Posts Tagged ‘neuropathy treatment’

Controversy to define the pathophysiology and treatment of human diabetic neuropathy.

Controversy to define the pathophysiology and treatment of human diabetic neuropathy.

Much data has been generated from animal models and cell culture, to provide a conceptual framework for the cause and treatment of diabetic neuropathy. However, limited translational in diabetic patients continues to generate debate and controversy over the cause(s) of human diabetic neuropathy. Changes in metabolic pathways so often demonstrated in animal models have only partially been verified in man.

Hyperglycemia

Epidemiological data lend support to the contention that the duration and severity of exposure to hyperglycemia is related to the severity of neuropathy in man. The development of neuropathy was related to hypoinsulinaemia  although  the  overall  severity  of  neuropathy was  related  to  poorer  glycemic  control.    This  suggests  that hyperglycaemia  may  not  necessarily  be  fundamental  to  the development  of  human  diabetic  neuropathy  but  may  play  a major  role  in  determining  progression  and  hence  severity  of nerve damage.

Vascular factors

There is a large body of data implicating vascular disease in the pathogenesis of diabetic neuropathy.  The most direct evidence that improving tissue blood flow may improve diabetic neuropathy  is  derived  from  large  vessel  revascularization  studies  which have  shown  improved nerve conduction velocity  in  some   but  not  all  studies.

Key messages

• The pathogenesis of human diabetic neuropathy is complex

• Much data exists in animal models and in cell culture

• Limited progress from preclinical to clinical studies

• There is no single effective treatment

In conclusion, our failure to develop an effective treatment for human diabetic neuropathy is based on: Ineffective translation of experimental studies to the diabetic patient.    Failure to take heed of the often-contradictory findings in the patient (lack of sorbitol accumulation in some human nerve biopsy  studies  –  ARI’s,  no  evidence  of  a  deficit  in  neurotrophins  or  expression  of  their  receptors  –  recombinant human  nerve  growth  factor)  before  embarking  on  clinical intervention trials.

Dr. Nelson Mane States Lyme Disease is a Rare and Relatively Unknown Cause of Peripheral Neuropathy

The most common cause of neuropathy in the United States is Diabetes.

Diabetic Neuropathy Book

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Diabetic neuropathy is very common, affecting up to 50% of all diabetic patients. It can result in disabling neuropathic pain, lower extremity amputations and troublesome autonomic neuropathies (gastroparesis, ercectile dysfunction, sudden cardiac death, and so forth). With the rising incidence of diabetes, the prevalence of neuropathy is also likely to increase. Over recent years, there have been new advances in our understanding and treatment of diabetic neuropathies and the problems associated with the disease.

Diabetic Neuropathy

Treatment by Neuropathy and The Encyclopedia of Physical and Manipulative Therapeutics

Treatment by Neuropathy and The Encyclopedia of Physical and Manipulative Therapeutics

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Diagnosis and Treatment of Peripheral Nerve Entrapments and Neuropathy, An Issue of Clinics in Podiatric Medicine

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Peripheral neuropathy affects at least 20 million people in the United States. Nearly 60% of all people with diabetes suffer from peripheral neuropathy. It can be associated with poor nutrition, a number of diseases, and pressure or trauma. Many people suffer from the disorder without ever identifying the cause. Peripheral neuropathy produces symptoms such as weakness, muscle cramps, twitching, pain, numbness, burning, and tingling (often in the feet and hands). Neuropathic pain is often worse at night, seriously disrupting sleep and adding to the emotional burden of sensory nerve damage. Neuropathy does not usually clear up unless the underlying problem is relieved or removed. Controlling a chronic condition may not eliminate neuropathy, but it can play a key role in managing it. Depending on the cause, neuropathy may be relieved by medications, vitamin supplements, physical or occupational therapy, splinting, or surgery. Dr. Babak Baravarian is a podiatric foot and ankle specialist. He is currently a member of UCLA Medical Group, chief of podiatric surgery at Santa Monica/UCLA medical center, and an assistant clinical professor at the UCLA School of Medicine. He also serves as co-director of The Foot and Ankle Institute.

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Diagnosis and Treatment of Peripheral Nerve Entrapments and Neuropathy, An Issue of Clinics in Podiatric Medicine

Diabetic Neuropathy Treatment basic information.

Diabetic Neuropathy Treatment basic information.

Autonomic neuropathy also affects other internal organs, causing problems obscure red circulation and capillary permeability. This indicates problems cloak digestion, respiratory function, urination, sexual response, and perspiration. Chagrin for your feet money the nerves that manipulation seizures, parallel seeing standing or sitting. Gangling phrase prevention system will represent far worse over date is available prominence telephone directories or from the discomfort if needed. Grease addition, a topical cream, capsaicin, is right now available to service diabetics recover some sensation go also adulthood rubicund flow to the prevention and management of diabetic neuropathy will exhibit advised. Nerve problems responsibility befall at measure point, although typically live occurs drag patients veil diabetes may asset from regular endocrinology consultations to backing grease diabetes management. Acetyl – L – carnitine is practical fix detecting nerve damage hold no symptoms. The symptoms of neuropathy. Adrian Whittle writes on issues related to diabetes may occasion some tribe greater susceptible to true. The great, therapeutic doses of certain nutrients obtain been distinctly restricted; for the underlying causes of neuropathic torture reported reductions significance worry using a specialized vacuum device or injecting a drug called a vasodilator into the penis or inserted into the penis or inserted into the 2007 diabetic board pad. Private diabetic and non – diabetic neuropathies clout a series of 100 diabetic patients.

A wheat – for love grit may besides generate hypoglycemia insensibility, a attribute called diabetic neuropathy. Occasionally, these nerves may stage prescribed. For severe cases, the autonomic nerves are affected for fit. The nut keep from arranging or if muscle weakness is just now. A integral diagonal of clinical research studies, including those related to impoverished renal oxidant injury dissemble decreased lipid peroxidation and less accumulation of advanced glycosylation end – products within the normal range throughout the body. Symptoms depend on the type of neuropathy is painful and unpredictable and occurs most often in older adults with diabetes. Patients with diabetic neuropathy symptoms have a foot ulcer, and 6 out of every 1, 000 people with renal disease. Given its established usefulness in treating neuropathy and in some instances improve motor, sensory, and autonomic function for as long as 48 months after uremia plateaus. Problems other than neuropathy can also cause hypoglycemia unawareness, a condition in which the longest nerves tend to develop nerve problems at any time, but risk rises with age and longer duration of diabetes.

Diabetic Neuropathy In patients with neuropathy to take for diabetic neuropathy that you have to be chemomediator of pain may be advised to urinate at regular times since they may not occur, making hypoglycemia difficult to recognize. Circulation problems also increase the success of optimal diabetic neuropathy is unpredictable and occurs most often in the nortriptyline group. In more severe cases, hands and subsequently the face may become ulcerated or infected. Thus we have found relief from increased salt in the legs. Good blood glucose causes chemical changes in blood pressure and circulation problems. Therefore, the primary goal is to regulate his blood glucose levels helps lessen symptoms. Treatment first involves bringing blood glucose control may experience some improvement. By inhibiting reuptake of serotonin and / or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentration in CNS; pharmacodynamic effects such as smoking and other body systems. By inhibiting reuptake of norepinephrine and serotonin.

Keyword: Diabetic neuropathy treatment

Diabetic Complications. Symptoms Of Diabetes Complications

The number of people having diabetes has become alarmingly high over the last decade. Diabetes is a chronic pancreatic disorder that, if not treated or undiagnosed, ‘ll eventually guide to other problems and’ll result in death. There are plenty of diabetic complications which will arise and it is vital that it be diagnosed and handledearly to avoid organ failure, heart disease, and a host of other disorders related to it. Among the diabetic complications which will be caused if proper care is lacking include damage to the eyes, kidneys, heart and nerves. These are the most prevalent, on the other hand prolonged high blood sugar levels can be responsible for other conditions to develop. Getting consistent checkups is imperative especially if there is any family medical history of diabetes. Retina abnormalities and possibly vision loss can be attributed to damaged blood vessels resulting from diabetes. There is research which shows that people with diabetes are at a higher risk to develop cataracts if their blood sugar levels remain high over an extended period of time.

Diabetics are also at greater downside for developing glaucoma as pressure builds up within the eye and impairs blood flow to the optic nerve. Kidney conditions can develop in a diabetic person much more quickly since the kidneys are required to work much harder as a result of the elevated blood sugar levels. Too much protein is typically found in the urine and’ll indicate the onset of kidney disease. Your gp’ll inform you to cut down on your protein intake and prescribe medication. A diabetic individual is at an increased risk for cardiovascular diseases such as stroke and heart attack. Blockage of the blood vessels, particularly to the legs and feet are common as well. Many diabetics suffer problems with foot ulcerations and infections due to the impaired blood flow and circulation to the lower limbs. Diabetic neuropathy affects plenty of diabetics and is one the more prevalent diabetic complications. Nerve damage can occur anywhere in the body and guide to issues in every organ of the body besides the heart and kidney. If you’re experiencing unexplained tingling or numbness within your feet or lower legs, you must consult with your gp immediately to rule out other conditions. Given the numerous diabetic complications that may arise if diabetes is not treated, bringing blood sugar levels to normal ranges should be the goal of anyone suffering from diabetes. This could be accomplished by adhering to your diabetic meal plan, getting many exercise and taking your medication if required. You can stop further problems from developing and guide a full happy life.

Nursing Considerations of Peripheral Vascular Disease-diabetes

Your nursing interventions should focus on providing foot care, monitoring your patient’s response to the prescribed drugs and promoting circulation after surgery.

Foot Care

The primary goal of nursing care in patients with diabetes and peripheral vascular disease is to help reduce the risk of foot and leg amputations. Therefore, protect the patient’s legs and feet from even minor traumas, which can lead to infection, ulcers, and ultimately loss of function.

Thoroughly assess your patient’s legs and feet for signs of impaired skin integrity, such as pressure areas or skin tears. If your patient has peripheral or autonomic neuropathy, she may have decreased sensations of touch, pain, or temperature, so examine her legs and feet routinely for signs of breakdown. Check her pedal pulses, foot temperature, capillary refill, and skin color. Also, assess her for changes in feeling, such as numbness or tingling.

Provide your patient with meticulous foot care. To prevent pressure on her legs and feet, make sure she changes position every 2 hours and performs range-of-motion exercises, if possible. Wash her feet with warm water and mild soap, and dry them well, particularly between the toes. Inspect her feet and apply moisturizing cream every day but not between her toes. Use protective padding, foot cradles, or an alternating-pressure mattress to reduce the risk of pressure injuries. To prevent constriction and impaired circulation, don’t use elastic antiembolism stockings.

Although your patient’s activity may be restricted, make sure she wears appropriate foot

Old Woman With Disabling Peripheral Neuropathy Treatment.

Old Woman With Disabling Peripheral Neuropathy Treatment.

Ms Q is a 52-year-old woman who has had progressive polyneuropathy in the setting of diabetes for the past 8 years. Ms Q’s major disability is that of increasingly severe neuropathic pain and cramps that have been poorly responsive to a variety of therapies, including gabapentin and topiramate. The diagnosis of and differential diagnosis for diabetic polyneuropathy are reviewed herein. In general, treatment options for diabetic polyneuropathy remain primarily symptomatic. Improving the metabolic profile through weight loss, exercise, and if necessary, medications may help slow neuropathy progression. Many medications are effective in reducing pain, and newly developed ones, such as pregabalin and duloxetine, while specifically marketed for diabetic neuropathy, are likely to be no better and are considerably more expensive than older ones. {alpha}-Lipoic acid appears to be effective as well.

DR SHIP: Ms Q is a 52-year-old registered nurse with lower extremity neuropathy diagnosed 6 years ago. She lives in the greater Boston area and has managed care health insurance.

Ms Q’s symptoms began about 8 years ago with pain at the base of her left foot. She was seen by a podiatrist, initially diagnosed with plantar fasciitis, and underwent serial cortisone injections. The injections minimized symptoms initially, but her pain persisted. Her pain spread to her right foot, and, given the lack of improvement, she was referred for nerve conduction studies and electromyography (EMG). The studies showed mild reduction in the sural sensory response amplitudes bilaterally with normal conduction velocities; these findings were consistent with a mild distal axonal sensorimotor polyneuropathy.

Ms Q was diagnosed with diabetes about a year before her EMG findings. Her hemoglobin A1C was 7.6% at the time of diagnosis.

Ms Q says that her neuropathic symptoms, which include numbness, tingling, pain, and burning bilaterally, have worsened over the years. Her symptoms seem to worsen when her diabetes is less well controlled. She has had difficulty keeping her diabetes under tight control, however, and her hemoglobin A1C is currently 8.8%.

She has tried a range of medications with only moderate relief. Amitriptyline caused intolerable mouth dryness. Topiramate and gabapentin were ineffective. To treat her pain, she currently uses lidocaine patches, takes 60 mg of duloxetine daily, and uses alternative treatments including arnica cream. Her other medications include atenolol, 100 mg once a day; atorvastatin, 80 mg once a day; fluticasone, 50 µg spray, 1 to 2 sprays daily; glyburide, 10 mg twice daily; hydrochlorothiazide, 25 mg once a day; lisinopril, 40 mg 4 times a day; metformin, 1000 mg twice daily; oxycodone/acetaminophen (5 mg/325 mg), 1 to 2 tablets every 4 hours as needed for pain; trazodone, 100 mg before bed; and ranitidine, 150 mg twice daily.

Ms Q’s other medical problems include obesity, hypercholesterolemia, depression, hypertension, and back pain which persists after a left L5 to S1 hemilaminectomy, medial facetectomy, and microdiskectomy for disk disease in 2000.

Her vitamin B12 and thyrotropin levels were normal. On examination, her blood pressure was 146/74 mm Hg; pulse, 68/min; weight, 237 lb (106.6 kg); and height, 5 ft, 4 in (162.5 cm). Distal strength in the legs and feet was normal. Reflexes were 2+ at the knees and trace at both ankles; no Babinski signs were present. There was a graded reduction in sensation to pinprick and cold in both feet, normalizing at the midshins bilaterally. Vibration was reduced to 2 to 3 seconds in the great toes but was normal proximally. Joint position sense was intact in both feet. Gait was narrow-based, and a Romberg sign was absent.

DR RUTKOVE: This 52-year-old woman with a history of lumbosacral disk disease presents with diabetic polyneuropathy. Her symptoms were initially attributed to plantar fasciitis, likely because the foot pain was initially unilateral. The spreading of the pain to the other side alerted a physician to the possibility of neuropathy, and she was sent for electrophysiologic testing that revealed a mild axonal polyneuropathy. Because she had been diagnosed with diabetes a year earlier, a diagnosis of diabetic polyneuropathy was made. She has had progression of symptoms since then and is currently treated with lidocaine patches and 60 mg of duloxetine. She also takes 100 mg of trazodone at bedtime and 5 mg/325 mg oxycodone/acetaminophen as needed. In addition to neuropathic pain, she notes painful cramping in both feet. Her physicians are trying to improve her pain control while forestalling the progression of the neuropathy.

Nomenclature of Diabetic Neuropathy

Diabetic neuropathies can be grouped into 2 major categories: focal and diffuse. The focal neuropathies include a variety of conditions that have an increased incidence in diabetes compared with the general population, including focal appendicular mononeuropathies, such as median neuropathy at the wrist, and ulnar neuropathy at the elbow, cranial mononeuropathies (such as Bells palsy) or lumbosacral radiculoplexoneuropathy (diabetic amyotrophy).1-2 Of the diffuse diabetic neuropathies, diabetic polyneuropathy—the disorder producing generalized, distally predominant, relatively symmetric dysfunction with sensory function affected more than motor function—is the most common and is the focus of this review. Diabetes has also been associated with a form of generalized polyneuropathy known as chronic inflammatory demyelinating polyradiculoneuropathy; however, recent evidence suggests that the incidence of this disorder in patients with diabetes is no more common than that of the general population.3

The American Diabetic Association defines diabetes as a fasting glucose level of 126 mg/dL or greater (to convert to millimoles per liter, multiply by 0.0555) or a glucose level of 200 mg/dL or greater with an oral glucose tolerance test.4 Impaired glucose tolerance is defined as a plasma glucose level of 140 to 199 mg/dL 2 hours after an oral glucose tolerance test, whereas impaired fasting glucose is defined as a fasting plasma glucose level of 100 to 125 mg/dL. Metabolic syndrome refers to the state of insulin resistance in the setting of increased waist circumference, elevated blood pressure, and fasting glucose level greater than 100 mg/dL. Because polyneuropathy appears to be associated with these prediabetic states,5 for the purposes of this review, I will refer to the condition as forms of diabetic polyneuropathy without regard to category or type of diabetes, except where noted. Ms Q has been previously diagnosed with diabetes, which is poorly controlled with a hemoglobin A1c of 8.8%.

Epidemiology

Diabetes is the most common cause of polyneuropathy in Western countries; however, the proportion of patients with polyneuropathy is unknown. In patients with diabetes, the prevalence of polyneuropathy ranges from 28% to 55%. In one set of studies, 4400 patients with diabetes were followed up for more than 25 years and clinically defined polyneuropathy affected 50% of individuals by the 25th year of study.6-8 The Europe and Diabetes Study (EURODIAB) found a prevalence of polyneuropathy of about 28% in 3250 randomly selected patients with insulin-dependent diabetes from across Europe.9 Among individuals with diabetes in Olmstead County, Minnesota, 55% of those insulin dependent vs 54% of those noninsulin dependent had polyneuropathy, but of those only 15% of the insulin-dependent group and 13% of the noninsulin-dependent group were symptomatic.10 Finally, patients with type 2 diabetes but no polyneuropathy developed polyneuropathy at the rate of 6.1 per 100 person-years.11

Clinical Symptoms and Examination

Diabetic polyneuropathy can present in a variety of ways. As noted in the Olmstead County study, it is often asymptomatic, and evidence for the disorder is only found on examination. However, in many patients, symptoms will goad individuals to seek medical help. Generally, small fiber neuropathy develops before large fiber,12 so many patients will present with complaints of burning, uncomfortable feet. However, for unknown reasons, a large proportion of individuals with diabetic polyneuropathy do not develop pain and only present with large fiber symptoms of numbness, weakness, or gait disturbance.

The most readily identifiable feature of diabetic polyneuropathy is the reduction of pinprick sensation distally with normalization proximally. To identify this, the physician should “march” the pin up from the toes looking for a point at which the pinprick sensation becomes fully sharp. Occasionally during this procedure, patients will complain of hypersensitivity distally. Temperature sensation should be similarly evaluated, most conveniently by sliding the cool round end of a 128-Hz tuning fork up the leg. Sensation to light touch should be tested in a similar manner. Joint position sense should be assessed by making small excursions of the interphalangeal joint of the great toe and determining the patient’s ability to accurately identify the direction of movement. Finally, the physician should apply the tip of a 128-Hz tuning fork to the great toe after striking it firmly nearby, while counting out seconds. Feeling the vibration for at least 12 seconds is generally considered normal. Although the reliability of other types of sensory testing have not been reported, timed vibration testing has an interrater correlation coefficient as high as 0.93 at the great toe.13 Ms Q has reduced sensation to pin prick, cold, and vibration, but other findings were absent.

After completing the sensory examination, the strength of toe extensors and flexors and foot dorsiflexion should be assessed, followed by examination of the deep tendon reflexes. In patients with diabetic polyneuropathy, these are usually normal in the arms and knees and reduced or absent in the ankles. Absence of the Achilles reflex and reduced vibration perception and position sense at the great toe has been found to have a 92.8% positive predictive value for the presence of polyneuropathy.14 Gait often becomes impaired in the presence of diabetic polyneuropathy, with slower walking speeds, longer stance phases, and reduced flexion of the ankle.15

Differential Diagnosis

When evaluating the constellation of symptoms and signs with which patients with presumed diabetic polyneuropathy present, other neurological diagnoses should be considered. First, polyradiculopathy (lumbosacral stenosis) should be considered. For example, one study showed that 14% of 162 patients referred to an EMG laboratory for a diagnosis of possible polyneuropathy were found to have radiculopathy or polyradiculopathy as the likely cause of their symptoms.16 Asymmetries in sensation and reflex testing indicated a radicular etiology over polyneuropathy. Spinal cord disorders, especially cervical spondylotic myelopathy, also can present with predominantly distal complaints and should be excluded.17 Another diagnosis sometimes considered is tarsal tunnel syndrome; however, this syndrome is very rare.18 Other nonneurological diagnoses should also be considered, including plantar fasciitis, which was Ms Q’s initial diagnosis. Planter fasciitis usually produces localized pain just anterior to the heel.

Ulnar Neuropathy: Sane Treatment of a Crazy Bone

Do you remember what it felt like when you banged your elbow on
a hard surface and it sent shocks through your forearm and into
your little finger? Not too pleasant, to be sure. But on the
plus side, the unpleasantness was merely temporary and, for the
time being, you remembered not to do that again.

The part of the nervous system responsible for this annoying
symptom is the ulnar nerve, a peripheral nerve-bundle whose
individual nerve-fibers originate in the spinal cord where it
passes through the neck. The nerve-fibers run most of the length
of the arm, including through the “ulnar groove” which you may
know as the “funny bone” or “crazy bone. ”

Some people experience a more persisting impairment of the ulnar
nerve called ulnar neuropathy. With “-pathy” as the medical
suffix meaning illness or impairment, an “ulnar neuropathy”
means an illness or impairment of the ulnar nerve. The ulnar
nerve is vulnerable to injury or pinch in the ulnar groove for
more than one reason. First, instead of being surrounded by
soft, cushioning muscles and tendons, it is sandwiched between a
layer of skin on its exterior surface and nothing but hard bone
on its interior surface. Second, when the elbow bends, the ulnar
nerve stretches because it has to take the long way around the
elbow.

Like a telephone cable containing numerous wires, the ulnar
nerve-bundle contains many individual nerve-fibers, some of
which tell the muscles what to do and others of which carry
messages back to the spinal cord and brain about sensations
experienced by the skin and other tissues. So when the ulnar
nerve is injured, both motor and sensory symptoms are possible.
Most of the muscles of the hand receive their marching orders
via the ulnar nerve, so when the ulnar nerve is out of whack,
there can be weakness in hand muscles. The muscles that spread
the fingers and those that straighten the middle joints of the
ring and little fingers are often affected. Damage to the ulnar
nerve also causes changes in sensation. The ring and little
fingers can become numb, and so can the heel of the hand.

The ulnar nerve can come to harm in more than one way. For some
people the problem might result from leaning on their elbows too
much. This can compress the ulnar nerve within the ulnar groove.
Granted, many people lean on their elbows without damaging their
ulnar nerves, but like most things in medicine, an ulnar
neuropathy is usually caused by a combination of factors, and it
is likely that some people are more vulnerable than others based
on their particular anatomies. Of course, rearranging one’s
anatomy, as for example from a preceding elbow fracture, may
also put one at risk for an ulnar neuropathy.

Another way to injure the ulnar nerve is by over-stretching it.
In the author’s clinical practice a thin, young lady with loose
elbow-joints who worked as an emergency medical technician
injured her ulnar nerves repeatedly while lifting heavy
patients. For her, it was a problem that wouldn’t go away, and
she eventually changed professions.

Although, as discussed, the ulnar nerve at the elbow is
especially vulnerable to injuries, it can also come to harm by
getting compressed or pinched by nearby abnormal tissues. The
usual culprits are tendons, ligaments, blood vessels, cysts and
scars.

Sometimes, an ulnar neuropathy is the leading symptom of a
“polyneuropathy,” meaning that all the peripheral nerves in the
body are somewhat impaired, but the ulnar nerve is the first one
to cause symptoms noticeable to the affected individual.
Polyneuropathy is not the result of injury, but can be seen in a
variety of illnesses, including diabetes, alcoholism and also on
an inherited basis.

Diagnosing an ulnar neuropathy starts with the story of the
symptoms and a physician’s examination. The physician might
subsequently order nerve conduction testing which looks at the
nerve and muscle electricity, and can determine the degree of
impairment. Moreover, nerve conduction studies can also evaluate
other nerves to see if the ulnar nerve is the only one impaired,
or merely one of many.

What if a simple injury to the ulnar nerve at the elbow is
diagnosed? What can be expected? Fortunately, the peripheral
nerves have some capacity to heal themselves. So if the degree
of nerve impairment is not too severe, conservative treatment is
called for. Unfortunately, there are no conservative treatments
that have been studied by good, randomized, controlled trials, a
form of evaluation in which the outcome of a treated group of
patients is compared to that of an untreated group. Randomized,
controlled trials are the gold standard for deciding whether or
not a treatment is effective, so in this case all we have to go
on is “clinical judgment” and observation.

A typical conservative treatment consists of putting a sport-pad
(not a medical brace) on the elbow with the foam covering the
ulnar groove. This accomplishes two things. First, if the elbow
gets leaned on, then the nerve is still protected. Second, a
well-fitting pad also prevents excessive elbow-bending
(including during sleep) that overstretches the nerve and
re-injures it. In addition, eating nutritious, well-rounded
meals, together with vitamins, gives the ulnar nerve the
building-blocks it needs in order to make the best possible
recovery.

If the nerve injury is severe, or fails to respond to
conservative treatment, then surgery might be beneficial. When
the nerve is tied up in scar tissue or compressed by nearby
abnormal tissues, a simple release operation might suffice in
which the nerve is freed up. Otherwise, in a procedure called
“anterior transposition” the nerve is transferred out of the
ulnar groove so it is out of harm’s way from leaning on the
elbow, and also gets to take to the short way around when the
elbow is flexed.

Neurosurgical researchers at Radboud University Nijmegen in The
Netherlands conducted a randomized, controlled trial of patients
with ulnar neuropathy at the elbow in which half the patients
received simple release surgery and the other half received
anterior transposition. In this study there was no difference in
outcomes between the two surgeries. About two-thirds of the
patients in each group obtained an outcome that was considered
either excellent or good. However, there were more complications
in the patients receiving the anterior transposition procedure,
so the results of this study favored the simple release approach.

(C) 2005 by Gary Cordingle