Main Topic 1: Parkinson's disease and movement disorders: expanding the boundaries of current pra...

1. P. Krack

1.1. DeepBrain Stimulation

1.1.1. PD

1.1.1.1. Post operative apathy

1.1.1.1.1. thobois et al 2010

1.1.1.1.2. Clinical predictors of postoperative apathy

1.1.1.2. Dopmaine dysregulation syndrome and impulse control disorders

1.1.1.2.1. Witjas 2005

1.1.1.2.2. Ardouin 2006

1.1.1.2.3. Lim 2009

1.1.1.3. picture

1.1.1.3.1. picture

1.1.2. Gilles de La Tourette

1.1.2.1. picture

1.1.2.1.1. Limbic GPi vs thalamic stimulation

1.1.2.2. JL houeto 2005

1.1.2.3. ML Welter 2008

1.1.2.4. Servello 2009

1.1.3. OCD

1.1.3.1. A day filled with rituals

1.1.3.2. STOC study group

1.1.3.2.1. after DBS normal life

1.1.3.2.2. YBOCS scale 18-20 --> 1-1 after surgery

1.1.3.2.3. Mallet 2008

1.1.3.3. DBS

1.1.3.3.1. Greenberg 2008, Molecular psychiatry

1.1.4. Depression

1.1.4.1. Lozano 2008, Biol Psychiatry

1.1.4.2. Malone 2009, Biol psychiatry

1.1.4.2.1. stimulation of ventral capsule/ventral striatum for treatment resistent depression

1.1.4.3. Bewernick 2009, Biol psychiatry

1.1.4.3.1. Nucleus accumbens

1.1.5. Addiction

1.1.5.1. Not discussed due to time

1.1.6. All targets

1.1.6.1. picture

1.1.6.2. it's a mess

1.1.6.2.1. Neurologists are used to reason

1.1.6.3. DBS from neurology to psychiatry?

1.1.6.3.1. picture

1.1.6.3.2. slide 2

1.1.6.4. What's needed?

1.1.7. Conclusion

1.1.7.1. DBS in psychiatry is still experimental but huge potential

2. J.J. Ferreira

2.1. Parkinson's disease beyond 10 years

2.1.1. What happens after the first 10 years of disease progress?

2.1.1.1. picture

2.1.1.2. picture with errors - Fereira JJ

2.1.1.2.1. pre-motor

2.1.1.2.2. signs and symptoms

2.1.2. Hoehn Yahr Staging

2.1.2.1. milestones

2.1.2.2. picture

2.1.2.2.1. picture

2.1.3. PD progression focused on motor complications

2.1.3.1. picture

2.1.3.1.1. Elldopa trial

2.1.3.1.2. Ahlskog JE, Mov. Disord 2001

2.1.4. PD progression focused on clinical trials population

2.1.4.1. De Novo patients or early stage

2.1.4.2. Motor fluctuations

2.1.4.2.1. wearing off

2.1.4.3. PD Dementia / psychosis

2.1.4.4. picture

2.1.4.5. Clinical characteristics

2.1.4.5.1. "wearing-off patients"

2.1.4.5.2. DBS

2.1.4.5.3. PD Dementia

2.1.5. After 10 years

2.1.5.1. Selection

2.1.5.1.1. Late stage / end-stage

2.1.5.1.2. Clinical staging: HY 4 and 5

2.1.5.1.3. Longer disease duration

2.1.5.1.4. specific clinical markers

2.1.5.1.5. Other

2.1.5.2. Clinical characteristics: motor symptoms

2.1.5.2.1. Coelho, J. Neurol 2010

2.1.5.2.2. S. papapetropoulos, 2007

2.1.5.3. Non-motor complications

2.1.5.3.1. Coelho J Neurol 2010

2.1.5.4. IS dementia inevitable?

2.1.5.4.1. picture

2.1.5.5. Placebo-adverse events at different disease stage

2.1.5.5.1. dyskinesias

2.1.5.5.2. hallucinations

2.1.5.5.3. Pain

2.1.5.5.4. Anxiety

2.1.5.5.5. Peripheral edema

2.1.5.6. Phenotype is different between clinical stages

2.1.5.6.1. Picture

2.1.5.6.2. Coelho 2010

2.1.5.6.3. Aarsland j am geriatr soc 2000

2.1.5.6.4. Clinical markers

2.1.5.7. Medication

2.1.5.7.1. Picture

2.1.5.8. Mortality

2.1.5.8.1. picture - w lots of authors

2.1.5.9. Conclusions

2.1.5.9.1. picture

2.1.5.9.2. Late / end stage is an orphan domain

2.1.5.10. Initial slide on progression late stage redesigned

2.1.5.10.1. picture

2.1.5.11. Implications for clinical practice

2.1.5.11.1. picture

2.1.5.12. Implications for research

3. Kailash Bhatia

3.1. Ion channels & movement Disorders

3.1.1. Basics on Ion channels

3.1.1.1. picture

3.1.1.1.1. picture

3.1.1.2. most abnormalities in alfa subunits

3.1.2. Ion channel disorder

3.1.2.1. jouveneau 2000

3.1.2.1.1. picture

3.1.2.2. Graves and Hanna 2005

3.1.2.2.1. review

3.1.2.2.2. classification of neurological channelopathies according to channel

3.1.2.2.3. http://www.ncbi.nlm.nih.gov/pubmed/15640425

3.1.3. The paroxysmal dyskinesias

3.1.3.1. often diagnosis is missed

3.1.3.2. Gowers 1885

3.1.3.2.1. called it epilepsy

3.1.3.3. Mount and reback 1940

3.1.3.3.1. first clear description

3.1.3.4. Paroxysmal dystonic choreoathetosis

3.1.3.5. Lance 1977

3.1.3.5.1. PKC

3.1.3.5.2. PED

3.1.3.5.3. PDC

3.1.3.6. picture

3.1.3.6.1. these slides go fast...missed some nice ones. - could not even read them

3.1.3.7. Hypnogenic episodic ataxia

3.1.4. Episodic ataxias

3.1.4.1. There are similarities between paroxysmal dyskinesia and episodic ataxias

3.1.4.1.1. picture

3.1.4.1.2. EA type 1

3.1.4.1.3. EA type 2

3.1.4.1.4. Houser et al, 1999

3.1.4.1.5. Bruno et al 2004

3.1.5. Pathophysiology

3.1.5.1. picture

3.1.5.2. picture

3.1.5.3. picture

3.1.5.3.1. epilepsy theory

3.1.6. Bhatia publications

3.1.6.1. http://www.ncbi.nlm.nih.gov/pubmed/10830404

3.1.6.2. http://www.ncbi.nlm.nih.gov/pubmed/11346027

3.1.7. PDC/PNKD

3.1.7.1. picture

3.1.7.2. treatment

3.1.7.2.1. no specific drug

3.1.7.2.2. anticonvulsants help rarely

3.1.7.3. Recent gene found

3.1.7.3.1. Oxidative stress product

3.1.7.3.2. Bruno et al neurology 2005

3.1.7.3.3. myofibrillogenesis regulator 1 gene mutations cause paroxysmal dystonic choreoathetosis

3.1.7.4. Paroxysmal dyskinesia due to glucose transporter 1 defect

3.1.7.4.1. Weber, JCI 2008

3.1.7.5. GLUT1 deficiency

3.1.8. Autosomal dominant nocturnal frontal lobe epilepsy

3.1.9. Diagnostics

3.1.9.1. Serum and CSF glucose studies

3.1.10. Treatment of GLUT1 deficiency

3.1.10.1. ketogenic diet

3.1.11. Autoimmune channelopathis causing movement disorders

3.1.11.1. central nervous system

3.1.11.2. peripheral nerve system

3.1.11.2.1. Isaac's syndrome

3.1.12. Summary

3.1.12.1. picture

3.1.12.2. picture

3.1.12.3. picture

3.1.12.4. picture