Peripheral Neuropathy:
A Diagnostic Case Study


by Hsien Young, MD, neurologist, neurophysiologist and sleep medicine specialist at Santa Barbara Neuroscience Institute at Cottage Health System


Diagnosing peripheral neuropathies can be an intimidating, confusing and costly process. Focused history-taking and a thorough neurological exam-with attention to the pattern of involvement and time course of symptoms-narrows the differential diagnosis, helps focus evaluation and expedites treatment. A systemic approach using an algorithm can be very helpful. A peripheral nerve algorithm based on key elements of history and physical examination helps focus workup and evaluation of any patient with neuropathy complaints and suggests the timing of neurological consultation.


Peripheral neuropathies are disease processes that affect any region of the peripheral nervous system, including the cranial nerves, the spinal nerve roots, the dorsal root ganglia, and the peripheral nerve trunks and their terminal branches. Nerve cells are composed of cell bodies and axons. The axons can be large myelinated, small myelinated or small unmyelinated. The most common neuropathies are those involving small myelinated and unmyelinated fiber types and are called small-fiber neuropathies.


Factors in Diagnosis

The workup of peripheral neuropathy should focus on three key points: 1) sensory and/or motor involvement; 2) symmetry; and 3) temporal progression. Motor weakness and cranial nerve involvement often indicate malignant disease. When present, early neurological consultation is always recommended.




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The most common neuropathies, such as diabetic neuropathy, are often symmetrical. Asymmetric neuropathies include common compressive neuropathies such as carpal tunnel syndrome. When the neuropathy is symmetrical, a proximal versus distal pattern becomes important. Toxic and metabolic neuropathies usually present with symmetrical and distal symptoms. Proximal sensory neuropathies are very rare, with porphyria as the main differential. Predominantly motor neuropathies, including Guillain-Barré Syndrome, are often proximal.



The temporal course of a neuropathy varies widely based on the etiology. With trauma or ischemia, the onset is acute, with maximum symptoms at onset. Inflammatory and some metabolic neuropathies have a subacute course extending over days to weeks. A more chronic course over weeks to months is the hallmark of most toxic and metabolic neuropathies. The very slowly progressive neuropathy over many years is the usual pattern of hereditary neuropathies or of chronic inflammatory demyelinating polyneuropathy.


The clinical assessment should

include a detailed medical history. Many systemic diseases, such as diabetes or hypothyroidism, can   A) Normal  B) Axonal neuropathy  C) Demyelinating neuropathy

 be associated with neuropathy. Many medications can cause a peripheral neuropathy. Social history regarding illegal drugs, alcohol, exposures to heavy metals, chemicals, solvents, HIV risk, travel involving potential exposure to leprosy or Lyme disease, dietary nutritional deficit, and vitamin use (such as megadoses of vitamin B) should be documented. A detailed family history should include inquiries as to the presence of hammertoes, high arches, weak ankles and gait abnormalities in immediate and extended family members.


Possible causes

Peripheral neuropathy has a dizzying array of causes, including hereditary, toxic, metabolic, infection, inflammatory, ischemic, trauma and paraneoplastic disorders. The use of an algorithm can help the busy practitioner navigate the diagnostic process by identifying a pattern in the patient's history and examination results and then including or excluding diagnostic possibilities based on clinical knowledge and training.


To learn more about diagnostic services at Santa Barbara Neuroscience Institute at Cottage Health System and/or to download a copy of the clinical algorithms that support this article, visit



Case Study

Peripheral Neuropathy


A 58-year-old overweight male with a history of borderline diabetes and mild carpal tunnel syndrome presented to his family doctor with increasing numbness and tingling of his hands. He was noted to have had flu-like symptoms with diarrhea two weeks earlier, which had since been resolved. The patient was suspected of having carpal tunnel syndrome exacerbation and was sent home with new wrist splints.


Two days later, the patient complained to his wife that his feet were tingling and slightly numb. The following day, while walking on the beach with his wife, the patient fell multiple times. He was unable to finish this exercise, which had to that point been part of the couple's daily routine. His wife called their family doctor, who advised them to go to the emergency room immediately.


In the ER, the patient was found to have weakness in all extremities, absent of reflexes, with patchy distal sensory deficits. Neurology consultation confirmed the ER physician's findings with high suspicion of Guillain-Barré Syndrome (GBS). Lumbar puncture, cerebrospinal fluid (CSF) examination, was ordered after computed tomography scan confirmed it was safe to proceed. CSF protein was 157, supporting the diagnosis of GBS.


The patient was admitted to the hospital and started on intravenous immunoglobulin (IVIG) treatment. The following day, nerve conduction studies confirmed asymmetrical sensory motor neuropathy consistent with a diagnosis of GBS.


Over the next week, the patient received four more IVIG treatments. He had steady recovery with improved nerve conduction study results. He required intensive rehabilitation, with physical and occupational therapy, over three months, resulting in full recovery of neurological function.