drugs → brain structures ap mst. bipolar disorder
TRANSCRIPT
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Drugs → brain structures
APMST
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Bipolar disorder
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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
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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)
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NICE
Before a rapid cycling BD is diagnosed consider:
Erratic compliance hypothyroidism, AD, suboptimal medication
regimes Lithium withdrawal
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NICE
Consider a diagnosis of BD before Axis II if there are mood swings
During treatment consider compliance before considering a personality disorder
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NICE
Treatment (1/3)
Inform the patient Contraception and risk of pregnancy See patients once / (1|2) week (for 3 months)
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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
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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
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Mania, which treatment ?
3 weeks
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Mania, which treatment ?
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Mania, which treatment ?
Change in mania rating scores
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Mania, which treatment ?
Risk difference for treatment responders
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Mania, which treatment ?
Risk difference for drop outs
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Conclusion 1
Use second generation AP (risp, olanz, quet) for the treatment of acute mania (3 weeks)
Mood stabilizers are second choice
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Acute depression, which treatment ?
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Acute depression, which treatment ?
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Acute depression, which treatment ?
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Symptom remission
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Conclusion 2
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
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Maintenance, which treatment ?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
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Maintenance → lithium
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Lithium 41% vs 61% placebo
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Conclusion 3
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
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neuroimaging
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lithium
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neuroimaging
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1.9 years base-1st fu4 years base-2nd fu
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Valproate and AP
Overall, no significant brain volume modification in bipolar patients taking valproate or AP
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Valproate
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ant
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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
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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
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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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Conclusion 4
The molecular events that drive the efficacy of mood stabilizers are related to GSK-3, IPP and
prosurvival genetic expression
The dopaminergic-serotoninergic-glutamatergic balance is central to the activity of AP in the prefrontal cortex. Scaffolding proteins are
thought to be relevant
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imaging
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Conclusion 5
Lymbic structures and the PFC are key relay points for the efficacy of pharmacological
treatments in BP
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Schizophrenia
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skz
Treatment
First episode → oral AP, address to specialized unit, write a care plan in collaboration with the patient and send it to the GMP, include a crisis plan
Provide information and discuss the benefits and disadvantages
Chose the AP with the patient, taking into consideration extrapyramidal side effects and metabolic side effects
Assess the cardiovascular risk (ECG)
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skz
Start with the lower dose of AP Justify and record reasons for dosages outside the
range given by guidelines Monitor efficacy, side effects, adherence, physical health Record the rationale for continuing, changing or stopping
medication and the effects of such changes Trials for one medication should last 4-6 weeks Do not “neuroleptisize” your patient Rapid tranquillization
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skz
Which drug ?
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Conclusion 6
Second generation AP are more effective for the treatment of Skz
Use Olanzapine and Risperidone when possible
The side efffect profile must nevertheless guide the clinical choices
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imaging
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Conventional antipsychotic agents led to an increase of basalganglia volume while ongoing multifocal gray matter loss
Modern atypical agents rather tend to turn increased basal ganglia volumeback to normal while increasing the volume of thalamus and of
gray matter in different key regions
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II AP → ↑ glutamatergic turnover and inhibit NMDA receptors
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17 (8m/9f) acute psychotic recurrent-episode (chronic) patients treated with
haloperidol or risperidone
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30 medication-naive first-episode patients and 36 matchedhealthy controls participatedAtypical antipsychotic treatment
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Effect of practice on brain activation in the left dorsolateral prefrontal cortex (DLPFC)
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8 skz and 8 controls
Treated with risperidone for 6 weeks
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Conclusion 7
II AP increase the DLPC activity This event correlates with outcome
Variations in the NAc may be involved during withdrawal