added at the end to show that the article is based on research and not just alternative theory.

Acupuncture Treats Peripheral Neuropathy
Wednesday, May 06, 2009 by: Melissa Sokulski

Neuropathy, or Peripheral Neuropathy, is defined as having numbness, tingling or pain in nerves apart from the spine or brain, often in the hands and feet (1). It is a fairly common symptom, occurring in people with spinal injuries, diabetes, and genetic conditions such as Charcot-Marie-Tooth Syndrome (2,3). Acupuncture can be an effective way to treat these symptoms, bringing energy, life and feeling back into the extremities.

Neuropathy is a serious symptom, which often affects people`s quality of life. When people don`t feel parts of their bodies, they are more prone to injury and infection, as well as finding difficulty in daily tasks such as walking, fine motor work, or gripping. People who have this symptom as part of a genetic disorder also deal with the fears and hopes that go along with having a rare medical disorder(4).

Acupuncture is a powerful tool not only to balance qi - or energy - in the body, but to bring peace, hope and alignment into the mind, emotions and spirit as well.

When there is numbness in the periphery, there is not enough qi reaching these areas, according to traditional Chinese medicine. This can be for a variety of reasons, but mainly either:

1) there is too little energy in that organ system/meridian (energy pathway)

2) something is blocking the energy from reaching the area.

Sometimes there will be a combination of the two, and often multiple organ systems/meridians are involved. There are also different causes for the condition. Each of these things is considered and addressed by the acupuncturist, and a treatment plan which best suits the patient is mapped out.

In general, treatment would involve selecting points that promote circulation of energy in the meridians. If heat or cold is the cause, treatment would include either dissipating heat or warming coldness.(5)

Sometimes, weakness and flaccidity in the extremities is classified as wei syndrome. According to Traditional Chinese Medicine, this results from malnourishment of the tendons due to depletion of body fluids, caused by "excess heat" remaining in the body after illness.(6) Wei syndrome often requires longer periods of treatment.

Acupuncture often brings immediate relief - especially when there is pain - though it will likely take a series of treatments for the feeling and strength to come back completely and for the body to stay in balance, providing lasting effects. How often or how long treatment should proceed will be individual, depending on the cause and the overall constitution and health of the patient. As mentioned above, Wei syndrome can require a long course of treatment.

Acupuncture works by treating the person as a whole, balancing body, mind and spirit and allowing the body to do what it needs to do to heal itself. Acupuncture helps remove blocks, helps the body focus on increasing energy in areas of deficiency, and helps the patient be more present and focused, but ultimately it is our own bodies and energy that are able to heal.

Footnotes:
1) http://en.wikipedia.org/wiki/Neuropathy
2) http://www.medicinenet.com/peripheral_neuropathy/article.htm#1whatis
3) Charcot-Marie-Tooth Disorders (from CMT Facts III, Special Report, p.24):
- CMT is the most common inherited neuropathy, affecting about 125,000 Americans
- CMT is also known as peroneal muscular atrophy and hereditary motor sensory neuropathy
- does not affect life expectancy
- can vary greatly in severity, even within a family
- is the focus of significant genetic research
4) Flapan, Mark, p.10 of CMTA Special Report.
5) Xinnong, p.444
6) Xinnong, p.443

References:

CMTA Special Report: CMT Facts III. Published by Charcot-Marie-Tooth Association. 2700 Chestnut Parkway. Chester, PA. 19013.

Flapan, Mark. Living With A Rare Disorder: Hope and Fear. CMTA Special Report: CMT Facts III. Published by the Charcot-Marie-Tooth Association.

Maciocia, Giovanni. The Foundations of Chinese Medicine: A Comprehensive Text for Acupuncturists and Herbalists. Second Edition. Churchill Livingstone. 2005.

Xinnong, Cheng. Chinese Acupuncture and Moxibustion. Foreign Languages Press. Beijing. 1990.

http://www.naturalnews.com/026211_acupuncture_neuropathy_energy.html

Anodyne Therapy for Neuropathy

Today's post is from Podiatrytoday.com (see link below) and concerns, Anodyne therapy, a light-therapy treatment for neuropathy that you may have read or heard about. It's one of those things which has lots of claims concerning it's effectiveness but true, evidence based research is more difficult to find. If you feel that it may be something for you and you can afford it (it is generally not covered by insurance policies) then of course it may be worth a try. Remember however, to prepare for possible disappointment. It seems to work for some people but by no means all (something all too familiar for neuropathy patients!)

Is Anodyne Therapy The Answer For Peripheral Neuropathy?
Author: Brian McCurdy, Associate Editor

Peripheral neuropathy is prevalent among people with diabetes and has a strong correlation to the majority of diabetic foot ulcers and diabetes-related amputations. One potential option for helping these patients is Anodyne Therapy, a non-invasive treatment that has garnered praise in clinical studies and anecdotal kudos from podiatrists and their patients.
The device, which received FDA approval in 1994, reduces pain and increases circulation, according to the company Anodyne Therapy. How does it work? The Anodyne Therapy System uses monochromatic infrared energy (MIRE) to release nitric oxide from the patient’s red blood cells. The company says this improves nerve function and is important for making new blood vessels and healing wounds. As the company notes, “low levels of nitric oxide are common in people with diabetes and are a major factor in the poor circulation, loss of sensation, chronic falls, foot ulcers and pain of diabetic peripheral neuropathy.”

The manufacturer also emphasizes that Anodyne Therapy has been clinically proven to increase local microcirculation and reduce pain. It says there are several clinical studies that demonstrate significant clinical outcomes including restoration of protective sensation in patients with diabetic peripheral neuropathy, pain reduction, increased nerve conduction and faster healing of diabetic ulcers and other chronic wounds. Podiatrists also tout the product’s benefits.

What Podiatrists Are Saying
“We actually had very good results,” says Timothy Shea, DPM, a Certified Wound Care Specialist at the John Muir Wound Care Center in Walnut Creek, Calif. “So far, it seems to be a good, proven, acceptable modality which is useful for patients.”
Dr. Shea, an Adjunct Associate Professor at the California College of Podiatric Medicine, has used the Anodyne Therapy System as an adjunct to wound care. One of his patients had peripheral neuropathy that doctors could not diagnose and described his pain level ranging from a 7 or 8 to a 10 with 10 being the most painful. If he undergoes treatment at home, the patient said his pain level dropped to 2 or 3, according to Dr. Shea.
Anodyne Therapy says performing three treatments per week for 30 to 45 minutes in your office and having the patient follow up with a weekly maintenance program at home will yield the best clinical results.
Stephen Barrett, DPM, says some patients who are not surgical candidates for nerve decompression can get relief from the system.
“We’ve had some patients that have had extraordinary results,” says Dr. Barrett, a Fellow of the American College of Foot and Ankle Surgeons.“We’ve also had some patients that have had mixed results. Overall, it’s been a very beneficial thing.”
Dr. Barrett says he also has initial neurosensory documentation with the pressure specified sensory device, which has shown significant improvement in two-point static discrimination after 12 treatments.
Glen Robison, DPM, has used Anodyne Therapy on patients with diabetic neuropathy, plantar fasciitis, ulceration and other problems. After therapy, most patients have said they can feel their feet. He says 90 percent or more of diabetics who use the product find their neuropathic numbness reversed.
“The success was overwhelming,” says Dr. Robison. “I have a steady flow of diabetics and non-diabetics with neuropathy who have greatly benefited.”

Final Notes
The company offers two systems, the Anodyne Model 480 Professional System and the Anodyne Model 120 Home System. The only contraindications are for pregnancy and active malignancy, according to the company.
As far as drawbacks go, Dr. Barrett notes some reimbursement problems with the device and Dr. Robison says insurance companies do not cover it. However, the company notes the device recently received a specific Medicare HCPCS code of E0221 that should facilitate reimbursement from Medicare and other insurance carriers.

http://www.podiatrytoday.com/article/1404

How To Turn Neuropathy Lemons Into Lemonade!

Today's short post from tellingknots.com (see link below) comes from a blog written by a lady living in Jerusalem, Israel and is a humorous look at an incident in her daily life with neuropathy. If only more of us could be able to bring a smile to other people's faces in such a way, living with neuropathy may not be such a daily grind.

Lemonade: A neuropathy kitchen ballet in one act 
Telling Knots 30th July 2014

Hot day in July, time to make lemonade. Sugar, lemon juice and a little hot water are already mixed up in the bottle. All that remains is to pour the cold water through the funnel and fill the bottle. Pouring from a Brita water-filter pitcher into the funnel. Left hand somehow loses grip on the funnel. Right hand somehow flips off the top of the Brita pitcher. Water, water of blessing, water of life, cold wet water flows over the kitchen counter, over me, onto the floor, onto the other counter, onto the floor of the next room.

I had no idea how much area a liter of water can actually cover.

Then comes the cleaning up part. My balance isn’t great today, but I need to make a choice: toss the floor cloth down and sort of skate around on it to sop up the water? Get down on my hands and knees (which means getting up again) to clean it up?

I start with the skating method, lose my balance (not a huge surprise) and fall over into the water. Nice and refreshing on this hot summer’s day. Since I’m down there anyway, I stay down and finish the clean up. Finally I crawl over to the bed and use it to hoist myself back up.

Cool – I did floor exercises today.
(This post appeared in almost identical form on my Facebook page. It made people smile, so I decided to post it here, too.)

http://www.tellingknots.com/archives/3490

The Shoe Problem For Neuropathy Sufferers

Today's post from pamspaulding.net (see link below) is a personal story of a woman trying to find the best shoes to suit her neuropathy symptoms. Many people will identify with her problems and although the suggestions are of American shoe brands, it does highlight the fact that we need to find footwear that is both reasonably stylish and comfortable and supportive. That's not an easy task!

When you have neuropathy-damaged feet, good (cute) shoes are hard to find. 
Posted by Pam Spaulding Saturday, June 8, 2013

 The stereotype is that lesbians wear "comfortable" shoes, as in unfashionable, or maybe work boots, I have no idea.

 Anyway, this lesbian has serious neuropathy in both feet. I've had insulin-dependent diabetes for 30 years, and thankfully my eyes and kidneys -- usual targets of long-term damage -- are fine, unfortunately the feet are what took the damage. My blood sugars have been in good control, but it's hard not to have some long-term effects having diabetes for this long. BTW, it runs on both sides of my family -- both of my parents had adult-onset but were not obese. My brother is fine; I seemed to be the one to get all of the horrid metabolic and immune disorders passed down. Even my RA, according to my rheumatologist, was spawned through the genes; my mom had sarcoidosis, which is in the same auto-immune family.

 Anyway, it's hard to describe what neuropathic pain feels like -- it's simultaneously numbness paired with extreme sensitivity at times to the touch, such as feeling like you're walking on hot coals, or someone is stabbing you with little knives on the soles of your feet. The duality of this is both frustrating and annoying because it can ramp up at any time. The worst-case scenario is an attack of it at night -- I've had pain so bad that even having the sheet touch my feet under the covers was excruciating.

 On the other hand, my feet are nearly completely numb to hot or cold, which can be dangerous. Burning hot water feels only warm on them; ice barely registers as cold. The numb aspect also makes it easy to slip in the shower, since my feet don't have the correct sensation to grip the wet floor well. I have to have bath mats all over the floor to make it to my slippers.

 One of the few topical things that help is capsaicin, derived from hot peppers. Mostly this is used by folks with osteoarthritis. In treating neuropathy, the heat sensation generated by it cancels out/breaks up the neuropathic signals causing the pain. Kate tried using it on a sore muscle and she couldn't bear the burning sensation; I barely feel anything warm on my feet, but after about a half-hour, some of the worst burning subsides and I'm able to finally sleep.

 But back to shoes... 

 Almost all my old shoes -- nice dress shoes, sandals -- had to be tossed out over the last couple of years because they either 1) hurt my feet by causing neuro-pain, or 2) didn't provide enough shock absorption to prevent knee and hip pain that I have from RA. What's left to wear? Well, lots of styles that look like Grandma Shoes. At this point, the only brand I trust to be comfortable are Easy Spirit's Athletic family. At least they come in all sorts of cool colors and styles.

 I took a risk on one shoe that looked kind of cool -- the Naturalizer BZees Mary Jane (right). While they aren't dress shoes or sneakers, they fall into middle ground for me. I'll wear these to work or out on the weekend. I've learned that comfort comes before style at this point. It's really not a choice.

 One of the brands that up until this about a year ago that I could reliably trust were Jambus and J-41s. I wore one pair last week and boy did I pay for it. They seemed comfy enough -- they have memory foam insoles -- but the next day my left knee and hip hurt so bad that I was limping for two days. I had to fall back on my trusty Easy Spirit Mary Janes to get enough support and shock absorption. I was crestfallen. I love those J-41s. I wanted to make a bargain with myself that I can still wear them in some limited way...oy.


 http://www.pamspaulding.net/2013/06/when-you-have-neuropathy-damaged-feet.html

Why Is An Idiopathic Neuropathy Diagnosis A Problem

Today's longer post from neuropathysupportnetwork.org (see link below) is written by Lt Col Eugene B Richardson, who is a well-known and respected activist when it comes to dealing with neuropathy, especially when related to agent orange. Here he discusses the diagnosis 'Idiopathic neuropathy' which basically means that they cannot identify or trace the origin of your neuropathy. The problem is, that this can then encourage assessors to see your neuropathy as being more psychosomatic than genuine. Lt Col Richardson quite rightly takes them to task for this and again quite rightly insists that just because doctors haven't got a good enough testing system to accurately test for the cause of the nerve damage, doesn't mean that the nerve damage is in any way lessened for that. There are descriptions of a person's neuropathy that are far more accurate than just 'idiopathic'. The type of neuropathy can be identified and named, it's just the cause that can't be definitively established. This article is useful reading for everybody who is living with neuropathic symptoms - definitely worth a read.
 

The Problem with a Diagnosis of Idiopathic Neuropathy!
Posted November 15th, 2013 by LtCol Eugene B Richardson, USA (Retired) BA, MDiv, EdM, MS 

 Idiopathic Neuropathy according to medical experts writing in the Journal of the Peripheral Nervous System should be considered as a disease entity in and of itself. It is recommended that this condition be diagnosed as Chronic Idiopathic Axonal Polyneuropathy or (CIAP) as a major health problem. (See reference 1.)

I would ask, what does the word ‘idiopathic’ add to this diagnosis? Why not Chronic Axonal Polyneuropathy or (CAP)?

With the greatest of respect for the writers of the article, following forty-four years of living with neuropathy , a diagnosis of idiopathic neuropathy is a ‘failed diagnosis’ given the diagnostic tools and information medicine has available in 2013. Having been at the receiving end of idiopathic, primarily due to limited clinical skills or failed testing and/or failed interpretation of these tests by the experts, in my view and that of many patients the use of idiopathic in diagnosis fails the patient and doctor.

Read on to understand your patient mission: Help influence better awareness, clinical thinking and knowledge about Peripheral Neuropathy and the available tests in the health care system by learning, sharing documents, information, sources, and asking good “I” questions of your doctor. Become a partner in your own health care and a facilitator of change. In the process you may even get the help you need for your neuropathy.

We patients understand that there are NO tests to diagnose Peripheral Neuropathy per se, as this must be done based on the patients symptoms and medical history. The available tests can only either rule out a cause for the symptoms or confirm that damage has been done to the large or small fiber nerves.

However, failure to find either a cause or damage does not rule out a neuropathy. The symptoms of Peripheral Neuropathy are often present without the damage to the axon (nerve) or myelin (nerve covering) as that may occur later in the course of the disease. It is this focus in searching for a cause that sets the patient and doctor up for a diagnosis of idiopathic. As noted below, medical science does not know the cause for many diseases, yet they do not use the term idiopathic!

If you read the transcript of a recent Facebook chat on Idiopathic Neuropathy lead by Dr. Shanna K. Paterson it highlights a serious problem in using such a diagnosis as every patient question and the doctor’s excellent responses are focused on getting a “real” diagnosis and “real help” for the symptoms of peripheral neuropathy. (Dr. Paterson is the Assistant Clinical Professor of Neurology at Columbia University Medical College and Neurologist at St. Luke’s Roosevelt Hospital Center).

Medical experts must be trained to adequately interpretation the available tests whether it be the EMG, nerve conduct test, skin biopsy, blood work, spinal tap, evoked potentials, doctors examination, and the patients’ medical history of symptoms.

Understanding the results and meaning of these tests and information, combined with patient medical history often point to a more precise diagnosis, possible treatment options or at a minimum an idea that might help the patient.

I always loved Mims Cushing’s’ definition of idiopathic. In her book You Can Cope with Peripheral Neuropathy she defines it as being “idiot” for ‘idio’ and “pathetic” for ‘pathic’. In fact this bit of harsh humor hits the nail right on the head.

From the real world of the neuropathy patient it is difficult, with all due respect to health care professionals, to not agree with Mims definition of the term.
 
Idiopathic to doctors of course means of “unknown cause” and is a legitimate word when seeking the cause of some disease, but it is never used in MS or cancer and other ‘recognized or accepted’ diseases when the cause is not known! Why? Does research not focus on the cause of all disease to find answers that we still do not have?

The other issue is that for lawyers’ idiopathic means “no objective proof of a problem” providing the foundation for legal denial of help for the patient. Talk about frustrated patients! In both situations, this leaves the neuropathy patient without help that may be possible with a more precise diagnosis.

Medicine must cease at the clinical level the focus on neuropathy as simply a component of another disease. Peripheral Neuropathy must be acknowledged as a disease entity in and of itself, a disease of a major system of the human body.

Based on the available tests the doctor should be able to diagnose any of the following rather than fall back on the term Idiopathic Peripheral Neuropathy.

Examples to name a few, without including the word “idiopathic” which adds nothing but uncertainty, would include the following. You can add acute (two months) or chronic (beyond two months) or progressive (remits and relapses with increasingly worse symptoms) to any of these focused findings. While not exhaustive this list will provide you with the point being made.

peripheral neuropathy or polyneuropathy
axonal neuropathy or polyneuropathy
sensory neuropathy or polyneuropathy
motor neuropathy or Multifocal Motor Neuropathy
sensory/motor neuropathy or polyneuropathy
immune mediated neuropathy or polyneuropathy
large fiber neuropathy or polyneuropathy
small fiber neuropathy or polyneuropathy
autonomic neuropathy
autoimmune sensory neuronitis
entrapment neuropathy (carpel tunnel syndrome) (common in diabetic and immune mediated neuropathies)
Guillian Barré Syndrome
Distal Symmetric Polyneuropathy
Chronic Inflammatory Demyelinating Polyneuropathy and variants

Or when there is a possible suspected cause of the neuropathy:

Diabetic neuropathy
Celiac neuropathy
Chemotherapy/Radiation induced neuropathy
Neuropathy in a nutritional deficiency
Neuropathy in alcoholic abuse
Hereditary or genetic neuropathy
Neuropathy in Agent Orange exposure***
Toxic neuropathy
Drug induced neuropathy
Entrapment neuropathy
Neuropathy with IgM Monoclonal Gammapathy
Vasculitic neuropathy
Neuropathy in AIDS
Neuropathy in Lyme Disease
Diphtheric neuropathy
Sarcoid neuropathy
Neuropathy in cancer
Paraneoplastic neuropathy,
Neuropathy in myeloma or POEMS
Neuropathy in amyloidosis

(* **Supported by the findings of the Institute of Medicine in 2010 and confirmed by the Veterans Affairs Administration law in 2012 as presumptive to Agent Orange exposure. For guidance in submitting a claim to the VA go to this link: http://neuropathysupportnetwork.org/blog/2013/01/guidelines-for-veterans-va-proposed-law-agent-orange-and-peripheral-neuropathy/#more-1086 and send an E Mail to gene@neuropathysupportnetwork.org for more guidance.)

When left with a diagnosis of Idiopathic neuropathy, the patient is left without affirmation that is important in the strange world of neuropathy symptoms, robbing patients of self-esteem.

To name something that is real to the patient, is to provide an emotional/cognitive handle on the strange world of the neuropathy patient and their families.

From the experience of some neuropathy patients, a diagnosis of idiopathic often results in a not too subtle a suggestion that the patient has a mental illness (since all tests are normal and there is no cause in must be mental) and the statement is used as a club against the patient to send them on their way. Many neuropathy patients have been here including me.

I even remember the doctor in the military who asked me, “Why do you want something wrong with you?” when he said, “All tests are normal.” It was easier to attack the patient than acknowledge a lack of clinical knowledge and skill or that all they had determined was that these tests were normal, nothing more.

Even more shocking, an esteemed teaching neurologist at a major University Neuropathy Center in 2001 noted that the patient had reflexes upon compression. He then dismissed the obvious diagnosis, attacked the patient by writing in the medical record “patient is claiming to have something they do not have”, without knowing that sometimes reflexes are absent, sometimes they are diminished, and sometimes they are normal. He ignored all the objective tests to reach this conclusion and he is a highly respected teacher of neurology.

The impact on reflexes is hardly a standard on its own for the clinical diagnosis for the neuropathy patient and to ignore the actual results of the objective testing that was done and the long medical history was incompetence at the highest level.

To further frustrate the patient, if an employer finds about such a diagnosis, this can cost the employee their career. Been there and done that in my military and civilian career with supervisors who wanted to play doctor? Since the cause is unknown, it must be failure to handle stress both supervisors concluded.

Understand I did not receive even a diagnosis of idiopathic in the 1970’s all the way to 1999, so maybe with this use of idiopathic for a diagnosis, we patients can celebrate progress?

A diagnosis of Idiopathic neuropathy misses the clues of what might be done for the neuropathy, as options to consider are lost. It too often shows that the doctor does not have the clinical expertise to read the tests with current knowledge about neuropathy. This diagnosis fails the patient clinically in both diagnosis and any possible treatments or responses to the neuropathy.

Medicare in 2013 still leads the way in supporting the dismissal of neuropathy by not paying for the blood tests that a doctor orders under the neuropathy profile!

POINT: The real value of this chat on Idiopathic Neuropathy is that it raises the question as to why do we need such a diagnosis, when testing in 2013 combined with the patients’ medical history, a more precise and helpful diagnoses is possible, even if “chronic axonal neuropathy” is used?

The Peripheral Nerve Society has developed a great source of reliable information and challenges via their journal and other experts have done the same. (See the Journal of the Peripheral Nervous System.)

Have you ever heard of idiopathic cancer? How about idiopathic MS or idiopathic Alzheimer’s? Okay, with MS there are liaisons on the brain so there is a test to confirm the diagnosis, but there is no focus on the cause. With cancer the same is true, but with Alzheimer’s the symptoms are there as in PN, but tests are not available to actually confirm the diagnosis until autopsy. So the real problem is that we do not have an actual test to diagnose Peripheral Neuropathy so we focus on CAUSES.

Over the year’s comments such as peripheral neuropathy is best thought of as something caused by other disease processes and therefore is not really a disease encourages the wrong focus. Every disease is caused by or involves other disease processes and these ‘accepted’ diseases do not use the term idiopathic even when our knowledge is limited or absent.

There are many diseases for which we do NOT understand or fully understand the cause or causes and that are caused by or involve other disease processes.

As Dr. Thomas Brannagan of Columbia University states, the simple reason is that too many health care professionals do not have the clinical training for the proper diagnosis and treatment of the neuropathies.

The challenging question is, “Why not train them?”

I recently went on several health care websites and with very few exceptions, every major disease is listed, but there are too many who do not even list Peripheral Neuropathy and I struggled to have these sites to consider listing it when there are more patients with Neuropathy than MS. They always list MS. Why? (See the Journal of the Peripheral Nervous System Vol.17, Supplement 2, at Page 44 top left hand column.)

So why is idiopathic neuropathy even necessary when a more helpful diagnosis is possible when a trained physician knows how to use and interpret the EMG, the Nerve Conduct Study, the spinal tap, the nerve/muscle biopsy, the blood work, a skin biopsy, a genetic test, and actually think about the subjective information provided in the patients’ medical history?

Dr. Norman Latov of Weil Medical College at Cornell University, shared in 2006 that for “one quarter to one-third of patients, no cause can be found and the neuropathy is called “idiopathic.” He notes that these are usually “axonal and may be sensory or sensorimotor” and “classified according to the clinical presentation”, with “therapy primarily symptomatic.” But again, I ask, why refer to them as idiopathic with the strong focus on the cause for peripheral neuropathy when this is not true of other accepted diseases processes for which we often do not have a cause?

Why not think out of the box with trial treatments such as was suggested in the article years ago in the use of IVIg? I suffered for decades and then years while a doctor with limited clinical skill thought all neuropathy patients MUST have diabetes and others used the term idiopathic. My disease was a form of CIDP and the treatment was IVIg. What other trials of treatment are available given a general idea of what is happening in the neuropathy patient?

Patient Challenge:

I strongly recommend that patients never rest on a diagnosis of “idiopathic” neuropathy, as in the experience of many neuropathy patients, it means someone may have failed to do the diagnostic work and/or does not understand the meaning of the tests we do have available. For me such thinking resulted in my severe disability and unbelievable suffering without support over decades with failed diagnosis and lack of thinking outside the box.

I remember the neurologist who was not clinically trained who wanted in a desperate way to make me a diabetic while resting on idiopathic. He delayed treatment another four years until I gave him the article on a trial of IVIg that worked for me. He was not aware of the usefulness of the spinal tap for such a neuropathy 2004. Then in 2005 for the first time my doctor, Dr. Waden Emery III, Neurologist in Lighthouse Point, Florida asked, “Why did they not do a spinal tap?” Limited clinical training!

In 2013 military veterans who are seeking help were told by VA doctors and claim reviewers that unless they are diabetic they cannot have Peripheral Neuropathy! This is frightening clinical misinformation for these patients.

You may want to provide the doctor with a copy of the document recently published in Neurology Today, March 15, 2012, volume 12(6); pp 30, 32-33 by Mark Moran. Read the entire article at: How to Diagnose Peripheral Neuropathy? No Simple Answers Unfortunately, this great article does fail to mention the diagnostic value of the spinal tap, a procedure that would have resulted in my earlier treatment years before my disability was serious. If you want a copy of this document, send an e-mail to gene@neuropathysupportnetwork.org

If you want a good description of the symptoms and causes of Peripheral Neuropathy, read Dr. Norman Latov’s book (Listed on the Resource Tab) or go to these articles including linking to the website of the National Institute of Health. Give this information to the doctor if needed. Click here for the Link to the NIH:

Click here for the article on the NSN website:

Well, the Doctor may be insulted or get angry.

Yes, it may take a bit of skill using “I” messages such as “I wonder if it would be helpful to _____?” rather than ‘you’ messages to the doctor. ‘You’ messages are usually rejected and making the person defensive while ‘I’ messages sets the person free while stimulating thinking! This is true even if the thinking occurs after your appointment is over.

I remember when the military Men of the Chapel went fishing to catch sea bass off of Baltimore one year and we brought the large catch of fish to shore and gave it to the Priest who was feeding the poor of the city. In his office was a sign that read, “I give you fish and you sell fish. I am angry. So I refused to give you fish because you sell them. You are angry. Better you angry”.

Your mission: Help influence better awareness, clinical thinking and knowledge about Peripheral Neuropathy and the available tests in the health care system by learning, sharing documents, information, sources, and asking good “I” questions of your doctor. Become a partner in your own health care and a facilitator of change. In the process you may even get the help you need for your neuropathy.

REFERENCES:

Reference 1: Journal of the Peripheral Nervous System, Vol. 17, suppl. 2, Page 43-49 “Idiopathic Neuropathy: New Paradigms, New Promise”, 2010 and other issues of this scientific journal of the Peripheral Nerve Society.

Reference 2: Peripheral Neuropathy: When the Numbness, Weakness, and Pain Won’t Stop, by Norman Latov, MD PhD, AAN Press 2007. (Order from amazon by clicking here:).

Reference 3: “How to Diagnose Peripheral Neuropathy? No Simple Answers: Experts Offer Some Guiding Principles”, in Neurology Today, March 15, 2012, volume 12(6); pp 30, 32-33 by Mark Moran. (Send E Mail to gene@neuropathysupportnetwork.org)

Reference 4: Peripheral Neuropathy: A Practical Approach to Diagnosis and Management by Dr. Didier Cros, M.D. Editor, Lippincott Williams & Wilkins published 2001

Reference 5: You Can Cope with Peripheral Neuropathy: 365 Tips for Living a Full Life, by Marguerite (Mims) Cushing (Neuropathy Patient) and Dr. Norman Latov, MD, PhD, published 2009. (Order from amazon by clicking here:).

Reference 6: “Sick and Tired” Part I and 2, Season Five TV show, The Golden Girls.(Order from amazon by clicking here:). 

PATIENT TO PATIENT – Disclaimer: Patient to Patient articles are educational, not diagnostic or prescriptive and the patient is encouraged to seek help from their own private physician.

Copyright 2013: Network for Neuropathy Support, Inc., dba Neuropathy Support Network.

http://neuropathysupportnetwork.org/blog/2013/11/the-problem-with-a-diagnosis-of-idiopathic-neuropathy/

Optical Neuropathy And HIV

Today's post from sajhivmed.org.za (see link below) is a South African case report regarding optical neuropathy associated with HIV. Optical neuritis is one of the less well-known forms of neuropathy but it does occur quite regularly in third world countries as well as elsewhere and quite often amongst those living with HIV. This article looks at case studies as well as giving some guidance as to how these were treated. Everybody living with neuropathy has to understand that neuropathy is nerve damage of one sort or another and that damage doesn't always result in symptoms of the feet, legs and hands but can affect many other parts of the body too. It's always interesting to widen our knowledge of the scope of neuropathy and read about the more unusual of the more than 100 different types of the disease.

CASE REPORT
SUCCESSFUL TREATMENT OF BILATERAL VISUAL LOSS CAUSED BY IDIOPATHIC OPTIC NEURITIS IN AN HIV-INFECTED PATIENT  
Claire Cullen¹, MB BCh, FCOphth (SA), MMed (Ophth)

Baile Matlala¹, MB ChB, FCOphth (SA), MMed (Ophth)

Fatima Laher² ³, MB BCh, Dip HIV Man (SA)

Ané Pienaar¹, MB ChB, MMed (Ophth)

¹Department of Ophthalmology, Dr George Mukhari Hospital, University of Limpopo, Ga-Rankuwa, Gauteng

²Perinatal HIV Research Unit, University of the Witwatersrand, Johannesburg

³Wits Donald Gordon Medical Centre, Johannesburg

Optic neuritis is not an uncommon diagnosis in HIV-infected patients, but it is rarely idiopathic. We report a case of a young HIV-infected woman who developed optic neuritis as her presenting manifestation of HIV infection. She had initially experienced sudden-onset right-sided painful visual loss; the left eye had become involved within days. Bilateral swollen discs were apparent on fundoscopy. Investigations were performed for meningitis (including bacterial, cryptococcal, tuberculous and syphilitic types), auto-immune diseases, toxoplasma, rubella, cytomegalovirus, viral hepatitis, HTLV-1/2, HIV-1/2 and syphilis. The only positive result was a reactive HIV enzyme-linked immunosorbent assay. The CD4 count was 85 cells/µl. A post-contrast magnetic resonance imaging scan of the brain illustrated enhancement of the optic nerves. Treatment was 3 days of intravenous methylprednisolone
1 g daily, followed by 11 days of oral prednisone 60 mg daily. Highly active antiretroviral therapy was initiated after 2 weeks. Vision improved from day 6 after commencement of steroid therapy, with ongoing recovery at 5 months.

The human immunodeficiency virus (HIV) manifests in various ways in the eye. Several optic nerve disorders have been described, most commonly resulting from opportunistic infections, neoplasms and inflammatory causes.1 HIV infection as a direct cause of optic neuropathy has been postulated. It is an uncommon presentation and a diagnosis of exclusion, with only a few case reports and case series in the literature. Mwanza et al. describe a sub-group of neurologically symptomatic HIV-infected patients from the Democratic Republic of Congo: optic neuropathies occurred in 31%, although only 7% of cases were ascribed solely to HIV.1 We present a case of idiopathic optic neuritis in an HIV-infected person.

CASE PRESENTATION

A 26-year-old South African woman presented to the ophthalmology clinic of Dr George Mukhari Hospital in Ga-Rankuwa, Gauteng, on 6 January 2009. Her main complaint was a 1-week history of sudden-onset, painful visual loss that had originated in the right eye and had progressed over a few days to include the left eye. She described the pain as being ‘deep within the eye’ but unrelated to eye movements. On the second day she had attended her local community clinic, where she had been dispensed chloramphenicol eye ointment, which did not improve the condition.

There was no history of trauma. Her medical, surgical, ophthalmological and family histories were otherwise unremarkable, and she was not receiving any other medications.

General examination revealed a well-looking young woman. Her vital signs, including blood pressure, were within normal limits. Visual acuity of the right eye was recorded as counting fingers at 1 metre (less than 6/60), and testing with a Snellen visual acuity chart showed that of the left eye to be 6/60. A relative afferent pupil defect was present in the right eye. Extra-ocular movements were full and painless. On fundus examination, bilateral swollen optic discs with flame-shaped haemorrhages were apparent (Fig. 1). There were no cotton wool spots and no macular star in either eye. The cornea, anterior chamber, vitreous and retina were normal, as were intra-ocular pressure readings.

Optical coherence tomography objectively documented bilateral swollen optic discs (Fig. 2). Fluorescein angiography showed hyperfluorescence of the optic discs (Fig. 3).

The chest radiograph was normal. Although there were no unusual findings on computed tomography scanning of the brain, a magnetic resonance imaging scan of the brain illustrated enhancement of the optic nerves post-contrast. There were no periventricular plaques and no other abnormalities were noted.

Lumbar puncture was performed and the opening pressure was noted as being within normal range. Cerebrospinal fluid chemistry and cytology were normal. Gram stain and bacterial culture, India ink and latex antigen tests for Cryptococcus neoformans, CSF adenosine deaminase (ADA) for tuberculosis and TPHA (Treponema pallidum haemagglutinin assay) syphilis tests were all negative.

The full blood count showed slight leukocytosis (white cell count 12×109 /1) and neutrocytosis (83%). The erythrocyte sedimentation rate was slightly increased at 33 mm/h, but the C-reactive protein level was normal at 5.8 mg/l. Auto-immune studies (antinuclear antibodies, antimitochondrial antibodies, antiparietal cell antibodies and anti-smooth muscle antibodies) were negative. Serum angiotensin-converting enzyme for sarcoid was also negative. Vitamin B12 levels were normal. Tests for mitochondrial mutations associated with Leber’s hereditary optic neuropathy were judged unnecessary. Infectious studies were all negative, including blood tests for Toxoplasma, rubella, cytomegalovirus (CMV) pp65 antigen, viral hepatitis screen, HTLV-1 and 2, RPR and TPHA for syphilis. The HIV enzyme-linked immunosorbent assay was reactive and the absolute CD4 count was 85 cells/ul.

The patient was admitted on the day of her presentation to our clinic. After 3 days she was treated with intravenous methylprednisolone 1 g daily for 3 days, followed by 11 days of oral prednisone 60 mg daily with subsequent gradual tapering to prevent possible steroid withdrawal symptoms. A diagnosis of idiopathic optic neuritis was subsequently made by exclusion of other causes.

On the 6th day of treatment, the patient reported improvements in her vision. Visual acuity of the right eye was unchanged, but in the left eye it improved to 6/24.

Two and a half weeks after her initial presentation to us, she started highly active antiretroviral therapy (HAART).

At a follow-up visit 2 months after presentation, and 5 weeks after HAART commencement, vision had improved bilaterally to 6/18 on the right and 6/12 on the left. There was complete resolution of disc swelling bilaterally, but some residual optic nerve pallor (Figs 4 and 5).

By the 5th month after presentation, the HIV-1 viral load was suppressed at less than25 copies/ul and visual acuity remained 6/18 in the right eye but had improved to 6/6 in the left. The CD4 count improved to 265 cells/ul. 

DISCUSSION

Optic neuritis is an inflammation of the optic nerve and a cause of acute visual loss. It may be categorised as typical or atypical.

Typical optic neuritis, the most common type, occurs in demyelinating conditions such as multiple sclerosis (MS). The International Headache Society (IHS) outlines five diagnostic criteria describing dull retrobulbar pain in one or both eyes of maximum 4 weeks’ duration accompanied by impaired central or paracentral vision in the absence of a compressive lesion.4 It has been proposed that the diagnostic criteria be used in conjunction with biomarkers and radiological evidence of multiple sclerosis.4

Atypical optic neuritis occurs in non-demyelinating conditions such as viral infections, toxin exposure, meningitis, tumour metastases, syphilis and neuromyelitis optica (Devic’s disease), and in some cases it is idiopathic.3 Features suggesting atypical optic neuritis include age (less than12 years or more than 50 years), African or Asian race, bilateral disease, severe (no light perception) or progressive (more than 2 weeks) visual loss, unusual description of pain (painless visual loss or severe pain that restricts eye movements or wakes patient from sleep), unusual ocular findings (marked anterior and/or posterior segment inflammation), lack of any visual recovery within 5 weeks or continued deterioration in visual function, symptoms or signs of a systemic disorder other than MS, and corticosteroid-dependent optic neuropathy (deterioration in vision when corticosteroids are withdrawn).5

This patient had features suggesting an atypical optic neuritis, particularly haemorrhages that accompanied optic disc swelling. In addition to tests for auto-immune diseases, sarcoidosis, rubella, viral hepatitis and HTLV-1 and 2, investigations for opportunistic infections should also be done in the setting of HIV, and the possibility of false-negative results should be borne in mind. More sensitive tests include serum or CSF cryptococcal antigen for the fungus C. neoformans, serology for the protozoan Toxoplasma gondii, and pp65 antigen for CMV. Tests which should be interpreted with more caution include syphilis serology, which may revert to negative in HIV infection,10 and tuberculosis tests because – despite the availability of multiple methods of investigation including microscopy, culture, CSF ADA and imaging – tuberculosis is noted to be cryptic in HIV infection.

Neuro-ophthalmic manifestations of HIV tend to present at an advanced stage of the disease when CD4 cell counts are depleted below 200 cells/µl.6 Indeed, in patients with AIDS there is a 3 - 8% prevalence of neuro-ophthalmic diseases including eye movement disorders, cranial nerve palsies, neuroretinitis, retrobulbar optic neuropathy, anterior optic neuropathy, papilloedema, visual field defects, cortical blindness, optic atrophy and optic neuritis.1 The latter manifestation was the presenting illness of HIV in our patient, who reported no prior HIV-related diseases even though her CD4 count at presentation was 85 cells/ul.

In HIV-infected patients, opportunistic infections such as syphilis, toxoplasmosis, tuberculosis and cytomegalovirus are by far the most common cause of optic nerve disorders.7 , 8 In rare cases, mostly affecting males, mitochondrial toxicity caused by nucleoside reverse transcriptase inhibitor antiretroviral drugs such as stavudine and didanosine may trigger acute painless central visual loss if the 14484 mitochondrial DNA mutation of Leber’s hereditary optic neuropathy is present.9 We did not test for this mutation because the patient had not been on antiretroviral drugs, was not male, and had no family history of sudden visual loss.

To our knowledge at least 10 cases of idiopathic HIV-associated optic neuritis have been reported in the English literature.8 , 10 In the 6 instances where CD4 counts were documented, they were well below 350 cells/µl in all cases except one of acute HIV syndrome. Nine of these 10 patients presented with decreased visual acuity in one or both eyes. Of the 9 cases where visual outcomes were reported, there was improvement in 16 eyes and 2 eyes remained unchanged.

A direct causal link between HIV and optic neuritis has been suggested previously.10 The mechanism by which HIV could cause primary optic neuritis remains unclear despite much research devoted to neurodegeneration in HIV infection.1 , 10 , 11 , 15 , 16 The current widely accepted theory suggests that the pro-inflammatory cytokine tumour necrosis alpha (TNFα) plays a key role.1 , 8 , 11 Other proposed mechanisms include damage secondary to activated microglia and macrophages releasing neurotoxic agents.1 Consistent with this proposed inflammatory pathogenesis, steroid responsiveness is thought to be a feature of idiopathic optic neuritis in HIV-infected persons.7 , 10

The use of steroids in typical optic neuritis is well established. The prospective randomised and controlled Optic Neuritis Treatment Trial reported that oral prednisone alone had no benefit over placebo and may increase the future risk of repeat episodes of optic neuritis, while intravenous methylprednisolone 1 g daily for 3 days followed by 11 days of oral prednisone 1mg/kg/day was associated with slightly faster visual recovery compared with placebo.17 Nevertheless, visual recovery within 2 weeks was marked for most participants, regardless of treatment arm.17

Treatment for atypical optic neuritis includes treating the underlying cause. The optimal treatment for optic neuritis in HIV- infected patients is controversial. On the one hand, spontaneous resolution of optic neuritis in HIV-infected patients after 2 weeks has been reported12 and some (but not all) studies have demonstrated accelerated disease progression with the use of even short courses of immunosuppressive doses of steroids in patients with advanced HIV.18 On the other hand, there are reported cases – ours being one of them – of visual recovery soon after the introduction of systemic steroid therapy.7 , 10 It is also possible that antiretroviral therapy contributed to visual recovery in the medium term.7 , 8 , 11

Some authorities advocate the inclusion of penicillin at neurosyphilis treatment doses as part of empiric management for optic neuropathies of cryptic origin in HIV-infected individuals,7 , 10 but we did not employ this strategy. The rationale underlying this approach reflects the attenuating sensitivity of laboratory tests for treponemal infection, which are antibody tests and may be non-reactive in advanced HIV illness.7
 
Conclusions

Underlying HIV should be considered in cases of atypical optic neuritis in patients at risk. Although uncommon, idiopathic optic neuritis in HIV-infected persons is a diagnosis of exclusion when there is a presentation of sudden visual loss and optic disc swelling. Management must include assessment for HAART, as the condition is linked with advanced disease. It may be reasonable to inform HIV-infected patients with optic neuritis about the possible risks versus benefits of steroid therapy and invite them to consent to the treatment of their choice.

Competing interests. The authors declare that they have no competing interests.

Author contributions. CC acquired and interpreted the data and drafted the manuscript. BM and FL critically revised ophthalmological and HIV-related sections of the manuscript, respectively. AP provided final review and approval of the manuscript.

Ethical considerations. The patient provided voluntary written informed consent to have her anonymous case details published.

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