Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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1. Recovery of function is a fragile state. For months after brain injury recovery of locomotion is vulnerable to transient disruption by drugs either blocking NA release, such as clonidine or by alpha-1 Noradrenergic antagonists such as prazosin. Animals recovered on beam walking tests when given either clonidine or prazosin show a transient reinstatement of hemipegic symptoms appearing as in the first week after injury. The doses of prazosin or clonidine have no effect in normal animals. This is important as stroke patients are often started on these drugs shortly after an infarct [8,9].

2. This vulnerability to reinstatement by prazosin remains unchanged for as long as a year after TBI. There is no tolerance to this effect and repeated administrations can produce hemiplegic symptoms which persist for over 9 hours. Correctional analysis indicate that the severity of symptom reinstatement months after injury is predictable by the severity of symptoms measured 24 hours after injury.

3. This r einstatement is not due to a nonspecific effect as it is produced by alpha-1 NA antagonists such as prazosin but not beta NA receptor blockers such as propranolol. Neither is it due to a soporific drug effect since a sedating dose of barbiturate does not produce a reinstatement of hemiplegia [5].

4. Apparently some minimal level of cerebral NA is required for the maintenance of functional recovery that is altered by brain injury [10]. It has been proposed that pharmacological increases of NA interacts with Physical Therapy to produce an enduring enhancement of functional recovery after stroke in laboratory and clinical studies [6,8,9].

5. The mechanism for the transient pharmacological reinstatement of deficits in recovered animals does not have a satisfactory explanation. Perhaps drugs reducing noradrenergic transmission or blocking alpha-1 NA receptors reinstate deficits by a perturbation of the metabolism of incompletely recovered neurons. There is evidence of a role for NA in lessening cerebral h ypometabolism after brain injury(12). The recovery to normal or adapted activity of these previously dysfunctional cells is apparently maintained by NA and may be one basis of recovery of function.

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