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Introduction to
Neuropsychology
Motor Behaviour
Example Exam Questions
1. How have neuropsychological investigations informed our current
understanding about the neural mechanisms behind motor
behaviour?
2. What differences exist between the behavioural deficits resulting
from damage to the cerebellum and damage to the basal ganglia?
3. How have investigations into motor disorders informed us about
the layout of motor representations in the brain?
Language
Lecture Outline
1. Cerebral Cortex
 Primary motor (M1)
 Sensori-motor
 Supplementary motor area (SMA)
2. Basal Ganglia
3. Cerebellum
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Basic Anatomy
The Motor System
Cerebral Cortex
(Penfield & Rasmussen, 1950; see Schott, 1993)
 „…a disorder of skilled movement not caused by weakness, akinesia, deafferentation,
abnormal tone or posture, movement disorders such as tremor or chorea, intellectual
deterioration, poor comprehension, or uncooperativeness‟‟ (Heilman and Rothi, 1993)
 A higher-order motor disorder not due to elementary sensory and/or motor
deficits (i.e. not a problem in moving the muscles themselves)
 Assessed (in order of severity) as impairment of:
 Movement on command of examiner
 Imitation of movement performed by examiner
 Appropriate movement in response to a seen object
 Correct handling of an object
 Detected in ~50% left and <10% right hemisphere patients
Cerebral Cortex
Apraxia
(Petreska et al., 2007; Zadifoff & Lang, 2005; Wheaton & Hallett, 2007)
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 Defined by errors and the manner in which they‟re elicited:
 Temporal errors
 Impaired timing and poor sequencing of movements requiring multiple
positioning
 Overall, movement is recognizable
 Spatial errors
 Abnormal amplitude, configuration orientation and body-part-as-object
substitution
 Content errors
 Perseveration
 “Other” errors
 Lack of response
 Entirely unrecognizable response
Cerebral Cortex
Apraxia
(Petreska et al., 2007; Zadifoff & Lang, 2005; Wheaton & Hallett, 2007)
Cerebral Cortex
Apraxia
(Petreska et al., 2007)
Cerebral Cortex
Apraxia
(Halsband et al., 2001)
A = Symbolic gestures; B = Actions towards body; C = Imagined tool use in extrapersonal
space
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Apraxia
Models
 Liepmann (1909)
 Disconnection between the “motor engram” (space-time plan) in left parietal
cortex and the “central region” (pre- and post-central gyri, and middle and
superior frontal gyri)
 Roy & Square (1985)
 “Conceptual system” provides knowledge about (1) the functions of tools and
objects; (2) actions independent of tools and objects; (3) the organization of
single actions into sequences
1. “Production system” incorporates a sensorimotor representation of the action and
mechanisms for movement control
 Heilman and Rothi (1993)
 Spatio-temporal representations of actions in inferior parietal lobule cannot be
sent to motor cortices
(Petreska et al., 2007)
 “…a disorder of the production component of the praxis system, i.e., sensorimotor
action programs that are concerned with the generation and control of motor
activity… It is characterized by errors in the timing, sequencing and spatial
organization of gestural movements...”
 Errors include:
 Temporal
 Increased or decreased rate of production of a pantomine,
 Addition, deletion, or transposition of movement parts
 Spatial
 When asked to pantomime teeth brushing , the fist is tight with no space for
the imagined toothbrush
 Improves on imitation and with use of actual tool, and transitive worse then
intransitive
 Impairment greater in clinical setting than everyday life
Cerebral Cortex
Ideomotor Apraxia
(Wheaton & Hallett, 2007 [but see Sunderland & Shinner, 2007])
Ideomotor Apraxia
Patient G.W.
(Rapcsak et al., 1995)
• Identify tools from verbal functional descriptions (10/10)
• Tool function identification (10/10)
• Tool selection (10/10)
• Verbally describe actions required for tool use (15/15)
• Verbal description of serial actions (flawless)
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 “…a disruption of the conceptual component of the praxis system, i.e., action
semantics memory… Patients with ideational apraxia are not impaired in the action
execution per se, but demonstrate inappropriate use of objects and may fail in
gesture discrimination and matching tasks.”
 Errors include:
 Content
 Impaired performance of single tool use - cannot associate tools/objects with
the corresponding action
 Unable to choose a hammer to drive a nail or correctly
 Impaired performance of action sequences requiring the use of various objects
 Impaired performance of multiple-step tasks
 Preparing a letter to mail (perseveration)
Cerebral Cortex
Ideational Apraxia
(Petreska et al., 2007)
Ideational Apraxia
Example Patient
 Lesion to “left parietal lobe”
 No signs of low-level motor disturbance
 “When asked to pantomime certain motions with either her right or left
arm (i.e. "Show me how you would use a key"), [she] would look down
at her hand and say, "I can't do it”… When asked if she understood the
question, [she] would verbally demonstrate comprehension, i.e. "Keys
are used for opening locks”.”
 “When the correct movement was shown… she was always able to
select the correct movement… [and] She was able to imitate in a
flawless manner.”
 “[She showed] no difficulty with multiple object sequencing (i.e. taking a
cigarette out of a pack, putting it in her mouth, lighting it, and then
smoking).”
(Heilman, 1973)
Cerebral Cortex
Apraxia
(Culham & Valyear, 2006; Iacoboni, 2006; Petreska et al., 2007)
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The Motor System
Basal Ganglia
 Input
 Striatum
1. Caudate
2. Putamen
 Output
3a. Globus Pallidus (internal)
4. Substantia Nigra
5. Subthalamic nuclei
3b. Globus Pallidus (external)
The Motor System
Basal Ganglia
(DeLong, 1990)
The Motor System
Basal Ganglia
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 Increased conduction through
indirect pathway
 Increased pallido-thalamic
inhibition
 Hypokinesia (PD)
 Increased conduction through
direct pathway
 Decreased pallido-thalamic
inhibition
 Hyperkinesia (HD)
The Motor System
Basal Ganglia
(DeLong, 1990)
Basal Ganglia
Parkinson’s Disease
 Hypokinetic
 Impaired movement initiation (akinesia); reduced velocity and
amplitude of voluntary movement (bradykinesia [1]);
 Muscular rigidity (dystonia [2]); resting tremor ; (L-DOPA
induced) dyskinesia; freezing (festination)
 Treatment with L-DOPA (“ON” vs. “OFF” phase)
Basal Ganglia
Parkinson’s Disease
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 Hyperkinetic
 Involuntary movements (dyskinesias)
Basal Ganglia
Huntington’s Disease
Basal Ganglia
Huntington’s Disease
 Dystonia and treatment by pallidotomy
(Obeso et al., 2000)
Basal Ganglia
Movement Disorders
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The Motor System
Cerebellum
(Fredericks, 1996)
 Contains more cells than the rest of CNS
 Ipsilateral control of motor behavior (cross twice)
 Inputs arrive from vestibular (inner ear), somatosensory, visual, and
auditory systems
 Outputs to deep cerebellar nuclei, which in turn send output to:
 Medial: Descending extrapyramidal nuclei (brainsteam)
 Lateral: Ascending projections to frontal and motor cortices via
thalamus
The Motor System
Cerebellum
(Fredericks, 1996)
 Consequential behavioural Impairments
 Hypotonia (antagonist); dysdiadochokinesia; dysmetria
(hypometria vs. hypermetria); cerebellar gait (postural instability)
Cerebellar Ataxia
Movement Disorders
(Fredericks, 1996)
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The Motor System
Cerebellum
 Cerebellar gait (Impairment of posture and fluidity in walking)
 Dysdiadocokinesia (Impairment of rapid movements )
The Motor System
Cerebellum