Chapter 023. Weakness and Paralysis (Part 4)

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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. A "pure motor" hemiparesis of the face, arm, or leg is often due to a small, discrete lesion in the posterior limb of the internal capsule, cerebral peduncle, or upper pons. Some brainstem lesions...

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Chapter 023. Weakness and Paralysis (Part 4) 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. A "pure motor" hemiparesis of the face, arm, or leg is often due to a small, discrete lesion in the posterior limb of the internal capsule, cerebral peduncle, or upper pons. Some brainstem lesions produce "crossed paralyses," consisting of ipsilateral cranial nerve signs and contralateral hemiparesis (Chap. 364). The absence of cranial nerve signs or facial weakness suggests that a hemiparesis is due to a lesion in the high cervical spinal cord, especially if
associated with ipsilateral loss of proprioception and contralateral loss of pain and temperature sense (the Brown-Séquard syndrome). Acute or episodic hemiparesis usually results from ischemic or hemorrhagic stroke, but may also relate to hemorrhage occurring into brain tumors or as a result of trauma; other causes include a focal structural lesion or inflammatory process as in multiple sclerosis, abscess, or sarcoidosis. Evaluation begins immediately with a CT scan of the brain (Fig. 23-3) and laboratory studies. If the CT is normal and an ischemic stroke is unlikely, MRI of the brain or cervical spine is performed. Figure 23-3
An algorithm for the initial workup of a patient with weakness. EMG, electromyography; LMN, lower motor neuron; NCS, nerve conduction studies; UMN, upper motor neuronSubacute hemiparesis that evolves over days or weeks has an extensive differential diagnosis. A common cause is subdural hematoma, especially in elderly or anticoagulated patients, even when there is no history of trauma. Infectious possibilities include cerebral abscess, fungal granuloma or meningitis, and parasitic infection. Weakness from primary and metastatic neoplasms may evolve over days to weeks. AIDS may present with subacute hemiparesis due to toxoplasmosis or primary CNS lymphoma. Noninfectious
inflammatory processes, such as multiple sclerosis or, less commonly, sarcoidosis, merit consideration. If the brain MRI is normal and there are no cortical and hemispheric signs, MRI of the cervical spine should be undertaken. Chronic hemiparesis that evolves over months is usually due to a neoplasm or vascular malformation, a chronic subdural hematoma, or a degenerative disease. If an MRI of the brain is normal, the possibility of a foramen magnum or high cervical spinal cord lesion should be considered. Paraparesis An intraspinal lesion at or below the upper thoracic spinal cord level is most commonly responsible, but a paraparesis may also result from lesions at other locations that disturb upper motor neurons (especially parasagittal intracranial lesions) and lower motor neurons [anterior horn cell disorders, cauda equina syndromes due to involvement of nerve roots derived from the lower spinal cord (Chap. 372), and peripheral neuropathies]. Acute paraparesis may not be recognized as due to spinal cord disease at an early stage if the legs are flaccid and areflexic. Usually, however, there is sensory loss in the legs with an upper level on the trunk; a dissociated sensory loss suggestive of a central cord syndrome; or exaggerated stretch reflexes in the legs with normal reflexes in the arms. It is important to image the spinal cord (Fig. 23- 3). Compressive lesions (particularly epidural tumor, abscess, or hematoma, but
also a prolapsed intervertebral disk and vertebral involvement by malignancy or infection), spinal cord infarction (proprioception is usually spared), an arteriovenous fistula or other vascular anomaly, and transverse myelitis, are among the possible causes (Chap. 372). Diseases of the cerebral hemispheres that produce acute paraparesis include anterior cerebral artery ischemia (shoulder shrug is also affected), superior sagittal sinus or cortical venous thrombosis, and acute hydrocephalus. If upper motor neuron signs are associated with drowsiness, confusion, seizures, or other hemispheric signs, MRI of the brain should be undertaken. Paraparesis may result from a cauda equina syndrome, for example, following trauma to the low back, a midline disk herniation, or an intraspinal tumor; although sphincters are affected, hip flexion is often spared, as is sensation over the anterolateral thighs. Rarely, paraparesis is caused by a rapidly evolving anterior horn cell disease (such as poliovirus or West Nile virus infection), peripheral neuropathy (such as Guillain-Barré syndrome; Chap. 380) or myopathy (Chap. 382). In such cases, electrophysiologic studies are diagnostically helpful and refocus the subsequent evaluation. Subacute or chronic paraparesis with spasticity is caused by upper motor neuron disease. When there is associated lower-limb sensory loss and sphincter involvement, a chronic spinal cord disorder is likely (Chap. 372). If an MRI of the
spinal cord is normal, MRI of the brain may be indicated. If hemispheric signs are present, a parasagittal meningioma or chronic hydrocephalus is likely and MRI of the brain is the initial test. In the rare situation in which a longstanding paraparesis has a lower motor neuron or myopathic etiology, the localization is usually suspected on clinical grounds by the absence of spasticity and confirmed by EMG and nerve conduction tests.