It is called an overuse strain injury, which occurs when the nerve that travels through the wrist is compressed. People whose work requires repeated motions with the wrist such as assembly-line workers, physical laborers, and those who use computer keyboards for prolonged periods are at greater risk. The damage to the nerve can result in numbness, tingling, unusual sensations, and pain in the first three fingers on the thumb side of the hand.
The person may awaken at night with numbness in their hand or discover that when they perform activities like using a hair dryer, the numbness is more noticeable. In time, carpal tunnel injuries can weaken the muscles in the hand. You may also feel pain, tingling, or burning in your arm and shoulder. Here are examples of other mononeuropathies that can cause weakness in the affected parts of the body, such as hands and feet:. Neuropathy can affect nerves that control muscle movement motor nerves and those that detect sensations such as coldness or pain sensory nerves.
In some cases, it can affect internal organs, such as the heart , blood vessels, bladder , or intestines. Neuropathy that affects internal organs is called an autonomic neuropathy. This rare condition can cause low blood pressure or problems with sweating. Polyneuropathy accounts for the greatest number of peripheral neuropathy cases. It occurs when multiple peripheral nerves throughout the body malfunction at the same time.
Polyneuropathy can have a wide variety of causes, including exposure to certain toxins such as with alcohol abuse , poor nutrition particularly vitamin B deficiency , and complications from diseases such as cancer or kidney failure. One of the most common forms of chronic polyneuropathy is diabetic neuropathy , a condition that occurs in people with diabetes.
It is more severe in people with poorly controlled blood sugar levels. Though less common, diabetes can also cause a mononeuropathy. Because people with chronic polyneuropathy often lose their ability to sense temperature and pain, they can burn themselves and develop open sores as the result of injury or prolonged pressure. If the nerves serving the organs are involved, diarrhea or constipation may result, as well as loss of bowel or bladder control.
Sexual dysfunction and abnormally low blood pressure also can occur.
The muscle is also directly weakened by the intracellular damage but also the loss of innervation and both macro and microvasculature damage, leading to atrophy, weakness, fatigue and slowing of contraction [ 18 ]. Patients with DN have been shown to have accelerated loss of strength, mass and quality of muscles compared to diabetics without neuropathy [ 19 ].
This simultaneous damage of sensation and strength greatly increases morbidity [ 20 ].
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Peripheral neuropathy is the classic, most common diabetic neuropathy. It is length dependent, striking the feet first in a stocking type pattern. There is a gradual and insidious multimodal loss of sensation that can present with a variety of combination of complaints including electric stinging, hyperanalgesia, burning, numbness, and imbalance in addition to other diabetic complications [ 21 ]. Physical signs of extensor digitorum brevis wasting, loss of ankle reflexes, foot drop and hair loss can be observed [ 13 ].
This can progress to a point to having motor nerves and upper extremities also involved in severe cases.
The loss of pedal sensation and places the patient at risk for foot ulcers and falls. True entrapment presents with slow progression and long lasting, requiring intervention differs from mononeurtis which presents acutely with pain and is self-limited in the distribution of the affected nerve [ 22 ].
Mononeuritis is called by vasculitis and ischemia to the nerve and is associated with weight loss. Mononeuritis and entrapment both affect similar nerves, including cranial III, IV, VI, VII , in addition to peripheral peroneal, sacral, femoral, median and ulnar, with median as the most common [ 23 ]. True entrapment is also worsened in diabetes, up to 3x the normal population, which is thought to be increased damage to areas of compression, poorer recovery to damage, metabolic changes and swelling [ 24 ].
Each focal neuropathy will present with loss of function and perhaps pain or tingling in same area. Multifocal neuropathy aka mononeuritis multiplex can also occur, with at least 2 nerves independently affected, presenting with asymmetric neuropathy with pain and similar to mononeuritis, be associated with weight loss [ 25 ]. While DN can show diffuse neuronal injury , the one of the rarer but concerning sites are the major nerve plexuses when it manifests as proximal diabetic neuropathy aka Diabetic amyotrophy, diabetic cervical radiculoplexus neuropathy, diabetic thoracic radiculoneuropathy, and diabetic lumbosacral radiculoplexus neuropathy.
The supraclavicular region is made up of the roots and trunks, with C5 and C6 joining to give the upper trunk; C7 becomes the middle trunk and C8-T1 joining to become the lower truck. Below the clavicle, there trunks split into anterior and posterior divisions and recombine below the clavicle to become the 3 cords named in according to their position around the subclavian artery. These then become the 5 terminal branches. Along the entire structure, eleven minor nerves exit at particular locations, which greatly aid in localization.
The lumbosacral plexus originates from the anterior divisions of the lumbar, sacral, and coccygeal nerve, with occasional supplementation from T It is well protected in the retroperitoneal space which makes it less prone to injury than the exposed brachial plexus. The major divisions are the obturator and femoral nerve from L lumbar plexus and the sciatic nerve from L4-S2 from the lumbosacral plexus which further separates to the tibial and peroneal nerves.
Diabetic Autonomic neuropathy DAN is one of the greater concerns of DN; given it is a significant source of morbidity and mortality [ 7 ]. Cardiac autonomic neuropathy has a 5 times increase in mortality, compared to those without [ 27 ]. Sadly it is also the most common nerve affected in DAN, given the vagal nerve is the longest parasympathetic nerve and the length dependent nature of the disease [ 27 ]. Unfortunately, DAN is often overlooked and not tested for despite the impact on quality of life [ 28 ].
Given the likely underlying pathology, glucose testing including hemoglobin A1c HbA1c , fasting blood glucose, and possible glucose tolerance test in those that test normal for HbA1c show be obtained.
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AAN guidelines also recommend B12 with methylmalonic acid and or homocysteine as well as protein electrophoresis [ 30 ]. In proximal neuropathy, laboratory studies in the disease can be variable with nonspecific inflammatory findings. Both Electromyography EMG and nerve biopsy have good negative predictive value at ruling out diabetic peripheral neuropathy but poor positive predictive value, and their utility is best used to give supportive information to the clinical diagnosis or rule out an alternate pathology [ 30 , 32 ].
Dyck et al. Given the relatively low diagnostic yield in a clear case of peripheral DN, EMG should be reserve for more atypical presentations and in cases concerning focal or proximal neuropathy. EMG in focal neuropathy can establish and confirm the nerve in question is impaired and others are relatively spared. In multifocal diabetic neuropathy, EMG will show a focal conduction block over short nerve segments away from entrapment sites, as illustrated by the loss of compound motor action potential amplitude across the block but preserved amplitude before and after the lesion [ 34 ].
Nerve conductive studies of proximal neuropathy are typically abnormal, however four weeks should be allowed for the emergence of the symptoms to permit EMG changes develop. Electomyographic changes are also related to timing with initial proximal muscles involvement with distal evidence appearing later, with a length dependent axonal general sensorimotor polyneuropathy [ 35 ]. Sensory responses can be absent or reduced with evidence of axonal loss as illustrated by reduced compound action potential amplitudes and proportionate slowing of conduction velocities [ 36 ].
Acute needling can reveal positive sharp waves, fibrillations and reduced recruitment of voluntary motor action potentials, while chronic cases will reflect neuropathic changes of increased amplitude and duration with reduced recruitment and polyphasic waves [ 35 ].
DAN can be confirmed by using the composite autonomic scoring scale; composed of QSART sweat test, orthostatic vitals, heart rate response to tilt and deep breathing, the valsava ratio, and beat to beat BP measurements during a variety of movements [ 38 ]. This composite is a specific and sensitive way to assess autonomic dysfunction [ 38 ].
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Other test can be used to assess the presence of autonomic dysfunction in other organ systems, including penile tumescence studies, and vaginal plethysmography and other imaging studies discussed below [ 39 ]. While diabetes can have nonspecific findings of increased cerebral microvascular disease and smaller cross sections of spinal cords, imaging is typically not indicated in peripheral DN or focal neuropathy unless another etiology is in the suspected after a thorough history and physical exam [ 40 ].
Imaging of the brachial and lumbrosacral plexuses is indicated in assessing proximal neuropathy, as it is a diagnosis of exclusion. When nerves are damaged because of an accident or injury, patients experience pain, weakness and muscle paralysis which can leave them disabled, and recovery rates are poor. The new study, published this week in the Journal of Neuroscience , suggests that omega-3 fatty acids could play a significant role in speeding recovery from nerve injury.
Omega-3 fatty acids could prevent and treat nerve damage, research suggests -- ScienceDaily
The study focused on peripheral nerve cells. Peripheral nerves are the nerves which transmit signals between the brain and spinal cord, and the rest of the body. These nerves have the ability to regenerate but, despite advances in surgical techniques, patients usually only have good recovery when their injury is minor. Omega-3 fatty acids are vital for the body's normal growth and development and have been widely researched for their health benefits.
Because the body cannot manufacture omega-3 fatty acids, they have to be consumed in foods such as oily fish. In the new study, researchers first looked at isolated mouse nerve cells. They simulated the type of damage caused by accident or injury, by either stretching the cells or starving them of oxygen.