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Drugs → brain structures

AP MST. Drugs → brain structures. Bipolar disorder. NICE. Diagnosis Full history of the patient (family, any episode, symptoms between the episodes)

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Drugs → brain structures

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  1. AP MST Drugs → brain structures

  2. Bipolar disorder

  3. NICE • Diagnosis • Full history of the patient (family, any episode, symptoms between the episodes) • Symptoms profile, triggers to previous episodes, social and personal functioning, comorbidities, physical health, current psychosocial stressors • Interview a family member

  4. NICE • BE CAREFUL • If (Psychotic symptoms, ↑ suicidal ideation, ↑ drug misuse) → late BD and not SKZ (minorities) • If alcohol | drug → wait 7 days before diagnosis • Late onset (>40yrs) → hypothyroidism, stroke, neurological disorders (dementia)

  5. NICE • Before a rapid cycling BD is diagnosed consider: • Erratic compliance • hypothyroidism, AD, suboptimal medication regimes • Lithium withdrawal

  6. NICE • Consider a diagnosis of BD before Axis II if there are mood swings • During treatment consider compliance before considering a personality disorder

  7. NICE • Treatment (1/3) • Inform the patient • Contraception and risk of pregnancy • See patients once / (1|2) week (for 3 months)

  8. NICE • Treatment (2/3) • Acute mania (and mixed→ AP, valproate, lithium, BDZ • AP (olanz, risp, quet)→ severe manic symptoms | marked behavioral disturbances • Valproate or lithium → previous response, good compliance, augmentation of AP • Lithium → not severe symptoms • NOT RECOMMENDED: CBZ, Gabapent, Lamo

  9. NICE • Treatment (3/3) • Acute depression • Add AP (quetiapine) to AD (SSRI better than TCI) • No AD → rapid-cycling, recent hypomanic, recent functional impairing and rapid mood fluctuations • Stop AD → after 8 weeks of symptoms relief (parox, venlafax → higher risk of discontinuation syndrome) • Avoid → Lamo a single treatment for BDI

  10. Mania, which treatment ? 3 weeks

  11. Mania, which treatment ?

  12. Mania, which treatment ? Change in mania rating scores

  13. Mania, which treatment ? Risk difference for treatment responders

  14. Mania, which treatment ? Risk difference for drop outs

  15. Use second generation AP (risp, olanz, quet) for the treatment of acute mania (3 weeks) Mood stabilizers are second choice Conclusion 1

  16. Acute depression, which treatment ?

  17. Acute depression, which treatment ?

  18. Acute depression, which treatment ?

  19. Symptom remission

  20. Use second generation AP (olanz, quet) for the treatment of acute depression during BD Mood stabilizers are less efficacious No strong evidence for using SSRI Conclusion 2

  21. the same regimen that successfully treated the acute bipolar mood episode attempt monotherapy. However, many bipolar patients require medication combinations First line: lithium, lamotrigine, risperidone (im) Second line: aripiprazole, valproate, quet, olanz Suicide risk → lithium Maintenance, which treatment ?

  22. Maintenance → lithium

  23. Lithium 41% vs 61% placebo

  24. For maintenance use the same drug started during acute phase If not possible use lithium, risperidone im, lamotrigine, valp Start with monotherapy, but multitreatment is more effective Conclusion 3

  25. neuroimaging

  26. lithium

  27. neuroimaging

  28. 1.9 years base-1st fu 4 years base-2nd fu

  29. Overall, no significant brain volume modification in bipolar patients taking valproate or AP Valproate and AP

  30. Valproate

  31. ant

  32. AP mechanism • Serotonin-glutamate Type II metabotropic glutamate receptors (mGluRs) and serotonin 5-HT(2A) receptors have been reported to form heterodimers that modulate G-protein-mediated intracellular signaling differentially compared to mGluR2 and 5-HT(2A) homomers

  33. Serotonin-Dopamine-Scaffolding The scaffolding protein PSD-95 is known to interact with N-methyl-D-aspartate (NMDA), D(2) and 5-HT(2) receptors, regulating their activation state

  34. Homer1a, the inducible member of the Homer family of PSD proteins that is implicated in glutamatergic signal transduction, is induced in striatum by antipsychotics with high dopamine receptor affinity and in the cortex by antipsychotics with mixed serotonergic/dopaminergic profile

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