Midline back pain is the most common presenting symptom (90%) (Gilbert et al. 1978; Sundaresan et al. 1985; Harrington 1988; Maranzano and Latini 1995). It is typically localized to the level of cord compression and, unlike degenerative disc disease, it is exacerbated by recumbency and improved by upright posture (Dodge et al. 1951). Radicular pain secondary to nerve root compression is less frequent but highly localizing. Symptom progression is usually slow with pain predating further neurologic changes by a median of 7 weeks (Quinn and DeAngelis 2000). Progression of neurologic dysfunction can, on occasion, take place over a matter of hours or days; therefore, new onset back pain in a cancer patient requires urgent evaluation.

Motor weakness is the second most common feature of cord compression. As a result of delays in both pre sentation and diagnosis, more than three-quarters of patients present with objective motor deficits (Gilbert et al. 1978; Harrington 1988). Regardless of the compression site, weakness begins in the legs and affects proximal muscle groups first (Quinn and DeAngelis 2000). Progression to paraplegia is typically a late event. Sensory changes are also common (50%) and occur soon after the onset of muscle weakness (Tazi et al. 2003). Symptoms include hyperesthesia at the level of compression or paresthesias and sensory loss in the toes with proximal ascent. Urinary retention, fecal incontinence, and impotence are usually late signs indicating autonomic dysfunction. An exception is cauda equina syndrome in which lumbar metastases cause compression of the conus medullaris. Autonomic dysfunction can occur early in this setting and sensory loss often assumes a saddle-like distribution.

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