Surgical management of knee dislocations with ligament reconstruction associated with a hinged external fixator.

INTRODUCTION: Knee dislocations are defined as ligament injuries involving at least two of the four most important knee ligaments. Results from recent studies have shown a tendency towards improvement of the functional outcomes with use of an articulated external fixator during the postoperative period following multiligament reconstruction. Our hypothesis was that good knee stability and early gain of range of motion could be achieved with the use of the external fixator after ligament reconstructions. METHODS: Fourteen patients with knee dislocations were evaluated after multiligament reconstruction in association with use of a lateral monoplanar external fixator for six weeks. Reconstructions were performed using grafts from a tissue bank. Range of motion was measured after one, two, three, six, twelve months and at the final evaluation at a mean time of 49 months. The assessments were made using objective and subjective IKDC, Lysholm and Tegner scales. RESULTS: The mean scores were 71.7 for the subjective IKDC score, 81.5 for the Lysholm score. No patient was able to return to previous Tegner score. Out of the 45 ligament reconstructions performed, only four failed during the follow-up time. The mean range of motion of the knee presented a progressive increase from the first to the twelfth month, from 67.8° to 115.7°. Two cases of superficial infection on the site of the external fixator pins were observed. CONCLUSION: The use of an external fixator enabled early rehabilitation with range of motion gains starting from the first postoperative month, a low rate of reconstruction failure and minimal complications. Nevertheless, none of the patients returned to the level of activity prevailing prior to the injury. LEVEL OF EVIDENCE: Level IV, retrospective therapeutic case series.

Differing neurotoxic potencies of methamphetamine, mazindol, and cocaine in mesencephalic cultures.

The potent reinforcing effects of methamphetamine and cocaine are thought to be mediated by their interactions with CNS dopamine neurons. Both stimulants share the ability to block dopamine uptake potently, and methamphetamine can release cytoplasmic dopamine as well. There is also abundant evidence demonstrating the neurotoxic effects of methamphetamine. There are, however, limited studies that attempt to discern the neurotoxic mechanisms of these agents. The purpose of the present study was to characterize and compare the chronic in vitro effects of methamphetamine, cocaine, and the dopamine uptake blocker, mazindol, on cultured fetal mesencephalic dopamine neurons. Our studies examined biochemical mechanisms to evaluate the contribution of reuptake blockade versus release of dopamine. Using a dispersed cell preparation of fetal mesencephalon, cultures were treated for 5 days with the three uptake blockers. Dopamine function was assessed by measuring high-affinity [3H]dopamine uptake and by examining cultures for the presence of tyrosine hydroxylase-immunopositive neurons. Nonspecific neurotoxicity was assessed by staining for neuron-specific enolase and measuring lactate dehydrogenase activity. The results indicate that repeated administration of high concentrations of methamphetamine (10(-4) and 10(-3) M) caused a generalized neurotoxicity whereas the effects of 10(-5) M methamphetamine appeared to be specific to dopamine cells. Likewise, treatment of the cultures with mazindol (10(-6) M) resulted in reduced dopamine uptake while not significantly affecting neuron-specific enolase or tyrosine hydroxylase immunostaining. On the other hand, repeated exposure to cocaine (10(-5) and 10(-4) M) did not alter dopaminergic function in these cultures. The different mechanisms of action of these stimulants may explain the differences in neurotoxic potency of these compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term cocaine administration is not neurotoxic to cultured fetal mesencephalic dopamine neurons.

The psychostimulants cocaine and methamphetamine produce their euphoric effects through an interaction with the mesolimbic dopamine system. Methamphetamine, unlike cocaine, has been shown to be neurotoxic to both dopaminergic and serotonergic systems. We have previously determined that a 6 day exposure to methamphetamine causes neuronal damage to tyrosine hydroxylase-immunopositive cells in our tissue culture model of the mesencephalon. Over the same exposure period, cocaine neither impaired neuronal function nor altered dopamine cell survival. To test whether a longer exposure period to cocaine would alter dopamine function, we added cocaine (100 microM) to the cultures once daily for either 8 or 11 days and examined changes in dopamine uptake, cell survival and morphology 24 h after the last administration. Cocaine did not produce any signs of neurotoxicity in the mesencephalic cultures.

Stimulant-induced alterations in dopaminergic and serotonergic function in fetal raphe neurons.

Methamphetamine and its structural analogues have been demonstrated to be neurotoxic to CNS dopamine (DA) and serotonin (5-HT) neurons both in vivo and in vitro. Our laboratory has been actively characterizing mesencephalic cultures and the effects of methamphetamine exposure on neurochemical and immunochemical indices. The purpose of the present studies was to extend our findings with mesencephalic cultures and compare them with methamphetamine-induced alterations in fetal raphe cultures that contain both DA and 5-HT cells. Methamphetamine (10 and 100 microM) was added to the cultures 24 h after plating and fresh daily thereafter. The effects of chronic methamphetamine exposure on [3H]-DA and [3H]-5-HT uptake were determined after 5 days of drug treatment. Additional cultures were immunochemically analyzed for the presence of DA- and 5-HT-containing cells and total neuronal density. Results indicate that repeated methamphetamine exposure decreased DA and 5-HT uptake. Furthermore, repeated exposure to the higher concentration of methamphetamine (100 microM) caused a significant reduction in the number of DA and 5-HT cells as well as reducing the total neuronal density. This would suggest that this higher concentration of methamphetamine results in generalized neurotoxicity. Exposure to 10 microM methamphetamine resulted in more specific effects on dopaminergic function. These findings indicate that repeated methamphetamine administration can induce similar alterations in both dopaminergic and serotonergic neurons in raphe cultures.