General Discussion

Patients with tingling and numbness in distal extremities bilaterally should prompt the clinician to consider peripheral polyneuropathy. Peripheral polyneuropathy can be either acquired or congenital. A pertinent family history asking about other family members must be included as part of the history. An assessment should be performed for peripheral polyneuropathy, as well as other causes for distal numbness. Note that peripheral polyneuropathy and other disorders can coexist. For example, patients with peripheral polyneuropathy are more prone to entrapment neuropathy, and peripheral polyneuropathy may exist in the setting of other disorders. In addition, it is important to assess the reason that patients has peripheral neuropathy, as that will affect the treatment plan.

When taking a history, ask patients about recent viral illnesses, any new medication they are taking, or if they have had any exposure to solvents or heavy metals.

Common Differential Diagnoses

• 1.
  

  Diabetic peripheral neuropathy —possible given the previous diagnosis diabetes, as well as poorly controlled blood sugars (as evidenced by elevated HbA1c levels).

  
  
• 2.
  

  Alcoholic peripheral neuropathy —patient has a long history of drinking alcohol. Alcoholic neuropathy can present after prolonged drinking.

  
  
• 3.
  

  Toxic peripheral neuropathy because of chemicals —patient worked as a janitor, and therefore might have been exposed to chemicals that are toxic to the peripheral nervous system (heavy metals, lead, mercury, arsenic, etc.).

  
  
• 4.
  

  Peripheral neuropathy because of other causes —could include undiagnosed thyroid disorder, human immunodeficiency virus (HIV), or other diseases.

  
  
• 5.
  

  Malignancy —Paraneoplastic syndrome can cause neuropathy. This is usually because of small cell carcinoma of the lung. This patient has a history of smoking, so is at increased risk for this type of neuropathy.

  
  
• 6.
  

  Nerve entrapment proximally in the legs —less likely given the symmetry of the symptoms, and the mild findings in the hands. Nerves can be entrapped anywhere in the legs. Common areas include:

  
  
  
  
  • a.
    

    Tarsal tunnel— commonly cause numbness in the plantar surface of the feet and spare the dorsum of the feet.

    
    
  • b.
    

    Peroneal neuropathy at the fibular head —commonly cause numbness on the top of the feet and spare the plantar surface of the feet.

    
    
  • c.
    

    Lumbosacral plexopathies— less likely because these lesions are rarely bilateral and patients usually present with numbness in a peripheral nerve distribution (as opposed to a stocking/glove distribution). Motor function is also likely to be affected.

    
    
  • d.
    

    Radiculopathy —less likely because the symptoms are bilateral and do not go above the ankles. Symptoms of radiculopathy would usually include back pain, motor weakness, and numbness in a nerve root distribution.

    
    
  • e.
    

    Spinal stenosis —less likely because spinal stenosis usually presents with back pain (improved with flexion), as well as pain and numbness that does not go distal to the knees. Symptoms can be bilateral.

  
  
  
  
• 7.
  

  Upper motor neuron lesion —a central nervous system lesion is less likely given the distribution of the sensory impairment (distal and bilateral, affecting upper, as well as lower extremities), as well as normal tone, negative Hoffmann, and down-going plantar reflexes.

  
  
• 8.
  

  Hereditary peripheral neuropathy— less likely given the lack of family history but should not be excluded.

  
  
• 9.
  

  Peripheral vascular disease— is usually distal and may mimic the symptoms of peripheral polyneuropathy. However, pulses on this patient were normal.

  
  
• 10.
  

  Diabetic amyotrophy —can occur in diabetic patients. It frequently presents with the acute onset of unilateral pain and weakness (however, it may be bilateral). This is followed by severe atrophy. Affected nerves are usually more proximal than in a distal peripheral polyneuropathy. This patient did not have proximal pain, the onset was chronic, and there was no muscle wasting.

  
  
• 11.
  

  Neuropathy as a side effect of medication— numerous medications can cause peripheral polyneuropathy as a side effect, including some cancer medications, antialcohol drugs, anticonvulsants, immune suppression medications, antibiotics, and heart or blood pressure medications.

  
  
• 12.
  

  Autoimmune inflammatory neuropathy— includes Guillain-Barré syndrome (acute inflammatory demyelinating polyneuropathy [AIDP], as well as chronic inflammatory demyelinating polyneuropathy [CIDP]). Patients may report an antecedent viral infection. Usually, in Guillain-Barré, the symptoms are acute and ascending. Here, the symptoms were more chronic and limited to a distal distribution.

  
  
• 13.
  

  Neuropathy caused by vitamin deficiency— can be secondary to vitamin deficiency, especially vitamin B12 and folate. This may be seen in patients with alcoholism.

  
  
• 14.
  

  Idiopathic neuropathy —up to 46% of patients develop peripheral polyneuropathy for which the reason is not clear.

  
  
• 15.
  

  Small fiber neuropathy —this type of neuropathy affects the small c fibers. Because nerve conduction testing only assesses for larger nerve fiber types, this type of neuropathy will yield a negative nerve conduction study (NCS)/electromyography (EMG).

Case Discussion

Our patient has several reasons to have a peripheral polyneuropathy, including diabetes, alcohol use, possible toxic chemical exposure, and smoking. He complains of numbness and tingling in the feet, but on physical examination, the hands are mildly affected as well. This is common in peripheral polyneuropathy because the nerves in the legs are longer and cooler than those in the arms. However, other diseases that can mimic peripheral neuropathy or coexist with peripheral neuropathy must be excluded.

The earlier EMG is helpful to further narrow down the differential diagnosis. Diabetic peripheral polyneuropathy typically presents as a distal sensory motor, axonal, and demyelinating peripheral polyneuropathy. The other main cause of this type of neuropathy is uremic peripheral polyneuropathy. Because kidney functions were normal, this is less likely. Distal denervation can be explained by the motor axonal component of the neuropathy. The patient’s laboratory results further indicate that the most likely reason for the peripheral polyneuropathy is diabetes.

Review of Proposed Pathology

The exact mechanism of injury to the nerves in diabetic peripheral polyneuropathy is not clear. The toxic effects of hyperglycemia probably play a role. Other factors include inflammatory, metabolic, and ischemic damage to the nerve.

Electromyography

EMG testing (especially the nerve conduction component of the test) can be used to differentiate peripheral polyneuropathy from other nerve involvement, including focal nerve entrapment syndromes (i.e., tarsal tunnel syndromes) and radiculopathy. It is also helpful in diagnosing nerve and muscle pathology that may coexist with the neuropathy. EMG can assess the type of neuropathy (axonal, demyelinating, or both; sensory, motor, or both; distal or proximal; uniform or segmental).

EMG testing can further help to prognosticate. The amount of conduction velocity slowing and increased distal latency indicates the severity of the demyelinating component. Dispersion of the compound motor action potential (CMAP) and sensory nerve action potential (SNAP) may also be noted, especially in acquired peripheral polyneuropathies. The reduction in amplitude indicates the severity of the axonal component. If distal denervation is severe, the motor units in that muscle are severely compromised. This indicates severe axonal damage and a poorer prognosis. Chronicity can be assessed by changes in the motor unit.

Other causes of peripheral neuropathy noted in the differential diagnosis can be excluded based on the findings of the EMG study ( Table 11.1 ). Alcoholic peripheral neuropathy usually presents as an axonal sensory motor neuropathy. Toxic neuropathies also usually present as axonal sensory motor neuropathies. Paraneoplastic syndrome peripheral neuropathy typically presents on EMG as a sensory axonal neuropathy. Entrapment neuropathies will typically demonstrate conduction velocity slowing across the area of entrapment or conduction block (neurapraxia). Radiculopathy will typically demonstrate normal nerve conduction studies, but may demonstrate denervation in a nerve root distribution. Spinal stenosis will typically show bilateral multilevel paraspinal denervation with few findings in the limb (but usually proximal findings more than distal findings). Upper motor neuron lesions will have normal nerve conduction studies and no denervation. There may be decreased recruitment in muscles affected by the central lesion. Hereditary neuropathies usually present with uniform demyelination as opposed to acquired neuropathies, where some segments have faster conduction velocities and some have slower conduction velocities.

Table 11.1

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