Does amantadine increase the endogenous release of dopamine

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High-density lipoproteins (HDL) are the "good" cholesterol. These little packages are more dense, and part of their job is to escort cholesterol from other parts of your body back to your liver-where it's then removed.

1. What is the maintenance dose of phenytoin in seizures arising as a complication of chronic renal failure?

2. I know that the loading dose of phenytoin in status epilepticus is 20 mg/kg with an upper limit of 1000 mg but if the same situation arose as a complication of chronic renal failure (on regular dialysis), should this dose remain the same or be reduced? If reduced, what should the dose be?

3. 1. What is the most effective antiepileptic for a patient with simple partial motor status epilepticus who is not responding to a loading dose of phenytoin?

2. How long does phenytoin, given in a loading dose, take to work?

4. Is valproate effective if given rectally in status epilepticus and, if so, what dose is recommended?

5. In simple partial motor status epilepticus, if the patient does not respond to diazepam and phenytoin, is it justifiable to proceed to anaesthetic medication?

6. What is the recommended upper limit dose of lamotrigine when combined with both carbamazepine and valproate?

7. Is a valproate-lamotrigine combination more effective than carbamazepine on its own against partial seizures?

8. Why is the incidence of parkinsonism less common in smokers?

9. Is it recommended to start the treatment of parkinsonism with dopamine agonists alone in elderly (over 60 years old) patients, and to delay using L-dopa until the disease has progressed much further? Is there a rationale for this protocol in younger patients?

10. Does amantadine increase the endogenous release of dopamine, thus aiding early treatment of parkinsonism?

Reference no: EM133870752

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