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Chapter 13



The complaint of weakness is common in emergency department (ED) patients and may be vague, subjective, and difficult to characterize. True loss of strength from a neurologic or muscle fiber lesion must be distinguished from other systemic conditions that result in fatigue, dyspnea, or imbalance because of inadequate substrate delivery to the nervous system or muscle unit. Such conditions may be described as weakness by the patient but are likely caused by cardiovascular, pulmonary, infectious, or metabolic processes. This chapter focuses on the evaluation of acute neuromuscular weakness; it may be focal or generalized and may originate in central or peripheral nerves, the neuromuscular junction (NMJ), or myofibers themselves. Other chapters provide more detail on peripheral nerve (Chapter 107) and neuromuscular disorders (Chapter 108).


There are a number of physiologic considerations for the patient with diffuse weakness (Box 13-1).

Focal weakness confined to one area in the face or body (left, right, distal, or proximal) indicates a localized problem arising in the brain, spinal cord, peripheral nerve, or muscle.

Conditions that affect the upper motor neuron (UMN) produce signs that include spasticity to extension in the upper extremities, spasticity to flexion in the lower extremities, hyper-reflexia, pronator drift, Hoffmann’s sign, and Babinski’s sign (upgoing toes). UMN signs signify a lesion within the cerebral cortex or corticospinal tracts (CSTs) of the brainstem or spinal cord. Although these findings are not always detectable in the acute period, the presence of even one of them indicates pathology within the central nervous system.

Weakness caused by lower motor neuron (LMN) dysfunction is often accompanied by flaccidity, decreased reflexes, fasciculations, or muscle cramps. Lesions in the anterior horn of the spinal cord and its axonal extensions at the nerve root and peripheral nerve produce these findings.

Conditions that have only peripheral effects at the NMJ and muscle have preserved reflexes.

Differential Considerations

In the diffusely weak patient, first consideration is given to a systemic deficiency in substrate delivery to the nervous system or skeletal muscle unit. In patients with cardiac disease, myocardial ischemia can also be a source of generalized weakness.

History regarding circumstances at onset, progression, exacerbating or alleviating factors, and any fluctuations in severity may help the emergency physician discern if weakness is a result of cardiovascular disease, pulmonary insufficiency, the metabolic demands of a recent infection, or cancer. Review of systems can reveal orthopnea and symptoms of congestive heart failure in the fatigued patient with significant cardiac disease, chronic blood loss in the anemic patient, or incontinence in an elderly person with urosepsis.

Vital sign abnormalities, including tachycardia, tachypnea, fever, hypothermia, or hypotension, prompt immediate intervention and a search for a systemic cause of weakness. Cardiac, pulmonary, skin, and mucous membrane examinations may give the emergency physician a sense of the adequacy of the cardiovascular system in delivering substrate to brain and muscle. In such patients the neurologic examination should not demonstrate focal changes of the central or peripheral nervous system.

If by history, physical examination, and bedside ancillary testing the patient does not appear to have derangements in intravascular volume or cardiopulmonary function, metabolic abnormalities, or a source of infection, the investigation turns to a neural or primary muscular cause for weakness. Often these patients will have some asymmetrical finding on their neurologic examination. The critical and emergent diagnoses for neuromuscular weakness are listed in Table 13-1.

Table 13-1

Critical and Emergent Causes of Neuromuscular Weakness

Critical Diagnoses  
Cerebral cortex or subcortical Ischemic or hemorrhagic cerebrovascular accident (CVA)
Brainstem Ischemic or hemorrhagic CVA
Spinal cord Ischemia, compression (disk, abscess, or hematoma)
Peripheral nerve Acute demyelination (Guillain-Barré syndrome)
Neuromuscular junction Myasthenic or cholinergic crisis
Tick paralysis
Organophosphate poisoning
Muscle Rhabdomyolysis
Emergent Diagnoses  
Cerebral cortex or subcortical Tumor, abscess, demyelination
Brainstem Demyelination
Spinal cord Demyelination (transverse myelitis)
Compression (disk, spondylosis)
Peripheral nerve Compressive plexopathy (hematoma, aneurysm)
Paraneoplastic vasculitis uremia
Muscle Inflammatory myositis

Diagnostic Algorithm

Deciphering loss of muscle power means following the pattern of a patient’s weakness from the myofiber back to a particular site within the central or peripheral nervous system (Fig. 13-1). Common clinical patterns of weakness can be classified and assessed as discussed in the following sections.

Unilateral Weakness with a Combination of Arm, Hand, or Leg with Ipsilateral Facial Involvement

This presentation is generally caused by a lesion in the contralateral cerebral cortex or the CSTs coursing down the corona radiata and forming the internal capsule. Mild forms can be limited to a loss of dexterity and coordination with hand movements. Moderate loss of power is termed paresis, and complete loss of motion is termed plegia. UMN signs are useful corroborative findings but may not always be present. Sensory disturbances commonly occur over the areas of weakness. Look for associated neglect, a visual field cut, or an expressive or receptive aphasia to localize the problem to the cortex.2 Patients with equal loss of strength to the face, hand, and leg are more likely to have a subcortical lesion disrupting all of these fibers as they funnel close together in the internal capsule. Concomitant headache is suggestive of a brain hemorrhage or mass lesion.3 Sudden onset of this weakness pattern implies hemorrhage or ischemia, whereas a gradual onset may be seen in demyelination or neoplasm.

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