Which clinical history findings are characteristic of toxic neuropathy?

Updated: Dec 06, 2017
  • Author: Jonathan S Rutchik, MD, MPH, FACOEM; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
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Answer

Patients with neuropathy typically present with symptoms of pain, tingling, or numbness in their feet, consistent with dysfunction affecting the longest and largest fibers of the PNS. In some cases, they may have weakness (distal more than proximal) or difficulty with gait. In other cases, patients may also present with symptoms of pain. This may suggest a small fiber neuropathy, which exists when small myelinated and unmyelinated fibers are involved. Clinically, pain may be accompanied by restless leg syndrome, a condition in which disagreeable leg sensations and an irresistible urge to move occur prior to sleep onset.

Additionally, other forms of autonomic dysfunction may be present such as hypohidrosis or hyperhidrosis, diarrhea or constipation, urinary incontinence or retention, gastroparesis, sicca syndrome, blurry vision, facial flushes, orthostatic intolerance, or sexual dysfunction. Autonomic dysfunction may present as cramping. In these cases, the examination reveals normal proprioception, vibration, power or bulk, reflexes, and normal findings on electromyography (EMG) or nerve conduction studies (NCS). [3]

The clinician needs to exercise a high index of suspicion to uncover toxic etiologies. A patient beginning a new medication in the last few weeks or months should raise a red flag. Certainly, the search for an underlying chronic disease is the most common workup ordered; however, new medications are commonly a culprit.

Toxic neuropathy due to recreational drug or chemical abuse may be more difficult to uncover than occupational or environmental exposures, since direct questioning of the patient may lead to incorrect information. In some cases, a dramatic systemic reaction leads to an emergency department (ED) visit because of an acute alteration of consciousness, heralding the diagnosis of drug abuse. The challenge for the ED clinician at this point is to uncover the agent of ingestion or inhalation. Neuropathy, in these cases, may present over a few days to weeks since the dose is often higher than in prescribed-medication settings.

Occupationally induced neuropathies may be secondary to low-level, long-term exposures. The differential diagnosis may not include a work-related exposure, since physicians often are not trained to ask questions about patients' work practices or environment. The presentation may coincide with other lifestyle and medication changes and recent medical diagnoses. After a high-level acute exposure, an occupational etiology for toxic neuropathy may be easier to consider.

Environmental exposure–induced neuropathies follow the same pattern as those from occupational exposures; however, they are omitted even more commonly from the differential diagnosis. For example, a physician is even less likely to ask questions about the patient's use of groundwater, proximity to pesticides, or household use of organic solvents than about occupational exposures. As with occupational exposure, environmental exposures often are very low level, but they are long term and more intensive than occupational exposures, lasting longer than a 40-hour workweek for the duration of employment. Patients who have had high-concentration acute exposure from an environmental accident may present with more obvious clinical symptoms. A differential diagnosis ruling out more common causes of neuropathy is mandatory to establish the cause of neuropathy. [4, 5]

Prior to appearance of symptoms, subclinical findings on EMG or NCV studies may be apparent and consistent with axonal or demyelinating abnormalities. Occupational or environmental exposure at doses approaching regulatory levels for duration or intensity may warrant such an evaluation. Often these are performed in field studies with the use of portable apparatus. Dysfunction associated with environmental exposure to TCE, mainly subclinical, is revealed by electrodiagnostic techniques.

Pain or numbness in the distribution of the trigeminal nerve suggests a disorder of that nerve.


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