Case 7.  Tunnel Vision

The patient had heart valve surgery six years ago and received a mechanical mitral valve implant. One day at work he abruptly collapsed unconscious. By the time EMTs brought him to the hospital, he had regained consciousness. In the emergency department, he was found to have "tunnel vision," i.e., he was blind except in the central parts of his visual fields. He could not remember new events or new facts for more than 40 to 50 seconds, and was therefore unable to learn any doctor's name or even to appreciate that he was in a hospital.

By the following afternoon, the blindness and inability to memorize new information began to gradually improve. Eventually, the only neurologic problem remaining was total amnesia for a period of about six weeks prior to this incident.

Diagrams
     

 

Expert Note Case 7.
Tunnel Vision
Diagrams

Likely a piece of thrombus that had formed on the surface of the mechanical heart valve broke off.  The resulting embolus probably passed through the systemic circulation and eventually reached the basilar artery, through which it traveled until it reached the narrow region just below the upper bifurcation. There it got stuck, suddenly blocking the vessel.

The patient's collapse and temporary unconsciousness were caused by the sudden interruption of input from rostral parts of the brainstem reticular formation to the cerebral cortex. Function was quickly restored when the embolus obstructing the basilar bifurcation broke apart.  However, the remaining fragments of the embolus entered both PCAs and briefly blocked cortical branches bilaterally before completely disintegrating. The nearly complete loss of vision reflected malfunction of much of the primary visual cortex due to ischemia. The eventual restoration of the patient's normal visual fields proved that these cortical neurons were not permanently damaged.  Throughout the episode, the patient's central vision was unaffected, suggesting that the macular representation within his brain lay in the MCA-PCA border zone. That region continued to receive adequate blood supply through distal cortical branches of the MCA.

The cortical branches of the PCA to the inferior medial temporal lobes also supply the hippocampal formation and its major output pathway, the fornix. These structures are important for specific memory functions, as illustrated by this case. The patient was able to converse with his physicians throughout the episode, so he remembered how to use language. Furthermore, he was able to briefly remember new people and factual information. However, he was incapable of retaining or retrieving this new information after more than a minute elapsed. This problem is sometimes described as a Korsakoff-type memory defect. The patient soon recovered normal memory function except for amnesia, a "hole in his memory," for events that occurred in the 3-4 weeks immediately prior to his stroke.

In this patient, brief ischemia involving the hippocampal formation and its connections permanently disrupted the consolidation of memories involving events just prior to the stroke. This suggests that the process of converting a block of temporally-related memories from a transient to a more permanent form occurs slowly, over a period of weeks. In this patient, the amnesia resulted from bilateral hippocampal damage. However, even unilateral PCA strokes can cause amnesia, particularly if the stroke occurs in the left hemisphere.