Spinal Cord
Lesions

( Return to Lesions Front Page )

1) HEMISECTION OF THE SPINAL CORD (BROWN-SEQUARD SYNDROME)

Pure hemisection of the cord rarely occurs but it is among the best cases for illustrating the features of spinal cord injury.

Briefly stated, symptoms include: spastic paralysis, loss of position sense, discriminative touch and vibratory sense on the side of the lesion - this represents involvement of the lateral corticospinal tract and the posterior white column on the side of the lesion. On the side opposite the lesion there is a loss of pain and temperature due to involvement of the lateral spinothalamic tract. At times, it is possible to also demonstrate a bilateral sensory deficit and flaccid paralysis at the level of the lesion.

A Sample Case: A young woman complained of pain in her left breast and progressive weakness of her left lower limb for a period of many months before finally visiting her physician.

The neurologic evaluation revealed weakness in the left lower limb. This was associated with spasticity (increased tone), hyperreflexia (increased deep tendon reflexes) at the knee and ankle, which also demonstrated clonus. On the left side there was loss of two-point touch, vibratory sense and proprioception at levels below the hip. The right side showed a loss of pain and temperature sensation below dermatome T-7.

The patient was determined to have an extramedullary tumor expanding from the dorsal roots at spinal cord levels T-5,6.

Explanation -

Ipsilateral paralysis below the lesion. Paralysis is the "Upper Motor Neuron" or spastic type; there is spasticity, slow (disuse) muscle atrophy, hypertonia, ankle clonus and a positive Babinski sign. Superficial reflexes, e.g., the abdominal and cremasteric are lost. Spastic paralysis is attributed to interruption of the lateral corticospinal tract and the accompanying lateral reticulospinal tract. Loss of these upper motor neurons deprives the anterior horn cells, i.e., lower motor neurons, of the impulses which generate contraction of skeletal muscle, hence, weakness (paresis) or paralysis. Hypertonia and hyperreflexia appear to result from loss of the inhibitory effects of these two descending motor pathways on the stretch reflexes, leaving them hyperexcitable to segmental muscle afferents .

It may be possible to also demonstrate a "Lower Motor Neuron Syndrome" or flaccid paralysis ipsilaterally at the level of the lesion. If the anterior horn cells supplying the skeletal muscles are injured at the level of the lesion then these muscles are denervated. This paralysis is of the flaccid type; muscles undergo rapid atrophy due to loss of the trophic influence of the nerves as well as disuse. Tone and tendon reflexes are diminished since they are reflex responses and the injured lower motor neurons are the "final common pathway" to the muscle in the stretch reflex, hence, there is no reflex.

Loss of conscious proprioception, two-point discrimination and vibratory sense ipsilaterally is due to interruption of the posterior white columns (fasciculus gracilis/cuneatus). This is frequently accompanied by a Romberg sign. A normal individual, standing erect with heels together and eyes closed, sways only slightly. Stable posture is achieve by 1) a sense of position from the vestibular system, 2) awareness of the position and status of muscles and joints by conscious proprioception and 3) visual input regarding our position. Closing the eyes has only slight effect on the normal individual's stance since the vestibular and conscious proprioception systems are sufficient. In a patient with an impaired posterior column conscious proprioception is diminished; when the eyes are closed loss of both systems renders the patient unstable and they are likely to sway or fall to the side.

Pain and temperature sensation is lost below the lesion, on the opposite side beginning about one dermatomal segment below the level of the lesion. These sensations are carried by the lateral spinothalamic tract whose fibers originated on the side opposite the lesion but which crossed in the anterior white commissure. Dorsal root afferents carrying pain and temperature synapse in the dorsal gray; the second order neuron crosses in the anterior white commissure along an ascending path for a distance of about one spinal segment. Because of the oblique ascent of the crossing fibers in the anterior white commissure, injury of the spinothalamic tract is not likely to be carrying sensation from that level.

A careful sensory evaluation may reveal that at the dermatomal level of the lesion there is a bilateral loss of pain and temperature sensation. Since the second order neurons from both sides cross in the midline below the central canal, a hemisection of the cord may interrupt the crossing fibers from both sides and produce this limited bilateral deficit.

The pain in the left breast was the result of the pressure of the tumor on the dorsal root.