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Acute peripheral neurologic lesions are a diverse group of disorders. By definition, they involve injury or disease in sensory and motor fibers outside of the central nervous system (CNS) extending to the neuromuscular junction. The peripheral nervous system (PNS) serves sensory, motor, and autonomic functions. The patient with a peripheral nerve lesion thus may have symptoms reflecting a disorder of any or a combination of these functions. Sensory symptoms may include numbness, tingling, dysesthesias, pain, or ataxia. Motor symptoms manifest as weakness. Autonomic disability may be noted as orthostasis, bowel or bladder dysfunction, gastroparesis, or sexual dysfunction. Acute peripheral neurologic processes may be due to Guillain-Barré syndrome, botulism, tick paralysis, focal compression, plexopathy, human immunodeficiency virus (HIV) disease, diabetic peripheral neuropathy, or others. Painful neuropathies alone are seen in approximately 15% of diabetics, 35% of HIV-positive patients, and 23% of patients with multiple sclerosis.1 Guillain-Barré syndrome or botulism has the potential to cause respiratory failure, so prompt recognition and treatment of these diseases is important. Most important, central processes, such as stroke or spinal cord injury, need exclusion before considering an acute peripheral lesion.


CNS and PNS neuroanatomy provides the best guide to distinguishing these lesions. Peripheral nerves contain varying amounts of motor, sensory, and autonomic fibers and follow well-described paths that make them prone to typical injuries. Thus, peripheral nerve lesions are more likely to be confined to one limb and to present with the involvement of multiple sensory modalities and motor symptoms. A typical example would be a nerve compression syndrome that involves weakness, numbness, and tingling in the upper forearm, which developed after the arm was in a peculiar position for a prolonged period during sleep and the symptoms of which worsen with change in position of the arm. However, weakness and numbness can be seen in both peripheral and central disorders. Hyporeflexia sometimes occurs with acute central lesions, but hyperreflexia and spasticity invariably develop with time. PNS disorders, like CNS diseases, can affect bulbar structures, resulting in diplopia, dysarthria, or dysphagia. Despite the potential overlap, CNS disorders frequently have other features that are not seen in peripheral diseases. For example, aphasia, apraxia, and vision loss are hallmarks of cortical disease. Perhaps the most important distinguishing component is the examination of deep tendon reflexes. Most CNS lesions will result in upper motor neuron signs: hyperreflexia, hypertonia (spasticity), and extensor plantar (Babinski) reflexes. The dorsiflexion of the great toe with fanning of remaining toes and flexion of the leg is a pathologic Babinski sign, indicating a central disruption of the pyramidal tract.


Although there can be many similarities between patients with CNS and PNS lesions, the distinctions are generally clear (Table 166-1). Lateralization of weakness, hyperreflexia, positive Babinski sign, or any other CNS finding requires further investigation for a central rather than peripheral disorder.

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Table 166-1 Differentiating Central from Peripheral Nervous System Disorders

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