1. 
   

   What are the symptoms and signs of peripheral neuropathy?

   
   
2. 
   

   Which patients with peripheral neuropathies require hospitalization?

   
   
3. 
   

   Which peripheral neuropathies are seen in the inpatient setting?

   
   
4. 
   

   What are the common causes of peripheral neuropathies?

   
   
5. 
   

   How are peripheral neuropathies evaluated?

   
   
6. 
   

   What are the best treatment options for peripheral neuropathy?

Nontraumatic peripheral neuropathy is present in 2.4% of the general population and in as many as 8% of individuals over the age of 55. Diabetes is the most common cause in developed nations. At least 60% of diabetics have objective evidence for peripheral neuropathy. Overall, diabetic neuropathy ranks third behind macrovascular disease and nephropathy in lifetime expenditures associated with diabetic complications. Neuropathy is responsible for more hospital admissions than all the other diabetic complications combined and is a causative factor in up to 75% of all nontraumatic amputations.

Peripheral neuropathy is classified by the level of anatomical involvement (Table 214-1).

Radiculopathy affects the spinal root, leading to pain, paresthesias, and weakness in the distribution of the nerve root. It is most often caused by herniation of an intervertebral disk. Other causes include Lyme disease.

Plexopathy involves either the brachial plexus or the lumbosacral plexus, with symptoms involving multiple nerves. Causes include trauma, tumor infiltration, bony or vascular compression, radiation injury, and viral infection. Plexopathy may occur acutely in-hospital as a procedural complication, as in lumbosacral plexopathy due to groin hematoma after cardiac catheterization, or brachial plexopathy from stretch injury after cardiothoracic surgery.

Mononeuropathy is dysfunction of a solitary peripheral nerve. This is typically due to trauma (as in footdrop from peroneal nerve palsy after fibular fracture), compression (as in “Saturday night palsy,” compression of the radial nerve in the axilla from falling asleep with the arm draped over a park bench or other hard surface, as seen in alcoholics), or entrapment (median nerve in carpal tunnel syndrome). Involvement of several noncontiguous individual nerves is referred to as multiple mononeuropathies or mononeuropathy multiplex; vasculitis is the most common cause.

Polyneuropathy affects many peripheral nerves simultaneously, with distal and more or less symmetric involvement. Symptoms typically begin in the feet before ascending to involve the legs and hands. It may involve sensory, motor, and autonomic nerves, either in isolation or varying combinations. Sensory symptoms may be persistent or intermittent. Positive sensory symptoms (dysesthesias or paresthesias) are described as tingling, burning, freezing, and electric-like. Negative sensory symptoms include numbness and anesthesia. Allodynia or dysesthesia occurs when innocuous stimuli are perceived as being painful. Loss of balance, incoordination, and gait difficulty may also occur with sensory neuropathies. Weakness, when present, is also generally distal and symmetric. Symptoms of autonomic neuropathy (Table 214-2) include lightheadedness or orthostatic hypotension, diminished sweating with heat intolerance, and diarrhea. They may be mistaken for nonneurologic illness. Autonomic neuropathy may be prominent in diabetes mellitus, Guillain–Barré syndrome, uremia, porphyria, and amyloidosis.

Polyneuropathy is classified by the temporal onset of symptoms (Table 214-3): acute (< 4 weeks’ duration), subacute (4–8 weeks’ duration), or chronic (> 8 weeks’ duration). Polyneuropathy may further be subclassified into axonal, demyelinating, or mixed injury, based on the results of nerve conduction studies.

Acute Polyneuropathy

Acute or subacute polyneuropathies tend to be inflammatory, infectious, or postinfectious in origin. Acute symmetric polyneuropathy with the rapid onset of ascending paralysis is usually due to acute inflammatory demyelinating polyradiculoneuropathy (AIDP), also known as Guillain–Barré syndrome. AIDP results from an autoimmune attack on peripheral nerves. It is preceded by recent Campylobacter jejuni infection in up to one third of cases. AIDP also occurs after viral infections, such as cytomegalovirus and Epstein–Barr virus. The diagnosis is based on the development of symmetric and ascending weakness of the limbs, hyporeflexia or areflexia, with variable sensory and cranial nerve involvement. Autonomic failure with fluctuating blood pressure and heart rate occurs in one third of patients and is a significant cause of morbidity. An elevated cerebrospinal fluid (CSF) protein without cells (albuminocytological dissociation) is diagnostic. AIDP has also been reported in the setting of recent human immunodeficiency virus (HIV) infection, viral hepatitis, Lyme disease, lymphoma, and systemic lupus erythematosus. Other causes of acute flaccid paralysis are listed in Table 214-4.