From the EM Model
12.0 Nervous System Disorders
12.7 Neuromuscular Disorders
Explore This IssueACEP News: Vol 32 – No 05 – May 2013
The evaluation and management of patients who present with peripheral neurologic complaints can cause anxiety and frustration for emergency physicians because of the wide variety of benign and life-threatening illnesses that are associated with those complaints and the fact that patients can present early in the disease process when it is more difficult to discern a specific diagnosis. Additionally, patients with peripheral neuropathies are generally only a small percentage of the patients that a typical emergency physician sees. In this review, an uncommon yet life-threatening peripheral neuropathy, botulism, will be described.
In order to diagnose a peripheral neuropathy, it is first important to differentiate it from a central neuropathy, which can be difficult because features of the history and physical examination for both overlap. Important elements to elicit in the history are the symptom onset, duration, provocative and alleviating factors, prodromal symptoms, and the degree of the neurologic deficit. The neurologic examination should focus on the following areas: sensory, motor, reflexes, and upper motor neuron signs. On the sensory examination, peripheral lesions are generally restricted to a single dermatome with a sharp border of demarcation.
With central lesions, especially spinal lesions, sensory symptoms are more commonly bilateral and involve multiple dermatomes. One area that is commonly overlooked on the sensory examination is the trunk. Specifically, patients with a thoracic spine lesion may have sensation that is symmetric and present over the legs, but in reality and in comparison to the trunk it is diminished but just not recognized by the patient or examiner.
The classic stocking-glove sensory deficit is a peripheral neuropathy that is most commonly seen with diabetes and chronic alcohol use. On motor examination, peripheral lesions usually cause unilateral weakness that is limited to the muscle group that is innervated by the involved nerve.
A central neuropathy will have weakness or paralysis distal to the site of the lesion. The findings with these central lesions are more commonly bilateral and can have associated upper motor neuron signs such as spasticity, hyperreflexia, and clonus. In some instances, the patient will complain of leg weakness but have no demonstrable weakness on the initial examination. One maneuver to help demonstrate weakness is to have the patient squat down and rise to the standing position without any assistance. Most patients without weakness are able to do this with only minor difficulty. If the patient is unable to rise or cannot rise without assistance then there is weakness.