Acute spinal cord transection syndrome. Complete transection of the spinal cord, whether of traumatic, neoplastic, vascular, or other origin, causes isolation of the segments below the level of the lesion. The upper portions of the cerebrospinal axis function normally, but motor, sensory, and autonomic functions are lost distal to the lesion. Acute spinal cord trauma initially produces so-called spinal shock, a clinical picture whose pathophysiology is incompletely understood. Below the level of the lesion there is complete, flaccid paralysis, and all types of sensation are lost. Bladder, bowel, and sexual function are lost too. There are also trophic changes below the level of the lesion e. g. decubitus ulcers). The upper border of the sensory deficit (the “sensory level”) is often demarcated by a zone of hyperalgesia. In the days and weeks after the causative event, the spinal neurons gradually regain their function, at least in part, but remain cut off from most of the centrally derived neural impulses that normally regulate them. They thus become “autonomous,” and so-called spinal automatisms appear. In many cases, a stimulus below the level of the lesion induces sudden flexion of the hip, knee, and ankle (flexor reflex); if the spinal cord transection syndrome is complete, the limbs retain the flexed position for a long time after the stimulus because of a spastic elevation of muscle tone. (In incomplete spinal cord transaction syndrome, on the other hand, the legs are initially flexed upon stimulation, but then return to their original position.) Defecation and urination gradually function again, but are no longer under voluntary control; instead, the bladder and bowel are emptied reflexively once they are filled to a certain point. Detrusorsphincter dyssynergia causes urinary retention and frequent, reflexive micturition. The deep tendon reflexes and muscle tone gradually return and can become pathologically elevated.
Progressive spinal cord transection syndrome. When spinal cord transaction syndrome arises gradually rather than suddenly, e. g., because of a slowly growing tumor, spinal shock does not arise. Progressively severe spastic paraparesis develops below the level of the lesion, accompanied by a sensory deficit, bowel, bladder, and sexual dysfunction, and autonomic manifestations.
Cervical spinal cord transection syndrome. Spinal cord transection above the level of the third cervical vertebra is fatal, as it abolishes breathing (total loss of function of the phrenic and intercostal nerves). Transection at lower cervical levels produces quadriparesis with involvement of the intercostal muscles; breathing may be dangerously impaired.
Thoracic spinal cord transection syndrome. Transection of the upper thoracic cord spares the upper limbs but impairs breathing and may also cause paralytic ileus through involvement of the splanchnic nerves. Transection of the lower thoracic cord spares the abdominal muscles and does not impair breathing.
Lumbar spinal cord transection syndrome. Traumatic transection of the spinal cord at lumbar levels often causes especially severe disturbances because of concomitant damage of the major supplying artery of the lower spinal cord, the great radicular artery (of Adamkiewicz). The result is infarction of the entire lumbar and sacral spinal cord.
Epiconus syndrome, caused by a spinal cord lesion at the L4 to S2 level. Unlike it is associated with spastic or flaccid paresis of the lower limbs, depending on the precise level of the lesion. There is weakness or total paralysis of hip external rotation (L4-S1) and extension (L4-L5), and possibly also of knee flexion (L4-S2) and flexion and extension of the ankles and toes (L4-S2). The Achilles reflex is absent, while the knee-jerk reflex is preserved. The sensory deficit extends from L4 to S5. The bladder and bowel empty only reflexively; sexual potency is lost.
Conus syndrome, due to a spinal cord lesion at or below S3, is also rare. It can be caused by spinal tumors, ischemia, or a massive lumbar disk herniation. An isolated lesion of the conus medullaris produces the following neurological deficits: detrusor areflexia with urinary retention and overflow incontinence, fecal incontinence, impotence saddle anesthesia (S3-S5), loss of the anal reflex, the lower limbs are not paretic.
Cauda equina syndrome involves the lumbar and sacral nerve roots, which descend alongside and below the conus medullaris, and through the lumbosacral subarachnoid space, to their exit foramina; a tumor (e. g., ependymoma or lipoma) is the usual cause. Patients initially complain of radicular pain in a sciatic distribution, and of severe bladder pain that worsens with coughing or sneezing. Later, variably severe radicular sensory deficits, affecting all sensory modalities, arise at L4 or lower levels. Lesions affecting the upper portion of the cauda equina produce a sensory deficit in the legs and in the saddle area. There may be flaccid paresis of the lower limbs with areflexia; urinary and fecal incontinence also develop, along with impaired sexual function.