Introduction | Case 1 | Case 2 | Case 3 | Case 4 | Case 5 | Case 6

Case 1.

A 24 year old male was brought into the emergency room following a motorcycle accident.  He suffered an apparent fracture of the spine in the lower back region.  Neurological examination revealed the following:

1. spastic paralysis of the lower left limb;
2. increased deep tendon reflexes of the lower left limb;
3. Babinski sign on the left;
4. loss of position sense, touch and pressure sensations of the lower left limb;
5. complete anesthesia of the L2 dermatome on the left side;
6. loss of pain sensations and thermal anesthesia of the L3-S4 dermatomes on the right side.

Case 1  is a classic example of the Brown Sequard Syndrome.  Damage to the left side of the cord produces the symptoms of an upper motor neuron disease in the left lower limb since the lateral cortical spinal tract has been severed on the left side of the cord (the descending cortical spinal tract has already crossed in the lower medulla at the decussation of the pyramids).  Complete loss of sensation on the left side at the L2 dermatome indicates that the injury is at the level of the second lumbar segment of the cord.  This is confirmed by the "crossed" loss of different sensations below the L2 dermatome.   Loss of proprioception and fine touch on the lower left limb is due to damage to the fasciculus gracilis on the left side of the cord.  These modes of somatosensory information ascending toward the brainstem have not yet crossed.  On the other hand, loss of pain and temperature in the right lower limb is due to damage to the anterior spinal thalamic tract on the left side - remembering that these modes of somatosensory information immediately cross in the anterior white commissure.

It is unlikely that these deficits would be seen immediately following the accident.  In fact, it is more likely that flaccid paralysis and the absence of reflexes would be noted at and below the lesion.  This is due to spinal shock, which may be a function of the sudden loss of numerous descending modulatory influences on motor function whose net effect are facilatory in maintaining motor tone.   It may take from days to weeks to recover from this shock depending upon the nature and extent of the damage.  It is important to remember that during this period that loss of bladder function and sensation of bladder fullness can become complicating factors.  Until reflexes recover, early catherization is required to minimize distention, infection and damage.