Case Study - 1. (Spinal Cord Case-1.)

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 visiting her physician.

The neurological evaluation revealed a weakness in the left lower limb, associated with spasticity, hypertonia, hyperreflexia at the knee, and ankle, which also demonstrated clonus.

On the left side there was a loss of two point touch, vibratory sense and proprioception at levels below the mid-trunk.

The right side showed a loss of pain and temperature sensation below dermatome T-7.

 

This classic hemisection (Brown-Sequard syndrome) at this upper thoracic level shows a left sided weakness, hyperreflexia, hypertonia, clonus and spasticity typical of upper motor neuron deficits due to a lesion involving the left lateral funiculus.

It might be possible to demonstrate a flaccid lower motor neuron type paralysis in those muscles innervated by the damaged anterior horn cells at this level. The loss of proprioception on the left is consistent with a lesion in the posterior funiculus.

The loss of the lateral spinothalamic tract at this level would explain the loss of pain sensation below dermatome T7 on the right. The pain in the left breast was the result of the pressure of the extramedullary tumor on the dorsal roots.

 

Extended Explanation


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


Briefly stated, the 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.


- Ipsilateral paralysis below the lesion. The paralysis is of the "Upper Motor Neuron" or spastic type. There is spasticity, slow (disuse) muscle atrophy, hypertonia, ankle clonus, and a positive Babinski sign.

Superficial reflexes, eg, the abdominal and cremasteric are loss. Spastic paralysis is attributed to interruption of the lateral corticospinal tract and the accompany lateral reticulospinal tract.

Loss of these upper motor neurons deprives the anterior horn cells (ie lower motor neurons), of the impuses which generates contract of skeletal muscle, hence, weakness of paralysis. Hypertonia and hyperreflexia appears to result from the loss of the inhibitory effects of the 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. The 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 achieved by:

    1) a sense of position from the vestibular system.

    2) awareness of the position and status of muscles and joints by conscious proprioception systems 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 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 spinal thalamic 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 cross 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. 

by 인체여행 | 2009/04/20 00:16 | Neuro Case Study | 트랙백 | 덧글(0)

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