Paraplegia and Spinal Cord Syndromes

Paraplegia and quadriplegia may result from a variety of systemic and primary central nervous system medical conditions as well as trauma at all segmental levels of the spinal cord ( Box 27.1 ). A spinal cord syndrome may develop from extramedullary and intramedullary pathological processes. Initial symptoms may be gradual in onset and progressive, including pain, dysesthesia, or subtle upper or lower extremity weakness. In other cases, such as an inflammatory myelitis, acute onset of severe motor, sensory, and autonomic deficits may develop without premonitory symptoms. Trauma from a cervical flexion-extension injury, for example, may produce a central cord injury of the lower cervical spinal cord with incomplete quadriparesis, whereas a complete transection injury at the lower thoracic spinal cord from a fall may result in complete paraplegia. Thus both the rostrocaudal segmental level of disease involvement or trauma and completeness of the lesion in the transverse plane anticipate the person’s impairments and disability. Details about the relationships between specific spinal cord segments and sensory dermatomes are reviewed in Chapter 31 , and the segmental innervations of specific muscle groups are reviewed in Chapters 32 and 33 . The sensorimotor clinical examination enables localization of the lesion ( Fig. 27.1 ).

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Characteristic sensory disturbances found in various spinal cord lesions in comparison with peripheral neuropathy.

When a patient who presents with paraparesis or paraplegia is being examined, a careful neurological examination is critical for planning additional diagnostic workup and care. Identifying distinct spinal cord syndromes and determining the likely location of the underlying pathological process will guide subsequent imaging and electrodiagnostic studies. As in most upper motor neuron or motor unit diseases, fatigability of strength occurs with repetitive movements against light resistance. For example, even when the initial manual muscle exam does not detect iliopsoas weakness, 10 leg raises from the supine position against light downward hand compression may reveal mild paresis upon immediately retesting hip flexion. Structural information about the integrity of the spine may be obtained from radiographic plain films and computed tomography (CT) for bone pathology. Myelography is indicated when extrinsic cord compression is suspected, especially when magnetic resonance imaging (MRI) is contraindicated. MRI with contrast best reveals intrinsic and extrinsic cord pathology. Spinal angiography identifies vascular pathology. A review of imaging of the spine is provided in Chapters 40 and 41 .

Acute and long-term patient care is influenced by the clinical presentation, severity of neurological deficits, underlying pathology, and prognosis for gains over time. Patients presenting with an acute spinal cord syndrome after trauma show both early (days to 3 months) and late (up to 2 years) changes in their motor and sensory deficits ( ). Both neurological improvements and clinical worsening may occur. When some sparing of sensation and movement is present in the first 72 hours after trauma, the prognosis for walking is rather good. Indeed, up to 90% of patients with a cervical central cord injury who have any spared sensation and movement below the level of injury by 4 weeks after trauma will become functional ambulators ( ). Thus serial and careful neurological examinations are important for monitoring the injury-related deficits, especially in the first weeks after onset. Rehabilitation of patients with paraplegia follows after the acute medical needs have been addressed. The aim is to promote as much functional independence as possible with and without assistive devices, decrease the risk of complications, and reintegrate the patient into home and community. Neurological rehabilitation for paraparesis after spinal cord syndromes is reviewed in Chapter 55 .