1. Week 6 Motor Control Corticospinal Damage Hemiparesis
(Dr Roger Newport)
Corticospinal Damage
Hemiparesis
Cerebellar Damage
Ataxia
Timing Issues
Motor Learning
Basal Ganglia Damage
Parkinson’s Disease
Huntingdon’s Chorea
Cortical Damage
Apraxia

2. Corticospinal Damage Hemiparesis and Hemiplegia Definitions
Hemiplegia: Paralysis
Hemiparesis: Weakness
The most common and obvious sign of stroke, but
can be caused by a variety of reasons including:
tumours
Infection (e.g. meningitis / encephalitis)
Metabolic imbalance
congenital disorders
Always as a result of damage to the corticospinal tract

3. Corticospinal Tract Originates in Primary Motor
Cortex and neighboring regions
Passes through Corona Radiata
Internal Capsule
Cerebral Peduncles
Pons
Pyramids
Crosses in the Pyramidal Decussation
Forms Anterior and Lateral
Corticospinal tracts

4. How can we tell where in the tract the damage is?
Doctor,
I’ve had a stroke
but you can’t afford
to give me a scan
Yes, if we follow a
few basic rules
Can we tell
where my lesion is?

5. RULE NUMBER 1
There are 4 major sites causing hemiparesis:
(1) Cortex
(2) Internal Capsule
(3) Corona Radiata
(4) Brainstem
RULE NUMBER 2
There is usually only one lesion.
Bilateral lesions do occur, but then there are bilateral signs
RULE NUMBER 3
If it is below the neck there will be no facial weakness.

6. Doctor, my lesion is in my spinal cord How do I know? Doctor,
Decussation
Midbrain
Pons
Medulla
Facial
nuclei
To right limbs
To left limbs
From
Right Cortex
Left Cortex SC X
Because I have no
facial weakness

7. Left-sided upper motor neurone facial weakness.
Cortical damage does not affect the entire side of the face. Because of the bilateral innervation of the upper third of the face, only the lower two-thirds of the face would be affected by cortical damage
To Upper
Facial Muscles
To Lower
Facialnerve
fibres
Crossed corticobulbar fibre
X &UnX
input
UnX
only
L Cortex
R Cortex
Uncrossed
Corticobulbar
fibre

8. RULE NUMBER 4
The face is always weak on the same side as the arm and leg if it is an upper motor neurone facial weakness -
except when the lesion is in the pons
A lesion in the pons can result in crossed hemiparesis, i.e. contralateral limb weakness and ipsilateral facial weakness

9. Doctor, my lesion is in my spinal cord How do I know? Doctor,
my pons
How do I know?
Decussation
Midbrain
Pons
Medulla
Facial
nuclei
To right limbs
To left limbs
From
Right Cortex
Left Cortex SC
To the
R face X
Because I have have
crossed hemiparesis

10. RULE NUMBER 4
The face is always weak on the same side as the arm and leg if it is an upper motor neurone facial weakness -
except when the lesion is in the pons
RULE NUMBER 5
If the lesion is above the neck then it is on the opposite side to the hemiparesis. EVERYTHING, absolutely everything crosses if it’s going to the hemispheres. Your left brain receives sensation and visual input from the right side and sends out its motor output to the right side.

11. RULE NUMBER 7: THE LAW OF EXPECTATIONS
If there is a left sided hemiparesis, which is an easy thing to observe: it follows that you can expect to find (if there is not a brainstem lesion):
Left-sided upper motor neurone facial weakness.
Left-sided sensory loss
Left homonymous hemianopia (can be cortical or subcortical)
If the lesion is in the cortex you expect cortical signs

12. Left Hemisphere Right Hemisphere Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Apraxia
Dysarthria (speech)
3Rs Difficulty
Right Hemisphere
Extinction of left-sided stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Spatial disorientation
Look at the eyes!
Eyes look at involved hemisphere
Eyes look away from the Hemiparesis

13. But what if the brainstem and pons have been ruled
Doctor,
my lesion is in
my cortex
How do I know?
Because I have
uneven arm and leg
weakness and show
cortical signs X
Doctor,
my lesion is in
my cortex
How do I know?
But what if the brainstem
and pons have been ruled
out and there are no
cortical signs?
Corona Radiata
Internal capsule
Remaining Candidates:
Internal capsule
Corona radiata

14. Fibres descending from the cortex are called the ‘corona radiata’
C.R.
I.C. To
LMN
Brainstem
Reticular
formation
These fibres funnel through the internal capsule which lies between the thalamus and basal ganglia on their way to the brainstem.
The reticulospinal tracts are two long descending pathways associated with the control of movements and posture. The lateral reticulospinal tract inhibit extensors.

15. So if input to the reticular nuclei is interrupted (as happens with a lesion of the internal capsule) extensor reflexes are no longer inhibited - result: the Babinski sign.
cortex
C.R.
I.C. To
LMN
Brainstem
Reticular
formation X
Normal plantar reflex
Babinski extensor reflex Up
Fanning
toes }

16. Doctor,
my lesion is in
my internal capsule
How do I know?
Doctor,
my lesion is in
my internal capsule
How do I know?
cortex
C.R.
I.C. To
LMN
Brainstem
Reticular
formation
Because I have
equal arm and leg
weakness and show
the Babinski sign X

17. Where is my lesion: summary?
Spinal cord No
Ipsilateral damage
Facial Weakness?
Yes
FW same side as limb W?
Pons No
Yes
Leg and arm equal?
Contralateral
damage
Internal Capsule
Yes No
Cortical signs?
Cortex
Corona Radiata
Yes No

18. But there is more to motor control than the corticospinal tract.
Thalamus
If you want to speak to the cortex, you’ll have to go through the thalamus
Much more.
Major components of the motor system
Transforming sensory
input into plans for
voluntary movement
Initiating and directing
voluntary movement
Movement learning,
motivation and initiation
Motor learning,
timing and coordination

19. The Cerebellum: where is it and what does it do?
Thought to be involved in:
Balance
Coordinating movement
Timing of movements
Timing of discontinuous movements
Motor learning - acquiring and maintaining
Sources of cerebellar injuries
Toxins (ethanol, chemotherapy, anticonvulsants, ethanol).
Autoantibodies (paraneoplastic cerebellar degeneration )
Structural lesions (strokes, MS, tumors, etc)
Inherited cerebellar degenerations ( e.g. Freidreich's ataxia)
Diagnosis usually by MRI

20. The cerebellum - basic divisions
Lateral
Hemispheres
Vermis
Paravermis
Anterior
Lobe
Posterior
Lobe
Flocculus

21. } Cerebellar Ataxia Midline effects Postural instability
e.g. fall to ipsilesional side
Truncal ataxia
Postural control and adjustment
e.g. Romberg sign
Gait ataxia
Extensor rigidity
Nystagmus
Eye deviation if unilateral

22. Cerebellar Ataxia Hemispheric effects Asynergia Dysarthia Dysmetria
Decomposition of movement
Dysarthia
Jerky speech pattern
Dysmetria
inability to stop a movement at desired point
Dysdiadochokinesia
inability to perform rapidly alternating movements
Hypotonia
decreased muscle tone, pendular knee jerk
Intention Tremor
usually evident during powerful movements, but absent or diminished with rest (contrast basal ganglia disorders)
Remember : Lesions to the cerebellum do not destroy movement, they disrupt it.
Ataxia = disordered movement

23. The Cerebellum and Timing
Cerebellum is thought be involved in the timing of movements because
cerebellum lights up in PET study of complex/novel timing tasks (Penhune et al. 1998) cerebellar patients are imparied at tasks like tapping along to a metronome beat
Two basic models:
40 Hz
25 ms
Pacemaker
10 pulses = 250 ms
20 pulses = 500 ms
30 pulses = 750 ms
Clock counter model
Pacemaker produces output to counter
Longer intervals represented by more pacemaker outputs in counter
250 ms
500 ms
750 ms
Interval model
Different intervals represented by distinct elements
Each corresponds to a specific duration

24. Multiple timer model
Must be independent (interval) timers for each effector (finger/hand/limb etc.) as unilateral cerebellar damage gives rise to unimanual timing deficit, but bimanual tapping improves performance.
Ivry, R.B. & Richardson, T. (2002).

25. Spencer et al (2003): Cerebellum is only responsible for stop-start movements, not continuous motion.
Continuous movements
can be set going and left
Discontinuous movements
have a specific temporal goal
This is what is controlled
by the cerebellum.

26. The Cerebellum and Motor Learning
The Cerebellum is thought to be involved in motor learning and the maintenance of movement accuracy because patients with cerebellar lesions are impaired at learning novel motor tasks.
Evidence from prism adaptation ( e.g. Thach et al., 1992)
No Prisms
Prisms On
Prisms Off
Example data

27. The Feedback Circuit: CORTEX Inferior Olive Spinal Cord Cerebellum
One theory of how the cerebellum might correct movement
CORTEX
Inferior
Olive
Spinal Cord
Cerebellum
Corticospinal Tract
Error
Correction
Feedback from
actual movement
cerebellar
Spino-
Tract

28. The basal ganglia
a collection of nuclei deep in the white matter of the cerebral cortex.
They include:
Caudate
Putamen
globus pallidus
substantia nigra
subthalamic nucleus
(the caudate nucleus and the putamen taken together all known as the striatum)

29.  The main input to the Basal Ganglia is exitatory from the frontal cortex (especially from the supplementary motor area SMA)
 The striatum (C+P) inhibit the Globus Pallidus whose output to the thalamus is also inhibitory
 The thalamic output to the cortex is exitatory.
 Striatum activity is modulated by the Substantia Nigra
There’s more:
Direct and indirect loops.
Direct Route
Striatum - GPi - Th - cortex
Indirect Route
detours via GPe and SN.
The release of dopamine stimulates D and inhibits InD routes
+ve
+ve
-ve
-ve
-ve
+ve
Mod -ve)

30.  What is the function of the Basal Ganglia?
Slow postural adjustments? - BG damage can cause postural disturbances
Initiating movements? - BG patients can struggle to start movements
Gate Keeper / Brake Regulator (e.g. Gazzaniga et al.)?
BG acts in a regulatory way to facilitate desired voluntary movements and inhibit unwanted, often reflexive, movements
The direct route enables the preferred action
The indirect route suppresses unwanted movements
Activity in the BG increases in anticipation of an intended movement 
Gate Keeper or Brake Regulator?

31. X +ve -ve -ve -ve +ve -ve Fixed by removal of STN
Lesions in specific nuclei tend to produce characteristic deficits.
the slow and steady loss of dopaminergic neurons in SNpc leads to:
Parkinson's disease,
3 symptoms usually associated with Parkinson's are:
Tremor (+ve) most apparent at rest
Rigidity (+ve) due to simultaneous contraction of flexors an extensors
Bradykinesia (ive) difficulty initiating voluntary movement
Akinesia illustrates intentional aspect of BG function
+ve
-ve
-ve
-ve
+ve X
-ve
Fixed by removal of STN
Remember the role of the GPi is inhibitory

32. X +ve -ve -ve +ve -ve Remember the role of the GPi is inhibitory
Whereas degeneration of the caudate and putamen (inhibitory) leads to:
Huntington's disease, or chorea,
a hereditary disease of unwanted movements.
produces continuous dance-like movements of the face and limbs
A related disorder is hemiballismus, flailing movements of one arm and leg, which is caused by damage (i.e., stroke) to the subthalamic nucleus.
+ve
-ve X
-ve
+ve
-ve
Remember the role of the GPi is inhibitory

33. Apraxia What is apraxia? Apraxia has an exclusionary definition:
It is a disorder of skilled movement that cannot be attributed to basic level sensory, motor or cognitive disturbances
It is therefore a disorder of high-level perceptual, cognitive and/or motor systems
What is apraxia?
Apraxia
Action system
 Three component approach
1. Perceptual processes
 vision, proprioception, haptics, vestibular, auditory
2. Cognitive processes
 attention, semantic memory, decision-making, response selection, motor representations
3. Motor processes
 convert movement plan into motor response, control muscle activation

34. Some basic tests for apraxia

35. But watch out for confounds

36. Brain areas involved Primary (Arcuate Motor Fasciculus) SMA cortex
(Broca’s area)
Primary
auditory
ortex
Primary
Visual
cortex
Angular gyrus
(Wernicke’s area)

37. Main types of Apraxia
Ideational apraxia
inability to produce a coherent action sequence - Kimura Box
Impairment in the concept of an action
ability to imitate gestures / produce movements on command spared
Thought to occur when the motor programming area is destroyed by damage to the supramarginal gyrus, impairing the conceptual representation of an action and leading to deficits in using tools or performing an action to verbal command while imitation is spared (Koski (on web))

38. Ideomotor apraxia
Impairment in the performance of skilled pantomime movements on verbal command or in imitation
most commonly caused by parietal damage in the dominant hemisphere (LH). In this case bilateral apraxia results. (In rare cases a lesion to the right-hemisphere SMA or to the corpus callosum may also produce ideomotor apraxia. In this case the apraxia is restricted to the left limb.)
Ideomotor apraxia occurs when the motor programming area is disconnected from the premotor and motor regions, so that the patient can conceptualize but not actually execute the action,
demonstrating spared recognition of tools but deficient
ability to use them appropriately or to imitate actions.

39. Ideomotor apraxia (cont.)
Can be ok with ipsilesional limb
Have greatest difficulty when imitating transitive movements (tool use)
Several types of errors
Use body parts instead of imagined tool (e.g. scissors)
Perseverative errors (do previous pantomime)
Sequencing (e.g open door twist before reach or pull before twist)
Most characteristic are spatial errors
Postural (e.g. wrong grip)
Spatial orientation (e.g. not cutting in one plane)
Spatial movement
(e.g screwdriver shoulder not wrist)
Impairment in knowing how,
rather than what to do

40. 2 forms of ideomotor apraxia (Heilman and Rothi, 1993)
Loss of praxicons in supramarginal or angular gyrus
Perform poorly to command, cannot comprehend gestures
2. Disconnection of praxicons from premotor and motor areas (caused by lesions anterior to SMG/AG. AG
SMA
Praxicon = stored spatiomotor gesture representations which provide the ‘‘time-space-form picture of the movement’’ (Liepmann & Maas, 1907)
a ‘movement formula’ if you like
But, Ochipa et al (1990)
Patient could comprehend
Panto and panto to command, but not imitate transitive gestures
Praxicons stored in dominant inferior parietal lobe

41. } Output praxicon 2 route model SMG/AG Auditory Analysis
Semantics (learnt actions) }
SMG/AG
Auditory Analysis
Auditory/verbal input
(command)
Innervatory patterns
(motor plan)
(SMA)
Visual Analysis
Visual input
(gesture or object)
Input praxicon
Motor sytems
lexical
route
Direct
Non-lexical
Any of above can still imitate meaningful and meaningless gestures
Input praxicon unable to recognise/comprehend gestures, but can do so to verbal command
Between input and output praxicon able to recognise, but not produce object gestures, but can do so to verbal command
Output praxicon can recognise/comprehend, but can’t produce
Direct route can do meaningful gestures only

42. Quick review
Damage to:
Input praxicon unable to recognise/comprehend gestures, but can do so to verbal command
Between input and able to recognise, but not produce object
output praxicon gestures, but can do so to verbal command
Output praxicon can recognise/comprehend, but can’t produce
Any of above can still imitate meaningful and meaningless gestures
Direct route can do meaningful gestures only

43. } Output praxicon 2 route model SMG/AG Auditory Analysis
Semantics (learnt actions) }
SMG/AG
Auditory Analysis
Auditory/verbal input
(command)
Innervatory patterns
(motor plan)
(SMA)
Visual Analysis
Visual input
(gesture or object)
Input praxicon
Motor sytems
lexical
route
Direct
Non-lexical
Problem is when a patient can do meaningless imitation, but not meaningful imitation
(MF (Bartolo, 2001))
Another patient that causes problems for this model is BG (Buxbaum, 2000) who can do tool-use gestures, but not other gestures, but whose meaningless imitation is worse than meaningful imitation

44. Lexical route
Direct route
In PPC
Buxbaum 2000
Dynamic interplay between knowledge of tool use and stored learnt gestures and body-centred representations of how to do actions (the body schema). The boxes on the left can supplement or boost the damaged processes of the right hand box.

45. A closer look at Patient BG:
gestures nearly normally with tool in hand
And recognises gestures quite well
 gesture representations can be accessed by visual input
more deficient in imitating meaningless gesture-like movements
than spatially matched meaningful gesture analogues
 direct route damaged?
But, unable to gesture to command , to sight of object or imitation
output praxicon damaged?
difficulty in matching gestures (but not objects),
especially when a spatial transformation is required
deficient processes not conceptual or visual,but spatiomotor

46. 1. What is the basis for the relative integrity of BG’s tool use?
2. Why does she fail to use the direct route upon provision of a model to be imitated?
One possibility is dual lesions to both lexical and direct route
more parsimonious explanation:
BG’s pattern reflects damage to a unitary set of procedures or representations common to both lexical and direct routes
(Buxbaum, 2000).

47. Apraxia summary
2 main types of apraxia
2-route model explains most functional characteristics of ideomotor apraxia are covered by the 2-route model, but
Cannot account for dissociation between being able to perform meaningless, but not meaningful gestures (patient MF (Bartolo))
Cannot account for preserved tool-use gesture with impaired other geture and impaired meaningless imitation (patient BG (Buxbaum)