In addition, alcohol interferes with intestinal absorption of thiamine, thereby further decreasing thiamine levels in the body. Thiamine is important in three reactions in the metabolism of glucose: the decarboxylation of pyruvic acid, d-ketoglutaric acid, and transketolase. A lack of thiamine in the cells may therefore prevent neurons from maintaining necessary adenosine triphosphate (ATP) levels as a result of impaired glycolysis. Thiamine deficiency alone could explain the impaired nerve conduction in those with alcoholic polyneuropathy, but other factors likely play a part.The malnutrition many alcoholics experience deprives them of important cofactors for the oxidative metabolism of glucose. Neural tissues depend on this process for energy, and disruption of the cycle would impair cell growth and function. Schwann cells produce myelin that wraps around the sensory and motor nerve axons to enhance action potential conduction in the periphery. An energy deficiency in Schwann cells would account for the disappearance of myelin on peripheral nerves, which may result in damage to axons or loss of nerve function altogether. In peripheral nerves, oxidative enzyme activity is most concentrated around the nodes of Ranvier, making these locations most vulnerable to cofactor deprivation. Lacking essential cofactors reduces myelin impedance, increases current leakage, and slows signal transmission. Disruptions in conductance first affect the peripheral ends of the longest and largest peripheral nerve fibers because they suffer most from decreased action potential propagation. Thus, neural deterioration occurs in an accelerating cycle: myelin damage reduces conductance, and reduced conductance contributes to myelin degradation.
Radial neuropathy  is a type of mononeuropathy which results from acute trauma to the radial nerve that extends the length of the arm. It is known as transient paresthesia when sensation is temporarily abnormal. Signs and symptoms
Symptoms of radial neuropathy vary depending on the severity of the trauma; however, common symptoms may include wrist drop, numbness on the back of the hand and wrist, and inability to voluntarily straighten the fingers. Loss of wrist extension is due to loss of the ability to move of the posterior compartment of forearm muscles. In the event of lacerations to the wrist area the symptom would therefore be sensory. Additionally, depending on the type of trauma, other nerves may be affected such as the median nerve and axillary nerves. Causes
There are many ways to acquire radial nerve neuropathy, including:
Upper arm - a fracture of the bone
Elbow - entrapment of the nerve
Wrist - elbow deformity and soft-tissue masses
Axilla - here the most common cause is compression. However, a dislocation of the humerus is a possible factor as well. It could also be due to brachial plexus compression. Mechanism
The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal degeneration. These would be caused via laceration or compression of the nerve in question. Diagnosis
Radial neuropathy may be diagnosed using MRI, ultrasound, nerve conduction study or electromyography (EMG).