The George Washington University Medical Center
Bipolar Disorder Symposium
About this Activity
Discussion Points
The Presentations
Speakers
Acknowledgements
From Neurobiology to Clinical Trials: New Approaches to the Management of Bipolar Disorder
Registration Information

Mission
The Presentations
Question and Answer Session:

The following questions were asked both during the presentations as well at the end of the event. Click the hyperlink next to each one to hear the response.

 

Dr. Goodwin (Play all of Dr Goodwin's answers)
 

1. How do you manage the weight gain associated with long-term Lithium use?

2. If a patient has breakthrough depression or cycling on Valproate then 1) Should Lithium be added? 2) Should Lamotrigene be added? After Lithium is added with improvement, should Valproate be stopped or at least decreased?

3. If studies have proved higher suicide rate from depakote then why is it still used as a mood stabilizer?

4. What do you mean that Lamotrigine stabilized “from below?”

5. What level of Valproic acid should we aim for for mood stabilization? What level of Lithium should be the goal for bipolar disorder?

6. Please comment on: 1) utility of psychotherapy focus on “energy management,” e.g., sleep, exercise, stress management, meditation, yoga, martial arts (e.g., Qi Gong), 2) Data on Mirtazapine and destabilization? Utility of Neurontin, Topamax, or Keppra as second mood stabilizer/augmentation strategy, and 3) Comorbid OCD – alternatives to SSRI’s?

7. Please comment on mood destabilization with newer atypical therapties, especially aripiprazole, ziprasidone. Also, Dr. Ghaemi concluded 20% bipolar patients still needed antidepressants. Please comment.

8. Do you feel that depression with psychosis is more likely to be a bipolar variant than purely unipolar (i.e., higher index of suspicion for bipolar)?

9. Please comment on the current role of Lamotrigine in the treatment of apparent unipolar depression, especially in more refractory cases.


Dr. Leibenluft (Play all of Dr Leibenluft's answers)
  1. For a child (pre-adolescent) with acute onset of depressions (never manic): 1) how can one distinguish between “unipolar” and “bipolar” depression? 2) If bipolar depression is suspected, what are reasonable choices for medications?

2. Are the severe mood dysregulation kids looked at neurologically (EEG, imaging studies) (i.e., cocaine, alcohol in mothers)?

3. One of the controversies in child psychiatry centers on co-morbidity of ADHD and bipolar disorder and treating both disorders. Given the role of amphetamines in activation of PKC, do we make things worse for a bipolar child by treating ADHD with stimulants, or can a mood stabilizer protect the child?

4 . How do you treat a patient with ADHD who then develops mania from the medications used to treat the ADHD? How then do you treat the ADHD long term and the mania? Do you avoid the stimulants?

5. What do you advise patients about their attention to circadian rhythm?

6. What proportion of severe mood and behavioral dysregulation patients become borderline personality disorders?

7. Could you comment on any interactive effects for women diagnosed with bipolar I or II during seasons of elevated hormone levels – e.g., pregnancy, menopause, or the introduction of estrogen-based birth control methods. Any treatment issues specific for this population?

8. What is the role of megavitamins in treatment of bipolar disorder?

9. Would Clonidine be a better treatment for ADHD and co-morbid bipolar than stimulants?

 

Dr. Manji (Play all of Dr Manji's answers)
  1. Do we know what effect Lamotrigine and Lithium have on Dopamine/Serotonin/Norepinephrine, or do they have their effect some other way?

2. Have mood stabilizing drugs shown benefit in recovery from episodes of multiple sclerosis?

3. Regarding Lamotrigine or Lithium, are there any known effects on gene clusters for energy metabolism, specifically in Mitochondria? (Or nucleur genes communicating with mitochondrial genes?)

4. What is the mechanism of Lithium neurotoxicity?

5. What is the role of Inositol in bipolar disorder?

6. Is Tamoxifen neuroprotective? Is Estrogen neurotoxic?

7 . Do any of the atypical antipsychotics or other anticonvulsants like Lamictal and Trileptal have protein kinase C effects?

8 . Is there any evidence that long-term mood disorders lead to an increased risk of Alzheimer's (i.e., via cell death in the hippocampus)?


Dr. Zarate (Play all of Dr Zarate's answers)
  1. Why does decreasing the activity of glutamate lead to clinical activation and antidepressant effect?

2. Would you comment on the utility of cholinesterase inhibitor and Restoring REM sleep?

3. Also comment on utility of Memantine in in organic bipolar disorder? (Brain injury, cerebrovascular disease, etc.).

     
 

GWUMC | CEHP

Last Updated: February 5, 2004
© 2003 The George Washington University Medical Center

 
 
Release Date: December 1, 2003 Expiration Date: December 1, 2006