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
Table 166-1 Differentiating
Central from Peripheral Nervous System Disorders
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