An easy approach to evaluating peripheral neuropathy

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Applied Evidence

An easy approach to evaluating peripheral neuropathy

J Fam Pract. 2006 October;55(10):853-861

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References

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When: The time course of signs and symptoms

Knowing whether the onset of neuropathy was definite and abrupt or was gradual is the most helpful temporal clue to possible underlying causes. The time course (ie, tempo) following onset is also important.

An acute/subacute onset with a definite date often suggests an immune-mediated or an infectious process (FIGURE). With respect to immune-mediated neuropathies, consider primarily autoimmune conditions (eg, Guillain-Barré syndrome, vasculitic neuropathy) and also paraneoplastic autoimmune syndromes (eg, subacute sensory neuropathy). In the latter case, a cancer presents to the immune system an epitope that is similarly found in the nervous system, prompting an autoimmune attack of the nervous system. Both autoimmune and infectious processes almost always have a rapid start on a definite date.

With an insidious onset, the patient won’t recollect a definite date on which the neuropathy began. The underlying mechanism usually is an inherited, metabolic, or toxic process—or idiopathic, if a cause cannot be identified.

FAST TRACK

Acute/subacute onset often suggests an immune-mediated or infectious process

The disease course sheds additional light on the causative mechanism. Onset and subsequent progression often correlate in a predictable manner, owing in part to the underlying mechanism. For example, an acute onset neuropathy often is followed by rapid disease progression, especially when caused by an autoimmune process (Guillain-Barré and vasculitic neuropathy). On the other hand, a neuropathy of insidious onset usually follows a slow or even static course. But there are exceptions that may make the diagnosis challenging and illustrate the need for clinical follow-up.

What setting

The patient’s medical history, medications, social and family history, and a review of systems can uncover known risk factors for neuropathic processes.

Common causes of acquired polyneuropathies are diabetes mellitus, chronic renal disease, and alcohol dependence. If a patient with distal, symmetric sensory complaints also has any of these conditions, a causal relationship should be considered. Another example is the patient with a history of bariatric surgery, which could lead to neuropathy as a result of malnutrition, particularly vitamin B₁ and B₁₂ deficiencies.¹³

The clinical setting may indicate a need for further evaluation by a neurologist. For example, a family history of inherited neuropathy in a patient with high arches and curled “hammer” toes would strongly suggest Charcot-Marie-Tooth (CMT) disease, also known as hereditary motor and sensory neuropathy. A patient with a monoclonal gammopathy may have a paraproteinemic neuropathy that warrants further evaluation by a neuromuscular specialist. Although more rare, a paraneoplastic cause would warrant consideration in a smoker, especially if the neuropathy was subacute. In many cases, neuropathic symptoms are the first clue of a new medical condition (eg, impaired glucose tolerance).

Electrodiagnostic testing: What it can and can’t tell you

Most polyneuropathies warrant additional electrodiagnostic evaluation in an electromyography (EMG) laboratory. Electro-diagnostic testing comprises 2 procedures: nerve conduction studies and needle electrode examination.

Preparing your patient. When ordering this study, be sure to discuss it thoroughly with the patient. The entire study typically takes an hour or longer. And it can be painful, though in our experience nearly every patient tolerates the procedure. Most important for the patient to understand is that information gleaned from electrodiagnostic testing may be essential to the diagnosis, as explained below.

Many benefits of the study. First, electrodiagnostic testing can confirm a peripheral neuropathic basis for a patient’s complaints.

Second, electrodiagnostic testing helps characterize a neuropathy as primarily demyelinating, primarily axonal, or mixed demyelinating and axonal. An example of this benefit is that a primary demyelinating characterization greatly narrows the list of possible causes (eg, Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy, Charcot-Marie-Tooth disease type 1).

Third, electrodiagnostic testing assists in characterizing the neuropathic process as sensory, motor or sensorimotor.

Fourth, electrodiagnostic testing helps localize the neuropathic process (the “where”).

Fifth, electrodiagnostic testing can gauge the severity of the neuropathic process.

FAST TRACK

Electrodiagnostic testing helps characterize a neuropathy as primarily demyelinating, axonal, or a mix of the two

Limitations of the study. When the study returns normal results, keep in mind it has limited sensitivity. For example, nerve conduction studies are only able to assess the function of larger myelinated nerve fibers; a neuropathic process solely in small fibers will not be evident with this test. Likewise, the needle electrode examination is unable to assess small nerve fiber status. We include this caveat in our electrodiagnostic testing reports of patients who have symptoms suggestive of pure small fiber polyneuropathy.

When might blood studies be useful?

Laboratory testing of blood is often of great value, but only after a particular polyneuropathy has been characterized and placed into one or more potential etiologic subgroups.