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Cerebellum,Cerebellum,
Psychiatric AspectsPsychiatric Aspects
& Routine Disorders& Routine Disorders
Dr Khalid Mansour
Consultant Psychiatrist
Priory Hospital Cefn Carnau
2014
Introduction
•10% of the weight of
the brain (Llinas et al, 2004).
•80% of brain neurones
(Herculano-Houzel, 2010)
•Traditionally:
cerebellum only >
posture, balance &
motor control.
•Not involved in
initiating motor
activity, but
coordinating them
(Flourens, 1824).
Introduction
•Abundant connections > non-
motor brain regions.
•Involved in coordinating all
non-motor functions e.g.
perceptions, emotions,
cognition, speech,
personality, etc.
•Cerebellar abnormalities
exist in most mental
illnesses.
•Mental illnesses exist in most
cerebellar disorders. 3
1.Anatomy
2.Models of Cerebellar
Functioning
3.Psychiatric Aspects of
Cerebellar Disorders
4.Cerebellar Abnormalities in
Psychiatric Disorders:
5.Cerebellar Mental Therapies.
6.Clinical Reflections:
4
Anatomy
5
Gross anatomy:
•Anterior lobe.
•Posterior lobe.
•Flocculonodular
lobe.
Cross sectional:
•Gray matter:
•White matter:
•Nerve fibre tracts
•Deep nuclei
6
Functional
Anatomy:
•Vestibulocerebellum
(flocculonodular
lobe).
•Spinocerebellum
(vermis &
paravermis).
•Cerebrocerebellum
(lateral cerebellar
hemispheres).
7
Deep
Cerebellar
Nuclei
•Dentate,
•Interposed
(Globose &
Emboliform)
•Fastigial
Nuclei.
8
Cerebellar Cortex
•Three layers:
•Granular Layer,
Granule cells and
Golgi cells.
•Purkinje Layer
•Molecular Layer,
•Dendrite of
Purkinje cells,
•Parallel Fibers
•Stellate cells and
Basket cells 9
Cerebellar Connections:
• Afferent:
• Brainstem, spinal cord and cerebrum > Mossy Fibers > Granule
cells> Parallel Fibers > Purkinje cell >
• Inferior Olivary nucleus > Climbing Fibers > Purkinje cells
• Efferent:
• Purkinje cell > Deep Cerebellar Nuclei > climbing and/or Mossy
fibers > Brainstem, spinal cord and cerebrum
10
Models of Cerebellar
Functioning
11
Marr & Albus Model for
Cerebellar Learning
(Eccles, Ito & Szentagothai,1967)
•Several theories about cerebellum
and learning.
•Most theories about Cerebellar
functioning / learning are derived
from early models of David Marr
(1969) and James Albus (1971).
•Albus (1971) formulated his model
as a software algorithm: Cerebellar
Model Articulation Controller, which
has been tested in a number of
computer applications.
12
David Marr
James Albus
Marr & Albus Model for Cerebellar Learning
(Eccles, Ito & Szentágothai,1967)
1. Feedforward processing.
2. Divergence and Convergence.
3. Modularity / Compartmentalization
4. Plasticity.
13
Cerebellar Perceptron,
James Albus
(1) Feed-forward Processing:
(Eccles, Ito & Szentágothai,1967)
•Signals move uni-
directionally from
input to output,
with very little
recurrent internal
transmission > a
quick and clear
response with no
reverberation.
14
(2) Modularity / Compartmentalization
(Oscarsson, 1979; Apps & Garwicz, 2005)
•Cerebellar cortex >
zones and micr-
ozones (1000
Purkinje cells).
•Interactions
within a micro-
zone much
stronger than
interactions
between different
micro-zones. 15
(3) Plasticity
(Mial et al, 1998; Ohtsuki et al, 2009)
•Purkinje cells normally > high
rate action potentials :
•Simple spike
•Complex spike
•Parallel fibre-Purkinje cell
synapse > long-term
depression (LTD).
•Repetitive firing of parallel
fibres alone > long-term
potentiation (LTP).
16
(4) Divergence & Convergence:
(Llinas et al, 2004; Apps & Garwicz, 2005)
•200 million MF > 50 billion
GC (1:500).
•Granule Cells > PF > spines
> 15 million PC
•PCs < 100000 PF (over
200000 spines) + 1 CF.
•Each micro-zone (1000
PCs) > 50 DNCs.
•100 MF > 10 billion spines
> 1 DNC 17
Adaptive Filtering(Fujita 1982; Dean & Porell, 2008; Dean et al, 2010)
• Elimination of noise
•Fine tuning
• Optimality /
Coordination
• Execution not
creativity
18
1. Feedforward processing.
2. Divergence and
Convergence.
3. Modularity /
Compartmentalization
4. Plasticity.
•Kenji Doya (2000):
•“Neural computation”.
•Katz & Steinmetz (2002):
•“Regulates brain processes”.
•Boydon (2004):
•“Makes fine adjustments to the
way an action is performed”.
•Masao Ito (2005):
•“Matches intentions with actual
performance”.
•Reeber et al (2013):
“computational task … recognizing
neural patterns … predict optimal
movements”. 19
Masao Ito
Kenji Doya
Cerebellar Learning: “Software Programmer”
Cerebellar Learning:
(Burguiere et al, 2010, Kalmbach et al, 2011)
•Cerebellum > develops
learnt behaviour with >
1.Minimum Errors
2.Minimum Time
3.Minimum Effort
4.Minimum Attention /
awareness
5.Maximum stability
20Chase Britton
Psychiatric Aspects of
Cerebellar Disorders
21
1 - Psychological Studies of Normal
Individuals with Reduced Cerebellar
Volume
•Individuals with
reduced cerebellar
volume > higher
scores on scales of
anxiety, type A
personality,
phobia,
tenderness and
hostility (Chung et al, 2010).
22Chase Britton
2 - Other Psychiatric Aspects of
Cerebellar Disorders: (Wolf et al, 2007)
23
3 - Psychiatric Aspects of Anatomically
Specific Cerebellar Abnormalities
•Vermal Agenesis >
severe LD & Autism (Tavano
et al, 2007).
•Vermal lesions > affective
and relational disorders
(Schmahman et al, 2007).
•Spinocerebellar Ataxia >
impairment in attention,
memory, executive
functions and theory of
mind (Garard et al, 2008).
24
4 - Cerebellar Cognitive Affective Syndrome
(Schmahman et al, 2007; Tavano et al, 2007; Levisohn et al, 2000):
25
Cerebellar Syndromes > motor
impairments +
Cognitive impairments:
Executive dysfunctions, visuo-
spatial abnormalities, linguistic
dysfunction.
Affective impairments: Anxiety,
lethargy, depression, lack of
empathy, ruminativeness,
perseveration, anhedonia and
aggression.
Jeremy
Schmahmann
Cerebellar Abnormalities
in Psychiatric Disorders:
General
26
Cerebellar Abnormalities in
Psychiatric Disorders
•Bipolar Affective
Disorder: e.g.
reduced Cerebellar /
Vermis volume (Glaser
et al, 2006)
•Anxiety: e.g.
cerebellar-vestibular
dysfunction (Levinson,
1989)
•Depression: e.g.
reduced posterior
cerebellar activities
(Fitzgerald et al, 2009)
27
ADHD:
•Smaller cerebellar
volume (Berquin et al 1998;
Giedd et al, 2001).
•Abnormalities in post-
inferior cerebellar
hemispheres and vermis
(Casey et al, 2007; Steinlin,
2007).
•Reduction in the activity
of cerebellum and
vermis (Mackie et al, 2007).
Cerebellar Abnormalities in
Psychiatric Disorders:
•Post Traumatic
Stress Disorder:
e.g. altered
function of the
vermis (Anderson et al,
2002)
•Alcohol abuse:
e.g. induced
reduction in
Cerebellar /
Vermis volume
(Glaser et al, 2006) 28
•Gender differences:
(Dean & McCarthy, 2008)
•Antisocial
Personality
Disorder: e.g.
reduced Cerebellar
volume (Barkataki et al, 2006).
•Alzheimer
Dementia: e.g.
cerebellar atrophy
(Wegiel et al, 1999)
Cerebellar Abnormalities
in Psychiatric Disorders:
Dyslexia, Schizophrenia & Autism
29
(1) Cerebellum & Dyslexia:
•Developmental Dyslexia:
(Stoodley & Stein, 2011; Nicolson et al,
2001; Pernet et al, 2009)
•Dyslexia > cerebellar
structural and functional
abnormalities in 80% of
cases.
•Dyslexia > impairment
in the ability to perform
skills automatically.
•Cerebellar syndromes >
impairments in reading
and writing characteristic
of dyslexia.
30
The Cerebellar
Deficit
Hypothesis of
Dyslexia: (Nicolson &
Fawcett, 1990; Nicolson et al,
2001): dyslexia is an
impaired
automatization of
high-order
sensory-motor
procedures in
reading.
(2) Cerebellum & Schizophrenia:
General Studies
• ↑ Imaging studies >
cerebellar abnormalities in
schizophrenia (Vernas et al,
2007):
• ↑ Cerebellar-Motor
Dysfunction in
Schizophrenia and
Psychosis-Risk (Bernard &
Mittal, 2014).
• ↓ Cerebellar volume (Bottmer
et al, 2005)
• ↓ Blood flow on PET scan
(Andreasen et al, 1996).
31
• ↓ Level of N-acetylaspartate
in Magnetic Resonance
Spectroscopy Imaging
(MRSI) studies (marker of
neurone density and viability) in
vermis and cerebellar cortex (Ende
et al, 2005).
• ↓ Volume in the cerebello-
thalamic-cortical network
(Rusch et al, 2007).
• Neuronal disorganisation in
the superior peduncle on
Diffusion Tensor Imaging
(DTI) studies (Okugawa et al,
2006).
(2) Cerebellum & Schizophrenia:
Specific Symptoms (Picard et al, 2008)
•Hallucinations (Shergill et al,
2003; Neckelman et al, 2006)
•Formal Thought Disorder
(Kircher et al, 2001; Levitt et al, 1999)
•Affect symptoms (Stip et al,
2005; Paradiso et al, 2003; Abel et al,
2003)
•Cognition (Szesko et al 2003;
Toulopoulou et al 2004)
•Attention (Eyler et al, 2004; Honey
et al, 2005; Aasen et al, 2005)
•Language (Shergill et al, 2003;
Boksman et al 2005; Kircher et al 2005)
•Memory (all types) (Mendrek et
al, 2005; Whyte et al 2006)
32
(2) Cerebellum &
Schizophrenia:
Cerebellar Glutamate
Theory
33
•Hypo-
functioning of
the Glutamate
NMDA receptors
in cerebellum >
cognitive
dysmetria >
schizophrenia.
• Yeganeh-Doost et al,
2011):
(2) Cerebellum & Schizophrenia:
Cognitive Dysmetria Theory
(Andreasen et al, 1998)
•The Cortico-Cerebellar-
Thalamo-Cortical circuit is
dysfunctional > poor
mental coordination >
(Cognitive Dysmetria) >
Schizophrenia.
•The theory has been
criticised by other
researchers (e.g. Kaprinis et al,
2002, Kaprinis et al, 2002; Shanagher et
al, 2006) Nancy
Andreasen
(2) Cerebellum & Schizophrenia:
Secondary Cerebellar Abnormalitites
•Schizophrenia >
increased dopaminergic
activities > cerebellar
disorder > motor
disorders in
schizophrenia (even
neuroleptics naïve)
(Mittleman et al, 2008;
Hoppenbrouwers et al, 2008;
Varambally et al, 2006; Picard et al,
2007).
35
(3) Cerebellar & Autism:
General Studies
•One of the most consistent
abnormalities found in ASD (DiCicco-Bloom
et al, 2006).
•95% of post mortem examinations of
autistic individuals (Delong, 2005)
•Consensus related to cerebellar
involvement in autism (Fatemi et al, 2012):
• Abnormal cerebellar anatomy,
• Abnormal neurotransmitter systems,
• Oxidative stress,
• Cerebellar motor and cognitive deficits,
• Neuro-inflammation
36
S. Hossein
Fatemi
(3) Cerebellum & Autism:
Cerebral Involvement
•Associated with mal-development of the frontal
lobe and any other brain regions > ASD (Carper &
Courchesne, 2000; Kuemerle et al, 2006; Reeber et al, 2013).
•Loss of modulatory control of Frontal Cortex >
ASD, (Catani et al, 2008).
•Cerebellum malfunction hinders neural development
(Wang et al, 2014).
Sam Wang
Cerebellar Mental
Therapies
38
Cerebellar Exercises / Training
(Schmahmann, 2010)
• Some claims (e.g. DORE) > Physical exercises (movement +
balance) > speed up information processing and improve
cerebellar functioning > improve dyslexia, ADHD and
Asperger’s syndrome:
• ? Could improve some mental illnesses like schizophrenia .
• No known scientific studies.
• Controversial treatments (Reynolds & Nicolson, 2007; Bishop,
2007; Rack, 2007)
39
Dance & Movement Therapy
(Levi, 1988; Jeong et al, 2005)
40
Cerebellar Transcranial Magnetic
Stimulation (TMS) (Schmahmann, 2010)
•Demirtas-Tatlidede et al (2010): stimulation of the
vermis in 8 schizophrenic patients > improvements in
mood, alertness, memory, attention, visual-spatial
skills and energy.
•Very early stages (Minks et al, 2010)
•No RCT
41
Cerebellum:
Clinical Reflections
42
Cerebellum: Clinical Reflections
Introduction
•Best way to make clinical judgment
> follow the model of motor
cerebellar functioning:
• Well studied
• Must be linked physiologically to non-
motor functioning.
•Two main fields:
• Cerebellar connections to mental
disorders specially dyslexia,
schizophrenia and Autism > very
promising and interesting but slow and
small impact .
• Mental equivalent to praxis and
dyspraxia > clearer and more promising 43
(1) Motor Learning vs Non-motor / Mental
Learning
Cerebellum > “motor”
and “non-motor / mental”
coordination.
a) Motor coordination
> “Motor Learning /
Praxis”.
b) Mental coordination
> Non-motor
coordination /
Mental
Coordination”
44
•Cerebellum failing in motor
coordination >
• (Motor) dyspraxia,
• Developmental Coordination
Disorder (DCD),
• Clumsy Child Syndrome, etc.
•Cerebellum failing in non-
motor / mental coordination >
• ? Mental Dyspraxia,
• ? Developmental Mental
Coordination Disorder (DMCD),
• ? Mentally Clumsy Child
Syndrome, or
• ? Mental Routine Disorder (MRD)
45
(2) Motor Dyspraxia vs Non-motor Dyspraxia
(3) Mental Routine Disorders (MRD):
A new chapter in psychopathology?!
1. Better understanding of a
major part of human
behaviour.
2. Widespread problem >
marked suffering > needs
attention.
3. Good room for effective
interventions
4. Enhance therapies for
major mental disorders
e.g. ASD.
46
(4) Prevalence of MRDs
• Motor Dyspraxia : 6-10 % in school children (Gibbs et al, 2007).
• Dyscalculia: 5-7% (Butterworth et al, 2011)
• Developmental Coordination Disorder (DCD): 5–6% (Blank et al, 2012;
Zwicker et al, 2012).
• Dyslexia: 5% - 17% of school-age children (USA) (Shaywitz & Shaywitz,
2003).
• Symptom: 40% reading below grade level (Shaywitz & Shaywitz,
2003).
• Special groups: 80% of individuals with LD (Shaywitz & Shaywitz,
2003).
• Complications: lower self-esteem and more emotional and
behavioural difficulties than those without dyslexia (Terras et al, 2009).
• comorbidity : 95% (Pauc 2005).
47
3- Assessment of MRDs:
(A) Doya’s Model of Motor Learning (Doya, 2000)
(also Imamizu et al, 2000; Hikosaka et al, 2002, Bosch-Bouju et al, 2013)
•Brain circuits:
•The cortico-cerebeller-thalamo-cortical
circuit
•The cortico-striato-thalamo-cortical
circuit
•Learning paradigms
•Cerebral cortex > unsupervised
learning
•Basal ganglia > reinforcement
learning
•Cerebellum > supervised learning
Kenji Doya
49
50
Ferreira et al, 2008
(B) The Four Primary Components
1. Failure to learn (problem
solving, adapting, planning,
etc.) e.g. LD.
2. Failure to eliminate anxiety
(threat) > marked disturbance
of functioning e.g. OCD.
3. Failure to reach satisfaction
without causing marked
disturbance of functioning
e.g. habit disorder
4. Failure to have smooth
functioning without errors e.g.
dyspraxia
51
(C)The Four Components Mixed
•Complex routine
abnormalities.
•1, 3 & 4 okay but 2
faulty > OCD with
inner resistance.
•3 & 4 okay but 1 & 2
faulty > rigid
obsessional routines
without inner
resistance. 52
Functional
Routines
Dysfunctional
Routines
Meaningful > Serves a
purpose
Bizarre (counting lamp posts /
eating flies).
Resilient (to stress):
stress > little disruption
Unstable: stress >
marked disruption
Adaptive (with novelty):
new data > little
disruption
Rigid: new data >
significant disruption
53
(4) Classification of MRDs:
a- Dysfunctional Routines
(4) Classification of MRDs:
b- Simple vs. Complex MRD
54
Simple Complex
− Single faulty
component (e.g.
OCD or drug
addiction)
− Highly functional
individuals
‒ Multiple faulty
components e.g.
routine problems in
Autism.
‒ Less functional
individuals
(4) Classification of MRDs:
c- Primary vs. Secondary MRD
55
e.g. primary
clumsiness
Secondary
clumsiness
− Clumsiness due to
faulty cerebellar
component
(Performance
clumsiness)
‒ Clumsiness due to
faulty cerebral
(cognitive)
component.
(Mentation
Clumsiness)
(5) Treatment of MRDs:
The Methods
• General Lines:
1. Medications.
2. Educational.
3. CBT.
4. Behavioural.
5. Others: e.g.
• GORE or Movement
Therapies
•Process-oriented approach
•Task-oriented approach
• Transcranial Magnetic
Stimulation (TMS)
• Specific:
• Depends on specific
conditions
56
“3 Dimensions” is not
the same as “2
Dimensions”:
•Integrating the
psychiatric dimension
into the
neuropsychological and
OT therapies for
dyspraxia > extra depth
and sophistications but
needs resources and
time.
(5) Treatment of MRDs :
The Strategy
58
Thank you
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Cerebellum 66

  • 1. 1 Cerebellum,Cerebellum, Psychiatric AspectsPsychiatric Aspects & Routine Disorders& Routine Disorders Dr Khalid Mansour Consultant Psychiatrist Priory Hospital Cefn Carnau 2014
  • 2. Introduction •10% of the weight of the brain (Llinas et al, 2004). •80% of brain neurones (Herculano-Houzel, 2010) •Traditionally: cerebellum only > posture, balance & motor control. •Not involved in initiating motor activity, but coordinating them (Flourens, 1824).
  • 3. Introduction •Abundant connections > non- motor brain regions. •Involved in coordinating all non-motor functions e.g. perceptions, emotions, cognition, speech, personality, etc. •Cerebellar abnormalities exist in most mental illnesses. •Mental illnesses exist in most cerebellar disorders. 3
  • 4. 1.Anatomy 2.Models of Cerebellar Functioning 3.Psychiatric Aspects of Cerebellar Disorders 4.Cerebellar Abnormalities in Psychiatric Disorders: 5.Cerebellar Mental Therapies. 6.Clinical Reflections: 4
  • 6. Gross anatomy: •Anterior lobe. •Posterior lobe. •Flocculonodular lobe. Cross sectional: •Gray matter: •White matter: •Nerve fibre tracts •Deep nuclei 6
  • 9. Cerebellar Cortex •Three layers: •Granular Layer, Granule cells and Golgi cells. •Purkinje Layer •Molecular Layer, •Dendrite of Purkinje cells, •Parallel Fibers •Stellate cells and Basket cells 9
  • 10. Cerebellar Connections: • Afferent: • Brainstem, spinal cord and cerebrum > Mossy Fibers > Granule cells> Parallel Fibers > Purkinje cell > • Inferior Olivary nucleus > Climbing Fibers > Purkinje cells • Efferent: • Purkinje cell > Deep Cerebellar Nuclei > climbing and/or Mossy fibers > Brainstem, spinal cord and cerebrum 10
  • 12. Marr & Albus Model for Cerebellar Learning (Eccles, Ito & Szentagothai,1967) •Several theories about cerebellum and learning. •Most theories about Cerebellar functioning / learning are derived from early models of David Marr (1969) and James Albus (1971). •Albus (1971) formulated his model as a software algorithm: Cerebellar Model Articulation Controller, which has been tested in a number of computer applications. 12 David Marr James Albus
  • 13. Marr & Albus Model for Cerebellar Learning (Eccles, Ito & Szentágothai,1967) 1. Feedforward processing. 2. Divergence and Convergence. 3. Modularity / Compartmentalization 4. Plasticity. 13 Cerebellar Perceptron, James Albus
  • 14. (1) Feed-forward Processing: (Eccles, Ito & Szentágothai,1967) •Signals move uni- directionally from input to output, with very little recurrent internal transmission > a quick and clear response with no reverberation. 14
  • 15. (2) Modularity / Compartmentalization (Oscarsson, 1979; Apps & Garwicz, 2005) •Cerebellar cortex > zones and micr- ozones (1000 Purkinje cells). •Interactions within a micro- zone much stronger than interactions between different micro-zones. 15
  • 16. (3) Plasticity (Mial et al, 1998; Ohtsuki et al, 2009) •Purkinje cells normally > high rate action potentials : •Simple spike •Complex spike •Parallel fibre-Purkinje cell synapse > long-term depression (LTD). •Repetitive firing of parallel fibres alone > long-term potentiation (LTP). 16
  • 17. (4) Divergence & Convergence: (Llinas et al, 2004; Apps & Garwicz, 2005) •200 million MF > 50 billion GC (1:500). •Granule Cells > PF > spines > 15 million PC •PCs < 100000 PF (over 200000 spines) + 1 CF. •Each micro-zone (1000 PCs) > 50 DNCs. •100 MF > 10 billion spines > 1 DNC 17
  • 18. Adaptive Filtering(Fujita 1982; Dean & Porell, 2008; Dean et al, 2010) • Elimination of noise •Fine tuning • Optimality / Coordination • Execution not creativity 18 1. Feedforward processing. 2. Divergence and Convergence. 3. Modularity / Compartmentalization 4. Plasticity.
  • 19. •Kenji Doya (2000): •“Neural computation”. •Katz & Steinmetz (2002): •“Regulates brain processes”. •Boydon (2004): •“Makes fine adjustments to the way an action is performed”. •Masao Ito (2005): •“Matches intentions with actual performance”. •Reeber et al (2013): “computational task … recognizing neural patterns … predict optimal movements”. 19 Masao Ito Kenji Doya Cerebellar Learning: “Software Programmer”
  • 20. Cerebellar Learning: (Burguiere et al, 2010, Kalmbach et al, 2011) •Cerebellum > develops learnt behaviour with > 1.Minimum Errors 2.Minimum Time 3.Minimum Effort 4.Minimum Attention / awareness 5.Maximum stability 20Chase Britton
  • 22. 1 - Psychological Studies of Normal Individuals with Reduced Cerebellar Volume •Individuals with reduced cerebellar volume > higher scores on scales of anxiety, type A personality, phobia, tenderness and hostility (Chung et al, 2010). 22Chase Britton
  • 23. 2 - Other Psychiatric Aspects of Cerebellar Disorders: (Wolf et al, 2007) 23
  • 24. 3 - Psychiatric Aspects of Anatomically Specific Cerebellar Abnormalities •Vermal Agenesis > severe LD & Autism (Tavano et al, 2007). •Vermal lesions > affective and relational disorders (Schmahman et al, 2007). •Spinocerebellar Ataxia > impairment in attention, memory, executive functions and theory of mind (Garard et al, 2008). 24
  • 25. 4 - Cerebellar Cognitive Affective Syndrome (Schmahman et al, 2007; Tavano et al, 2007; Levisohn et al, 2000): 25 Cerebellar Syndromes > motor impairments + Cognitive impairments: Executive dysfunctions, visuo- spatial abnormalities, linguistic dysfunction. Affective impairments: Anxiety, lethargy, depression, lack of empathy, ruminativeness, perseveration, anhedonia and aggression. Jeremy Schmahmann
  • 27. Cerebellar Abnormalities in Psychiatric Disorders •Bipolar Affective Disorder: e.g. reduced Cerebellar / Vermis volume (Glaser et al, 2006) •Anxiety: e.g. cerebellar-vestibular dysfunction (Levinson, 1989) •Depression: e.g. reduced posterior cerebellar activities (Fitzgerald et al, 2009) 27 ADHD: •Smaller cerebellar volume (Berquin et al 1998; Giedd et al, 2001). •Abnormalities in post- inferior cerebellar hemispheres and vermis (Casey et al, 2007; Steinlin, 2007). •Reduction in the activity of cerebellum and vermis (Mackie et al, 2007).
  • 28. Cerebellar Abnormalities in Psychiatric Disorders: •Post Traumatic Stress Disorder: e.g. altered function of the vermis (Anderson et al, 2002) •Alcohol abuse: e.g. induced reduction in Cerebellar / Vermis volume (Glaser et al, 2006) 28 •Gender differences: (Dean & McCarthy, 2008) •Antisocial Personality Disorder: e.g. reduced Cerebellar volume (Barkataki et al, 2006). •Alzheimer Dementia: e.g. cerebellar atrophy (Wegiel et al, 1999)
  • 29. Cerebellar Abnormalities in Psychiatric Disorders: Dyslexia, Schizophrenia & Autism 29
  • 30. (1) Cerebellum & Dyslexia: •Developmental Dyslexia: (Stoodley & Stein, 2011; Nicolson et al, 2001; Pernet et al, 2009) •Dyslexia > cerebellar structural and functional abnormalities in 80% of cases. •Dyslexia > impairment in the ability to perform skills automatically. •Cerebellar syndromes > impairments in reading and writing characteristic of dyslexia. 30 The Cerebellar Deficit Hypothesis of Dyslexia: (Nicolson & Fawcett, 1990; Nicolson et al, 2001): dyslexia is an impaired automatization of high-order sensory-motor procedures in reading.
  • 31. (2) Cerebellum & Schizophrenia: General Studies • ↑ Imaging studies > cerebellar abnormalities in schizophrenia (Vernas et al, 2007): • ↑ Cerebellar-Motor Dysfunction in Schizophrenia and Psychosis-Risk (Bernard & Mittal, 2014). • ↓ Cerebellar volume (Bottmer et al, 2005) • ↓ Blood flow on PET scan (Andreasen et al, 1996). 31 • ↓ Level of N-acetylaspartate in Magnetic Resonance Spectroscopy Imaging (MRSI) studies (marker of neurone density and viability) in vermis and cerebellar cortex (Ende et al, 2005). • ↓ Volume in the cerebello- thalamic-cortical network (Rusch et al, 2007). • Neuronal disorganisation in the superior peduncle on Diffusion Tensor Imaging (DTI) studies (Okugawa et al, 2006).
  • 32. (2) Cerebellum & Schizophrenia: Specific Symptoms (Picard et al, 2008) •Hallucinations (Shergill et al, 2003; Neckelman et al, 2006) •Formal Thought Disorder (Kircher et al, 2001; Levitt et al, 1999) •Affect symptoms (Stip et al, 2005; Paradiso et al, 2003; Abel et al, 2003) •Cognition (Szesko et al 2003; Toulopoulou et al 2004) •Attention (Eyler et al, 2004; Honey et al, 2005; Aasen et al, 2005) •Language (Shergill et al, 2003; Boksman et al 2005; Kircher et al 2005) •Memory (all types) (Mendrek et al, 2005; Whyte et al 2006) 32
  • 33. (2) Cerebellum & Schizophrenia: Cerebellar Glutamate Theory 33 •Hypo- functioning of the Glutamate NMDA receptors in cerebellum > cognitive dysmetria > schizophrenia. • Yeganeh-Doost et al, 2011):
  • 34. (2) Cerebellum & Schizophrenia: Cognitive Dysmetria Theory (Andreasen et al, 1998) •The Cortico-Cerebellar- Thalamo-Cortical circuit is dysfunctional > poor mental coordination > (Cognitive Dysmetria) > Schizophrenia. •The theory has been criticised by other researchers (e.g. Kaprinis et al, 2002, Kaprinis et al, 2002; Shanagher et al, 2006) Nancy Andreasen
  • 35. (2) Cerebellum & Schizophrenia: Secondary Cerebellar Abnormalitites •Schizophrenia > increased dopaminergic activities > cerebellar disorder > motor disorders in schizophrenia (even neuroleptics naïve) (Mittleman et al, 2008; Hoppenbrouwers et al, 2008; Varambally et al, 2006; Picard et al, 2007). 35
  • 36. (3) Cerebellar & Autism: General Studies •One of the most consistent abnormalities found in ASD (DiCicco-Bloom et al, 2006). •95% of post mortem examinations of autistic individuals (Delong, 2005) •Consensus related to cerebellar involvement in autism (Fatemi et al, 2012): • Abnormal cerebellar anatomy, • Abnormal neurotransmitter systems, • Oxidative stress, • Cerebellar motor and cognitive deficits, • Neuro-inflammation 36 S. Hossein Fatemi
  • 37. (3) Cerebellum & Autism: Cerebral Involvement •Associated with mal-development of the frontal lobe and any other brain regions > ASD (Carper & Courchesne, 2000; Kuemerle et al, 2006; Reeber et al, 2013). •Loss of modulatory control of Frontal Cortex > ASD, (Catani et al, 2008). •Cerebellum malfunction hinders neural development (Wang et al, 2014). Sam Wang
  • 39. Cerebellar Exercises / Training (Schmahmann, 2010) • Some claims (e.g. DORE) > Physical exercises (movement + balance) > speed up information processing and improve cerebellar functioning > improve dyslexia, ADHD and Asperger’s syndrome: • ? Could improve some mental illnesses like schizophrenia . • No known scientific studies. • Controversial treatments (Reynolds & Nicolson, 2007; Bishop, 2007; Rack, 2007) 39
  • 40. Dance & Movement Therapy (Levi, 1988; Jeong et al, 2005) 40
  • 41. Cerebellar Transcranial Magnetic Stimulation (TMS) (Schmahmann, 2010) •Demirtas-Tatlidede et al (2010): stimulation of the vermis in 8 schizophrenic patients > improvements in mood, alertness, memory, attention, visual-spatial skills and energy. •Very early stages (Minks et al, 2010) •No RCT 41
  • 43. Cerebellum: Clinical Reflections Introduction •Best way to make clinical judgment > follow the model of motor cerebellar functioning: • Well studied • Must be linked physiologically to non- motor functioning. •Two main fields: • Cerebellar connections to mental disorders specially dyslexia, schizophrenia and Autism > very promising and interesting but slow and small impact . • Mental equivalent to praxis and dyspraxia > clearer and more promising 43
  • 44. (1) Motor Learning vs Non-motor / Mental Learning Cerebellum > “motor” and “non-motor / mental” coordination. a) Motor coordination > “Motor Learning / Praxis”. b) Mental coordination > Non-motor coordination / Mental Coordination” 44
  • 45. •Cerebellum failing in motor coordination > • (Motor) dyspraxia, • Developmental Coordination Disorder (DCD), • Clumsy Child Syndrome, etc. •Cerebellum failing in non- motor / mental coordination > • ? Mental Dyspraxia, • ? Developmental Mental Coordination Disorder (DMCD), • ? Mentally Clumsy Child Syndrome, or • ? Mental Routine Disorder (MRD) 45 (2) Motor Dyspraxia vs Non-motor Dyspraxia
  • 46. (3) Mental Routine Disorders (MRD): A new chapter in psychopathology?! 1. Better understanding of a major part of human behaviour. 2. Widespread problem > marked suffering > needs attention. 3. Good room for effective interventions 4. Enhance therapies for major mental disorders e.g. ASD. 46
  • 47. (4) Prevalence of MRDs • Motor Dyspraxia : 6-10 % in school children (Gibbs et al, 2007). • Dyscalculia: 5-7% (Butterworth et al, 2011) • Developmental Coordination Disorder (DCD): 5–6% (Blank et al, 2012; Zwicker et al, 2012). • Dyslexia: 5% - 17% of school-age children (USA) (Shaywitz & Shaywitz, 2003). • Symptom: 40% reading below grade level (Shaywitz & Shaywitz, 2003). • Special groups: 80% of individuals with LD (Shaywitz & Shaywitz, 2003). • Complications: lower self-esteem and more emotional and behavioural difficulties than those without dyslexia (Terras et al, 2009). • comorbidity : 95% (Pauc 2005). 47
  • 48. 3- Assessment of MRDs: (A) Doya’s Model of Motor Learning (Doya, 2000) (also Imamizu et al, 2000; Hikosaka et al, 2002, Bosch-Bouju et al, 2013) •Brain circuits: •The cortico-cerebeller-thalamo-cortical circuit •The cortico-striato-thalamo-cortical circuit •Learning paradigms •Cerebral cortex > unsupervised learning •Basal ganglia > reinforcement learning •Cerebellum > supervised learning Kenji Doya
  • 49. 49
  • 51. (B) The Four Primary Components 1. Failure to learn (problem solving, adapting, planning, etc.) e.g. LD. 2. Failure to eliminate anxiety (threat) > marked disturbance of functioning e.g. OCD. 3. Failure to reach satisfaction without causing marked disturbance of functioning e.g. habit disorder 4. Failure to have smooth functioning without errors e.g. dyspraxia 51
  • 52. (C)The Four Components Mixed •Complex routine abnormalities. •1, 3 & 4 okay but 2 faulty > OCD with inner resistance. •3 & 4 okay but 1 & 2 faulty > rigid obsessional routines without inner resistance. 52
  • 53. Functional Routines Dysfunctional Routines Meaningful > Serves a purpose Bizarre (counting lamp posts / eating flies). Resilient (to stress): stress > little disruption Unstable: stress > marked disruption Adaptive (with novelty): new data > little disruption Rigid: new data > significant disruption 53 (4) Classification of MRDs: a- Dysfunctional Routines
  • 54. (4) Classification of MRDs: b- Simple vs. Complex MRD 54 Simple Complex − Single faulty component (e.g. OCD or drug addiction) − Highly functional individuals ‒ Multiple faulty components e.g. routine problems in Autism. ‒ Less functional individuals
  • 55. (4) Classification of MRDs: c- Primary vs. Secondary MRD 55 e.g. primary clumsiness Secondary clumsiness − Clumsiness due to faulty cerebellar component (Performance clumsiness) ‒ Clumsiness due to faulty cerebral (cognitive) component. (Mentation Clumsiness)
  • 56. (5) Treatment of MRDs: The Methods • General Lines: 1. Medications. 2. Educational. 3. CBT. 4. Behavioural. 5. Others: e.g. • GORE or Movement Therapies •Process-oriented approach •Task-oriented approach • Transcranial Magnetic Stimulation (TMS) • Specific: • Depends on specific conditions 56
  • 57. “3 Dimensions” is not the same as “2 Dimensions”: •Integrating the psychiatric dimension into the neuropsychological and OT therapies for dyspraxia > extra depth and sophistications but needs resources and time. (5) Treatment of MRDs : The Strategy