Weakness and paralysis

Clinical Manifestations Food-Borne Botulism After ingestion of food containing toxin, illness varies from a mild condition for which no medical advice is sought to very severe disease that can result in death within 24 h. The incubation period is usually 18–36 h but, depending on toxin dose, can range from a few hours to several days. Symmetric descending paralysis is characteristic and can lead to respiratory failure and death. Cranial nerve involvement, which almost always marks the onset of symptoms, usually produces diplopia, dysarthria, dysphonia, and/or dysphagia.

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Acute Monoparesis If the weakness is predominantly in distal and nonantigravity muscles and not associated with sensory impairment or pain, focal cortical ischemia is likely (Chap. 364); diagnostic possibilities are similar to those for acute hemiparesis. Sensory loss and pain usually accompany acute lower motor neuron weakness; the weakness is commonly localized to a single nerve root or peripheral nerve within the limb but occasionally reflects plexus involvement.

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Hemiparesis Hemiparesis results from an upper motor neuron lesion above the midcervical spinal cord; most such lesions are above the foramen magnum. The presence of other neurologic deficits helps to localize the lesion. Thus, language disorders, cortical sensory disturbances, cognitive abnormalities, disorders of visual-spatial integration, apraxia, or seizures point to a cortical lesion. Homonymous visual field defects reflect either a cortical or a subcortical hemispheric lesion.

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Quadriparesis or Generalized Weakness Generalized weakness may be due to disorders of the CNS or of the motor unit. Although the terms quadriparesis and generalized weakness are often used interchangeably, quadriparesis is commonly used when an upper motor neuron cause is suspected, and generalized weakness when a disease of the motor unit is likely. Weakness from CNS disorders is usually associated with changes in consciousness or cognition, with spasticity and brisk stretch reflexes, and with alterations of sensation.

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Lower Motor Neuron Weakness This pattern results from disorders of cell bodies of lower motor neurons in the brainstem motor nuclei and the anterior horn of the spinal cord, or from dysfunction of the axons of these neurons as they pass to skeletal muscle (Fig. 232). Weakness is due to a decrease in the number of muscle fibers that can be activated, through a loss of α motor neurons or disruption of their connections to muscle. Loss of γmotor neurons does not cause weakness but decreases tension on the muscle spindles, which decreases muscle tone and attenuates the stretch reflexes...

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Pathogenesis Upper Motor Neuron Weakness This pattern of weakness results from disorders that affect the upper motor neurons or their axons in the cerebral cortex, subcortical white matter, internal capsule, brainstem, or spinal cord (Fig. 23-1). Such lesions produce weakness through decreased activation of the lower motor neurons. In general, distal muscle groups are affected more severely than proximal ones, and axial movements are spared unless the lesion is severe and bilateral.

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Harrison's Internal Medicine Chapter 23. Weakness and Paralysis Weakness and Paralysis: Introduction Normal motor function involves integrated muscle activity that is modulated by the activity of the cerebral cortex, basal ganglia, cerebellum, and spinal cord. Motor system dysfunction leads to weakness or paralysis, which is discussed in this chapter, or to ataxia (Chap. 368) or abnormal movements (Chap. 367). The mode of onset, distribution, and accompaniments of weakness help to suggest its cause. Weakness is a reduction in the power that can be exerted by one or more muscles.

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