Motor and Planning Flashcards

(256 cards)

1
Q

What do we use muscle contractions for?

A
Moving limbs
Moving the external world
Moving yourself around
Communication - speech/gesture/writing
To move visual and somatosensory sensors
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2
Q

Define apraxia

A

Movements poorly prepared or planned
Inability to carry out purposeful sequences of action. Perhaps struggle to hold goal in mind while performing individual actions. Have functioning motor equipment

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3
Q

Define noise

A

Random variation in signals, both motor and sensory, which renders them imprecise

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4
Q

Define redundancy

A

There are many possible ways to achieve a goal - the ‘motor equivalence’ problem: which do you pick?

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5
Q

Describe biological delays

A
  • Conduction of AP delays signals
  • Muscle contracts slowly
  • Eye muscles 20ms to full force, limb muscles 30-50ms
  • Must specify when force reaches its peak to produce accurate movement
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6
Q

Define nonlinearity

A

Mixing individual motor commands doesn’t produce predictable results - force depends on length, load and velocity of shortening in a more complex way

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7
Q

Define non-stationarity

A

The behaviour of motor systems can change over time; muscle contraction depends on history e.g. thixotropy (gels becoming fluid when disturbed)

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8
Q

How many synapses does a motorneuron receive?

A

30K

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9
Q

How big is the EPSP of an excitatory synapse?

A

0.1mV

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10
Q

What is the spike threshold for a muscle?

A

> 10mV depolarisation (e.g -55mV)

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11
Q

What are the stages of simple shifts of position?

A

Acceleration (agonist)
Deceleration (antagonist)
Final position holding force (agonist)

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12
Q

What are the sensors of the outside environment?

A
Auditory
Visual
Somatosensory
Proprioceptors
Vestibular receptors
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13
Q

Define negative feedback

A

System that acts as a regulator to maintain a given parameter at a set point. Deviation from the set point is detected by sensors and a correction generated to nullify the deviation

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14
Q

Define closed-loop feedback

A

A negative feedback system that can shift state when the set point changes

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15
Q

What are the major problems with negative feedback loops?

A

Time delays in the feedback loop (sensory transduction, conduction to and from brain)Leads to instability and oscillation

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16
Q

How do cerebellar lesions affect feedback systems?

A

Damage ability to anticipate motor commands (feedforward), so only leave negative feedback?

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17
Q

Define feedforward/open-loop feedback

A

Sensory information is used to generate a prediction of what is needed in the future

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18
Q

Define internal model system

A
Simulator in the brain that represents the mechanics of the body and the behaviour of the outside world 
Can learn (with experience) to predict which motor commands would be useful in a given situation
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19
Q

Define inverse model

A

A representation of transformation from motoneuron activity to movement in reverse so that from the desired outcome, motor demands to generate it can be estimated

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20
Q

What are the problems with inverse models?

A

Small errors in the initial stages of the calculation lead to massive errors in the final stages

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21
Q

Define forward model

A

Predicts consequences of motor commands before the slow muscle movement is complete, using information on what the motor commands were via efference copy/internal feedback. This is used to predict the movement that will follow, so the predictions can be set to the desired result and follow up corrections can thus be set up for errors as they are in the process of occurring.

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22
Q

What is the main centres for feedforward control?

A

Cerebellum and motor areas of cerebral cortex

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23
Q

Where in the spinal cord are the alpha-motoneurons?

A

Ventral horn

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24
Q

Define motoneuron pool

A

The 200-500 motoneurons that innervate a given muscle

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25
What is the organisation of motoneurons within the ventral horn?
Proximal medial, distal lateral Flexor posterior, extensor anterior Somatotopic organisation
26
What is a motor unit?
The muscle fibres that one motoneuron innervates
27
How many motor units are in a muscle?
Several hundred
28
What are the three categories of motor unit?
1. Slow 2. Fast fatigue resistant 3. Fast fatiguable
29
Describe the anatomy, biochemistry, and physiology of slow fibres?
Red Anatomy: small fibres, few fibres/unit, highly vascular Biochemistry: oxidative, lots of myoglobin (red) Physiology: slow twitch, low tension, fatigue resistant, slow axons Used in endurance training
30
Describe the anatomy, biochemistry, and physiology of fast, fatigue resistant fibres?
Anatomy: intermediate fibres, intermediate fibres/unit, intermediate vascularity Biochemistry: intermediate oxidative and glycolytic, intermediate levels myoglobin Physiology: intermediate twitch, intermediate tension, intermediate fatiguability, intermediate speed axons
31
Describe the anatomy, biochemistry, and physiology of fast, fatiguable fibres?
Pale Anatomy: many fibres/unit, few capillaries Biochemistry: glycolytic, little myoglobin Physiology: fast twitch, high tension, fatiguable, fast axons Used in sprint training
32
What is the benefit of having motor units with different properties?
Slow units can use for continuous generation of small forces (finely graded, low force contractions) Fast fatigueable units can produce high forces over a short period (strength needed)
33
How is motor unit utilisation controlled?
1. Rate coding: vary motoneuron firing rate. Fuse into tetanus at quite low freq though 2. Motoneuron recruitment: recruit more motor units as more force is required
34
What is the size principle?
That motor units are recruited in an orderly sequence from lowest force to highest force units as force increases. Means that force always increments by finest available motor unit, and so is as smooth as possible.
35
How does the size principle work?
Developmental plasticity Motoneurons with low firing threshold innervate few muscle fibres and induce them to become slow twitch/low force/fatigue resistant. Motoneuons with the highest firing thresholds recruited last innervate many muscle fibres and induce them to become fast twitch. Reduces work of the motor system.
36
What are the 3 sources of synaptic input to motoneurons?
1. Afferent fibres from muscle spindles 2. Descending fibres: direct from brainstem or cerebral cortical structures, relatively rare but with an exception 3. Spinal interneurons: most numerous connection, most cases receive input from sensory pathways and descending pathways
37
What are the two types of reflex?
1. Targeted at specific small groups of muscles to regulate their force e.g. stretch reflex, associated reciprocal and recurrent inhibition 2. Complex reflexes that generate functional movements that involve multiple muscles e.g. nociceptive withdrawal reflex
38
Define a withdrawal reflex
Coordinated pattern of muscle contraction to move the stimulated part of the body away from the stimulus
39
Describe 'local sign' of the foot.
Different reflexes are evoked from different locations. Stim of plantar (bottom) surface of foot evokes leg flexion, stim of foot dorsum evokes leg (top) extension.
40
Where do nociceptive afferents terminate?
Substantia gelatinosa of the dorsal horn
41
What are proprioceptors?
Sensory fibres from muscles and joints that provide information on the musculoskeletal system. 1/5 of mechanoreceptors. 3 major groups: 1. Muscle spindle afferents = stretch receptors/length 2. Golgi tendon organ afferents = muscle tension receptors/force 3. Joint receptors = signal joint position and movement especially at the extremes
42
What are exteroceptors?
The receptors on the surface of the body, e.g. cutaneous receptors. Especially ruffini endings are involved in movement
43
What are teloceptors?
Receptors that sense the environment at a distance e.g. eyes, ears, nose
44
Define proprioception
The sense of position and movement of the body | Takes information from proprioceptors, exteroceptors, vision and vestibular systems
45
Describe muscle spindles
Proprioceptors: activated by stretch of the central regions of the intrafusal fibres Spindle-shaped structures embedded in muscles whose afferents signal muscle length and change in muscle length Comprises an encapsulated bundle of small specialised intrafusal muscle fibres Striated at the ends of their fibres - contractions change the sensitivity of the sensory nerve endings
46
How many spindles in a muscle?
20-100
47
What is the difference between extra and intrafusal muscle fibres?
Intrafusal aren't contractile, smaller than extrafusal which are contractile
48
What are the two types of muscle spindles?
Bag fibres: swollen centre and contain many nuclei, contractile ends. 2 forms Chain fibres: uniform diameter, uniformly contractile along length.
49
What are the sensory receptors that attach to intrafusal muscle fibres?
Primary/1a spindle afferents: very large and fast conducting axons with terminal branches that end in coils/annulospiral endings around the central region of the intrafusal muscle fibre Secondary/II spindle afferents: end adjacent to the central region of the intrafusal muscle fibre. Both activated by stretch
50
What are the motorneurons that attach to intrafusal muscle fibres?
Gamma motoneurons Innervate the ends of the intrafusal fibres (In some mammalian fibres, beta innervation) Different gamma neurons innervate bag and chain fibres
51
What is beta innervation?
In amphibian/reptile muscle, where alpha motoneurons innervate the intrafusal (as well as extrafusal) muscle fibres
52
What is the difference between what bag fibres sense and what chain fibres sense?
Chain fibres = uniform mechanical properties along length, so sensory endings esp II afferents, signal static muscle length linearly Bag fibres = esp 1a afferents, dynamic sensitivity to changes in stretch. Because central region isn't contractile, but elastic, so rapid stretches rapidly elongate it (rapid strong activation of afferents at stretch onset), which is subsequently relieved as the viscoelastic contractile ends of the fibres elongate - rapid adaptation.
53
What is the function of gamma innervation?
Innervate the ends of the intrafusal fibres Shorten Stretch central region of fibres where the receptors are located Increases both firing and sensitivity of receptors Lets the muscle signal length changes from different starting muscle lengths (a form of adaptation)
54
Define adaptation
Adjusting the receptor sensitivity to extend the range over which the sense organ operates
55
How come the brain isn't confused by both gamma motoneurons or muscle contractions being able to signal the same thing from muscle spindles?
Brain receives efference copies of the commands sent to gamma motoneurons
56
Describe Golgi tendon organs
Activated by active tension in the tendon Passive stretches of relaxed muscle doesn't increase tension in the tendon, but muscle contractions do. Signal strongly proportional to the load on the muscle
57
What is the stretch reflex?
Muscles respond to being stretched by contracting, e.g. knee jerk: tap patellar tendon, stretches muscle spindles, reflex contraction of quadriceps, close synergists, and excite interneurons that inhibit antagonist muscles
58
Which muscles do not have a stretch reflex?
Eye, tongue
59
What is reciprocal inhibition?
A spinal reflex. In stretch reflexes, agonist contracts, but also (via interneurone) reflexive relaxation of antagonist
60
What was Merton's proposal?
That movement was driven by gamma motoneurons altering set points such that the spinal cord itself determines the appropriate force required via negative feedback
61
What were the problems with Merton's proposal?
1. For this to work the stretch reflex would need a gain of one (it's actually less) 2. Delay which would lead to oscillation
62
What is clonus?
Oscillation following a muscle stretch in pathological situations following damage to descending corticospinal pathway systems such that the stretch reflex is exaggerated
63
What are the roles of proprioceptors?
1. Spinal reflex action 2. Kinesthesia (sense of position, movement and effort) 3. Information for supraspinal motor systems involved in predictive feedforward control
64
What do proprioceptors contribute to supraspinal control?
Information on current state of play at outset of movement to model predictions on Assessment of the outcome after the movement, critical for learning in the model system to ensure they are accurate
65
What was the Nashner experiment?
Move a platform backwards with a person on it, pulls feet, measure muscle response in gastrocnemius. The more you do it, the more the early stretch reflex response comes in. Did it again but tilt the platform: caused the same stretch, and get the same strong reflex, which induces a body sway as you expect the previous set of circumstances.
66
What type of synapse is there between 1a afferents and inhibitory interneurons?
Glycinergic
67
What is recurrent inhibition?
Renshaw cells Motoneuron axons have branches called recurrent collaterals within the spinal cord that innervate a type of inhibitory interneuron called Renshaw cells. Renshaw cells seem to regulate the timing of motoneuron firing, preventing synchrony and so jerkiness or tremor
68
What does it mean that Golgi tendon reflexes are context dependent?
In static positions, activation of tendon organs mainly inhibits the parent muscle In locomotion, activation of tendon organs mainly leads to excitation, where it supports contraction against a load
69
What are 3 neonatal reflexes that change with development?
1. Grasp reflex 2. Babinski's sign (plantar reflex) 3. Reflex stepping
70
Describe the grasp reflex
In first 6-12 months then disappears Babies grasp onto things and generate enough force to support the body Can reappear after brain damaged
71
Describe Babinski's reflex
Toes curl up in response to plantar stimulation (in adults they turn down) Neonatal reflex reappears after brain damage
72
Describe spasticity
Exaggerated stretch reflexes. Muscles are tense and stiff. Stretch elicits strong reflexes and clonus
73
Describe the clasp knife reflex
The limbs snap into flexion or extension during movement (not due to tendon organs)
74
What are central pattern generators?
Biological neural networks that produce rhythmic outputs with the absence of rhythmic inputs. Can function without input from higher brain areas, but are modulated by them. Can also function without sensory inputs, e.g. by cutting dorsal roots of spinal cord. Made up of spinal interneurons
75
How much do CPGs generate locomotion in man?
Little Pattern that greater encephalisation is associated with weaker ability to generate locomotion. Mammals less prone to produce movement after removal of the brain
76
Where do the two descending motor pathways sit in the spinal cord white matter?
Dorsolateral | Ventromedial
77
What do the ventromedial pathways control?
Axial and proximal limb muscles Role in whole body movement (posture/locomotion) Crossed and uncrossed
78
What is the ventromedial pathway divided into?
Reticulospinal from reticular formation Vesibulospinal from vestibular nuclei Tectospinal from superior colliculus (orientation of your head in space)
79
What are the dorsolateral systems?
Control goal directed movements of the limbs esp hands, feet, face, lips
80
What is the dorsolateral system divided into?
Rubrospinal pathway: Red nucleus in midbrain. Probably vestigial in man. Corticospinal tract: from motor areas of cerebral cortex, largest descending pathway in all mammals, the dominant descending control pathway in man. Crossed
81
What and where are the receptors for the vestibular system?
Hair cells in labyrinth of semi-circular canals and otolith organs (saccule and utricle)
82
Describe the utricle and saccule
Static information Hair cells project into jelly-like mass that gravity acts on Hair cells have different directional sensitivities Specific sets of hair cells activated when the head in different positions So inform on effective direction that gravity is acting - when immobile = head position
83
Describe the semicircular canals
Dynamic signal when the head starts or stops to move. Hair cells embedded in mass that almost closes the canal called the cupula Cupula neutrally buoyant in the endolymph in the canals so stationary when head is stationary Head moves --> fluid has inertia so tends to remain stationary but cupula fixed to head so cupula deflected --> activates hair cells.
84
Why do you feel dizzy when you drink alcohol?
Alcohol equilibrates more quickly into the cupula than endolymph cells, so the cupula becomes buoyant and you feel like you're constantly rotating
85
Which is more likely to provide signals for feedforward control: otolith or semicircular canals?
Semicircular canals
86
How does the vestibular system being activated affect posture?
Activation --> vestibulospinal pathways --> extensor/antigravity muscles
87
How can the vestibular system get damaged?
Labrynthitis, centrally through brainstem stroke or cerebellar damage
88
How does the body differentiate between body sway, when it needs to move, and head sway, when it doesn't
Efference copy from motor systems that move the head: if the predicted vestibular signals match the actual vestibular signals, the vestibular reflexes are cancelled
89
What is the point of gaze-fixing mechanisms?
Visual system is bad at resolving moving images, so eye needs to be kept fixed relative to the outside world as much as possible.
90
What are saccades?
Very rapid gaze shifting eye movements
91
What are the two major gaze fixing mechanisms in mammals?
Vestibuloocular reflex | Optokinetic reflex
92
Define the vestibuloocular reflex
Moves the eyes equal and opposite to the head
93
What does the MLF connect?
Medial longitudinal fasciculus | Semicircular canal afferents, vestibular nculei, motoneurons of oculomotor nuclei
94
Which bit of the cerebellum controls vestibuloocular reflexes?
Flocculus | Calibrates what oculomotor movement is needed to be done by the cerebellum
95
How many synapses are thee between the semicircular canals and the eyes moving?
4: 1 canal --> nerve 2 nerve to second nerve in vestibular nucleus 3. second nerve to third nerve in oculomotor nucleus 4. third nerve to eye muscle
96
What is the function of the optokinetic system?
Moves the eyes to follow slow movements of the visual field
97
What drives the optokinetic system?
Visual cortex
98
How does the optokinetic system work?
When eye deviates from it axis within the orbit, saccades reset the eye to the centre: nystagmus.
99
Define nystagmus
Drift and saccade eye sequence resulting in a 'sawtooth' motion of the eye Can occur physiologically due to optokinetic or vestibular stimuli, or pathologically after cerebellar or vestibular damage.
100
What is the pathway that drives gaze-shifting foveation?
Retina --> magnocellular pathway --> superior colliculus --> brainstem reticular formation --> oculomotor nuclei --> saccade Deep layers of colliculus --> tectospinal tract --> cervical spinal cord --> neck movmeents accompanying eye movements. Deep layers of colliculus also receive auditory input so can rapidly orientate to sound stimuli too.
101
Which cortical regions are involved in smooth pursuit?
Visual cortex and medial temporal cortex process visual signals, regions of frontal lobe anterior to motor cortex called frontal eye fields also do
102
What is smooth pursuit?
Gaze-shifting mechanism: slower eye movements to follow moving objects. Feedforward
103
Summarise the main gaze-fixing and gaze-shifting mechanisms:
Fixing VOR Optokinetic system Shifting Foveation Smooth pursuit
104
What is the function of the primary motor cortex?
Execution of voluntary movement via the corticospinal or corticobulbar tracts projecting onto motor neurons
105
What is the effect of unilateral mild stroke in the motor cortex?
Contralateral hemiparesis
106
Definition hemiparesis
One-sided weakness and partial paralysis
107
What is the effect of unilateral severe stroke?
Contralateral hemiplegia
108
Where do: ACA and MCA strokes affect?
ACA = lower limbs, MCA = upper limbs and face
109
What is the outflow of the motor cortex called?
Internal capsule
110
What is the pathway of the corticospinal tract?
``` M1 Forebrain internal capsule Midbrain cerebral peduncle Ventral brainstem Inferior olive of medulla --> corticobulbar fibres Medullary pyramid Pyramidal decussation Lateral corticospinal tract in dorsolateral funiculus of spinal cord (90%) Anterior uncrossed tract (10%) ```
111
How do you identify corticospinal tract fibres?
After a stroke that affects a movement, can find which fibres used to supply it by demyelination
112
What happens to the ventral corticospinal tract fibres?
Either cross or provide control for axial muscles | Don't control distal ipsilateral muscles: after stroke they are not used for recovery of function
113
What is an upper motoneuron lesion?
Motor cortex lesions that are complicated by spasticity
114
What is a lower motoneuron lesion?
Lesion of spinal cord or peripheral nerve which causes flaccid paralysis
115
What is the function of cortico-motoneuron connections? How do we know?
Direct, monosynaptic, bypass spinal interneurons. Allow for precise, independent movement of extremities (fingers) Lesions --> permanent deficits most prominent in finger movement and manipulation Comparative neuroanatomy --> projections to motoneurons appear in species that make independent finger movements but not species without Development --> evidence these direct projections are developed post-natally at 9months, which is when dexterity begins to develop
116
Describe the motor homunculus
A simple figure representing the motor cortex organisation
117
Why is the motor homunculus misleading?
Misleading in that it suggests the motor cortex contains an orderly representation of individual muscles in a fractionated map, and so that lesions in one location will affect a specific muscle or body part, which isn't the case
118
What is the representation of the body in M1?
 Individual neurons in M1 see sets of synergistic muscles that can be activated together in particular movements  Different groups of motor cortex neurons thus provide ‘alternative libraries’ of muscle synergies e.g. wrist extensors and finger flexors for a power grip
119
What are the sources of input to the primary motor cortex?
1. Motor association areas via direct cortico-cortical connections 2. Cerebellum via VL thalamus 3. Basal ganglia via VL thalamus 4. Sensory afferents via VL thalamus and sensory cortex (tactile and proprioceptive) 5. Subcortical areas via VL thalamus
120
What is the function of the sensory afferents reaching M1?
Rapid feedback correction of ongoing movement
121
What are the outputs of the motor association areas?
Cortico-cortical to M1 Direct to spinal cord Connections to cerebellum and basal ganglia, through which they can influence plans and preparation or future movement
122
What do the motor association areas do?
Plan movement SMA: Internally generated or self-paced movement, bimanual movement LPA: Movements that depend on a sensory trigger system
123
Where are the heaviest projections of the cerebellum and basal ganglia?
Cerebellum --> LPA | Basal ganglia --> SMA
124
What is the effect of a lateral premotor area lesion?
Inability to appropriately incorporate sensory information into motor actions, particularly grasping
125
What are mirror neurons?
Neurons that fire in relation to making a movement, but also in relation to seeing another person make the same movement
126
What is the evidence for the function of the SMA?
- PET Scans Activity in SMA also occurs during mental rehearsal of imagined movements Suggests SMA helps predict the sequence of movements needed to achieve a particular end point and in understanding their consequences - SMA more activated when subjects performing a learned sequence of finger movements rather than relying on external cues to signal a novel sequence of finger movements - Ablation of SMA in monkeys causes i) deficit in bimanual coordination, ii) failure to orient hands and fingers accurately as they approach food, iii) failure to raise hand in the absence of external cues in order to get peanut reward - Alien hand syndrome: patients with SMA pathology may have their actions divorced from conscious control. Hand responds to outside world but the can't control it.
127
What is the function of the prefrontal cortex?
Planning, cognitive and decision making skills | Plans for future strategic goals on which movements are based
128
What is the prefrontal cortex connected to?
Basal ganglia and cerebellum | Inputs into supplementary motor areas
129
What are the signs of cerebellar ataxia?
Hypotonia (weakness) Dysmetria (inappropriate displacement e.g. overreaching) Dysdiadochokinesis (inability to make rapid alternating movement) Decomposition of movement (lack of coordination of different joint movements)
130
How was cerebellar function found?
Lesion studies of WW1 soldiers
131
What is the type of synapse between Purkinje cells and deep nuclei?
GABAergic
132
Concisely define the function of the cerebellum
Construction of movements from appropriately timed, scaled and patterned contractions of specific groups of muscles Works out the parameters of movement
133
Describe the organisation of the cerebellum
Superficial molecular layer Purkinje cell layer Granular layer White cell layer (deep nuclei and output)
134
What are Purkinje cells?
Output of the cerebellar cortex Dendrites planar GABA inhibit cerebellar nuclie
135
What is the largest cerebellar nucleus?
Dentate
136
Where does the cerebellum project?
Superior cerebellar peduncle VL thalamus --> basal ganglia, primary motor cortex VA thalamus --> supplementary motor area
137
What are the 5 types of cell in the cerebellum?
1. Purkinje 2. Mossy 3. Climbing 4. Granule (excitatory) 5. Deep nuclear
138
What is the most numerous cell in the brain?
Granule cells
139
What is the function of the climbing fibres?
Teach the Purkinje cells which of the parallel fibres carry important information, so cerebellar circuitry could learn which outputs are appropriate to specific inputs Acts by initiating plasticity
140
Describe synaptic plasticity in the cerebellum
LTD | Parallel fibre pathways following conjunctive activation of parallel fibres andclimbing fibres
141
Describe the function of the basal ganglia
Decision making = action selection | Selection of movement patterns and triggering of movements
142
Define the basal ganglia
Collection of large subcortical forebrain nuclei: largest of these are the putamen and caudate, and globus pallidus
143
What is the striatum?
Nuclei with stripes of fibres crossing grey matter: putamen, caudate, globus pallidus
144
What are the 2 midbrain nuclei functionally connected with the basal ganglia nuclei?
Substantia nigra | Subthalamic nucleus
145
What are the inputs to the basal ganglia?
All lobes of the cerebral corte
146
What is the main output of the basal ganglia?
Inhibitory to the thalamus --> excitatory to frontal lobes
147
What are the signs of basal ganglia malfunction?
Excess or paucity of movement 1. Hyperkinesia - often of well coordinated movements at inappropriate times 2. Dyskinesia - unpredictable movements 3. Hypokinesia
148
What are the types of hyperkinesia?
Chorea (unexpected dancing movement associated with Huntington's) Athetosis (writhing movements of hands or face) Ballismus (flailing ballistic movements)
149
What are the types of hypokinesia?
1. Bradykinesia (slowness associated with Parkinsonism) | 2. Rigidity (stiff, fixed position)
150
What does the terminology pyramidal and extrapyramidal mean?
``` Pyramidal = stroke Extrapyramidal = basal ganglia disorders. Assumes an alternative descending pathway which is misleading as the main way the basal ganglia affects movements is via motor cortex and pyramidal tract) ```
151
What is the direct circuit?
Corticostriate fibres + caudate or putamen - internal globus pallidus - thalamus so + - - stim disinhibition
152
What is the indirect pathway?
Corticostriate fibres + different caudate or putamen neurons - external globus pallidus - subthalamic nucleus + internal globus pallidus - subthalamic nucleus + internal globus pallidus - thalamus so + -- + - net - inhibits movement
153
What is the physiology of hypokinesia in Parkinsonism?
Loss of dopamine --> imbalances in activity in different pathways as normally dopamine via D1 activates direct pathway, and inhibits via D2 the indirect pathway so loss --> more indirect pathway --> excessive internal globus pallidus activity --> increased inhibition in the thalamus
154
How do you treat Parkinsonism?
Radical neurosurgery Controlled lesions of globus pallidus (pallidotomy) Deep brain stimulation of subthalamic nucleus L-DOPA, can lead to too much dopamine and hyperkinesia
155
For the motor circuit | Cortical input and output?
Input: motor, sensory association, output, motor and SMA
156
For the oculomotor circuit | Cortical input and output?
Prefrontal and visual association | Frontal eye fields
157
For the association cortex | Cortical input and output?
About cognition Parietal and temporal association Prefrontal
158
For the limbic association cortex | Cortical input and output?
About emotion and motivation Temporal lobe, cortex and amygdala Output: cingulate, prefrontal
159
What are the dorsal and ventral striata?
``` Dorsal = related to motor function Ventral = related to limbic function ```
160
What stops all peripheral stimuli driving saccades?
Superior colliculus tonically inhibited by basal ganglia output (substantia nigra/globus pallidus) Cerebral cortex can activate appropriate cells in the caudate/putamen to inhibit the output cells, disinhibiting the superior colliculus BG thus determines whether and when the saccade occurs
161
What is the normal role of dopamine in the basal ganglia?
Mediates plasticity of the cerebral corticostriate inputs to the caudate and putamen If an output from the BG is successful, it reinforces the synapses that were active to generate the successful output, so that when those synapses were activated again, the output is generated again Underlies habit learning
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What are the non-motor roles of the basal ganglia?
Nucleus accumbens and ventral striatum project to the prefrontal areas of cortex, which are not usually considered to be overtly motor in function. Concerned with high level executive decisions on strategy, so BG seen to select between strategies or potential behaviours Also reward processes, DA involved in learning what are good decisions (so can be altered in mental illness)
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What are the characteristic signs of patients with prefrontal lesions?
Lack of initiative, poor planning ability and inability to cope in novel situations, poor social skills
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Define apraxia. What are the major types?
Motor disorder where there is a difficulty performing purposeful or voluntary movements 4 major types: limb, oral, agraphic, constricutional
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Define limb apraxia. What causes it?
Problems with arm, hand and finger movements, but general intent or planning of act intact Bilateral damage to parietal or premotor cortex Execution and recognition deficits parietal, execution but not recognition premotor (removal and loss of ability to store action plans)
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Define oral apraxia. What causes it?
Problems with programming movements of the tongue, lips and throat to produce sequences of speech
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Define agraphic apraxia. What causes it
A particular type of writing deficit
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Define constructional apraxia. What causes it?.
Inability to copy mental or visual pictures | Right parietal damage
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Define ideomotor apraxia
Represent the inability to perform purposeful movements either to command or on imitation
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Discuss the Kimura box test
illustrates impairments in learning new sequences of actions. Have to push top button with index finger, pull the handle and then press down on the bar with your thumb. Can’t
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Which areas of the brain when damaged are associated with apraxia?
Posterior parietal cortex and frontal premotor areas and the connections between them Post parietal --> hand and limb apraxias Ant premotor --> oral These two are the ideomotor apraxias
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What does the posterior parietal cortex do?
Rostral = integration of somatosensory and proprioceptive information relating the relative position of body segments to their movement Posterior = integration of visual information about events located in the external environment Mediates reaching into extra-personal space, mediates between spatial perception and the direction of action
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What is the evidence that the posterior parietal cortex mediates reaching into extra-personal space?
1. Posterior parietal lesions in monkeys impair sequential reaching movements e.g. removing polo mints from a bent wire 2. Recordings of the posterior parietal cortex from single units in monkeys demonstrate the existence of neurons within area 7 that i. Fire when the monkey detects a visual target, increase firing as an arm is projected towards the target and decrease firing when the target is reached (arm projection neurons) ii. Fire when the target is manipulated (manipulation neurons)
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What are the connections from the posterior parietal cortex?
Reciprocally connected to the lateral and medial premotor areas of the frontal lobes
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What is the evidence for the function of the lateral premotor area?
1. Ablations of PM in monkeys causes i) deficit in performing hand actions based on, or directed by, external cues 2. PET studies reveal greater activity in PM when subjects relying on external cues to determine a sequence of finger movements compared to when they are performing a sequence of finger movements from memory
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Explain 'release of reflexes'
Premotor areas (LPA, SMA) inhibit inappropriate actions, especially inappropriate reflexes. Many reflexes present at birth that become inhibited during development re-appear following damage to premotor areas e.g. suckling, rooting, grasping. Think mechanisms reside in the parietal lobe, normally inhibited by the frontal lobes
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What is the function of the inferotemporal area of the posterior cortex?
Feature attention
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What is the function of the rhinal cortex of the temporal lobe?
Recognition memory - declarative
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What is the function of the hippocampus?
Scene/episodic memory - declarative
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What is the function of Wernicke's area?
Speech comprehension
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What is the function of Broca's area?
Speech production
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What is the prefrontal cortex connected to?
1. Specialised processing modules in posterior cortex (parietal spatial attention and inferotemporal feature attention) 2. Declarative memory in temporal lobes (rhinal cortex recognition memory and hippocampus scene/episodic memory) 3. Limbic structures involved in emotional processing amygdala and hypothalamus 4. Basal ganglia – higher order control of action 5. Language processing in post + ant cortex: Wernicke’s and Broca’s
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Describe the Winsconsin Card Sort Test
Deficit in inhibitory control seen following damage to the lateral prefrontal cortex. Failure to inhibit previously relevant rules governing behaviour. If patients learn to sort a pack of cards according to colour, they are then unable to switch to sorting according to a different dimension, i.e. shape. Instead persevere with the previously correct dimension.
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Describe behavioural inflexibility
monkeys with prefrontal damage, after learning that one object, out of a pair, is associated with reward, cannot switch their responding to the other object when that object becomes rewarded instead
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Describe the evidence about spatial and feature detection in the prefrontal cortex.
subjects required to attend to one of three different perceptual features: colour, form or movement (selective attention conditions) or all three (divided attention). Dorsolateral Prefrontal cortex activated spatial, ventrolateral activated most when attending to visual features.
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Which brain areas are used in processing spatial info?
Posterior parietal cortex, dorsolateral prefrontal cortex
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Which brain areas are used in processing visual info?
Inferotemporal cortex, ventrolateral prefrontal cortex
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How does the ventrolateral prefrontal cortex influence the processing of visual information?
Top down control of selective attention Enhances processing of relevant information by enhancing activity in the sensory cortex involved in processing that information
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How does the dorsolateral prefrontal cortex influence the processing of spatial information?
Enhances activity for divided attention linked to spatial attentional mechanisms Thought dorsolateral region involved in learning and planning of higher-order strategies to achieve the goal
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What is the evidence for the prefrontal cortex's control of short term memory?
1. Delayed response tasks: Lesions of regions of prefrontal cortex impair delayed response tasks that require monkeys to remember spatial, object or proprioceptive information over a brief delay. Sample stage where monkey a) shown peanut hidden in one of two locations (spatial), b) shown one of two objects (object), c) or required to press a lever one or five times (proprioceptive). After a few s, choice stage, where monkeys choose the location/object/do the same response. Lesions of pfc do not affect this choice if there is no delay. Implicates the pfc in short term memory 2, Some neurons in lateral regions of pfc in monkeys have been shown to fire during the delay period of the spatial and object versions of the delayed response task
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Which region of the prefrontal cortex is involved in emotion?
Orbital regions of prefrontal cortex
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Describe monkeys with orbitofrontal damage
female monkeys normally submissive and solicitative of the advances of a male, when damaged, replaced either by indifference or aggression. Show indifference towards own offspring.
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What is the function of the prefrontal cortex?
Executive function - management and regulation of cognitive processes Seems like the prefrontal cortex inhibits complex behaviours, is involved in attention, is involved in short term memory, and enables emotions to contribute to complex decision making
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What are the different ways that you can divide the prefrontal cortex?
1. Type of information that they process | 2. Type of cognitive operations that they perform
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What is needed to select a goal?
1. Hold information in mind 2. Filter out irrelevant info (determined by what we have learnt in the past) 3. Choose an appropriate goal 4. Select appropriate responses to fulfil the goal 5. Inhibit inappropriate responses
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Are the pyramids dorsal or ventral?
Ventral
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Which neurons form the corticospinal tract?
Layer V pyramidal neurons of motor cortex
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What histologically distinguishes the primary motor cortex from other areas?
1. Layer V contains a population of giant pyramidal neurons only round in M1. 2. Motor cortex is thickest area of cortex, but contains few small rounded cells (so sometimes called agranular cortex)
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Where does the internal capsule run through?
Between basal ganglia nuclei and thalamus
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What is the boundary between medulla and spinal cord?
The motor decussation
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What is just deep to the peduncles in the upper midbrain?
The substantia nigra and the red nuclei
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Describe the vestibulospinal tracts
Descend in the ventral columns Arise in vestibular nuclei in the dorsal medulla Exerts actions mainly on extensor limb muscles and proximal muscles Involved in maintaining posture and equilibrium
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Describe the reticulospinal fibres
Originate from reticular formation of pons and medulla Several groups of neurons give rise to descending fibres, which are fast conducting and project through the length of the spinal cord Important for posture and coordinated body movement
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Describe the rubrospinal tract
From Red nucleus of midbrain Large nucleus in man but few fibres that descend to spinal cord Gets input from cerebellar nuclei and motor areas of the cerebral cortex and output mainly to inferior olivary nucleus (--> climbing fibres) Thought to function in motor skills learning
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What are the folds of the cerebellar cortex called?
Folia
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What is the fat middle part of the cerebellum called?
Vermis
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What is the flocculus?
Small, semi-detatched part of cerebellum Concerned with vestibular function In cerebello-pontine angle
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What are the tonsils?
Bilateral small parts of cerebellar cortex that overhang the dorsolateral aspect of the medulla
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What is the clinical importance of the tonsil?
In patients with raised intracranial pressure, risk of tonsils collapsing into the foramen magnum if CSF is withdrawn by lumbar puncture. Results in pressure on the brainstem and sudden death due to pressure on vital centres for respiratory and autonomic control: coning.
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What are the deep cerebellar nuclei?
Dentate nucleus Nucleus interpositus Fastigial nucleus
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How does the cerebellum output information?
All via deep nuclei | Except flocculus directly to vestibular nuclei in the medulla
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Where do each of the cerebellar peduncles come from?
``` Superior = deep nuclear output --> thalamus Middle = pons Inferior = medulla ```
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Where and what can you see regarding the superior cerebellar peduncle?
Midbrain dorsally Can see decussation in low midbrain Then sends some fibres to the red nucleus Bridge between the two is the roof of the rostral part of IV ventricle
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Where do the ventrolateral and ventroanterior thalamic nuclei project to?
VL --> primary motor cortex | VA --> premotor and supplementary motor
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What is the projection through the middle cerebellar peduncle? What does it carry?
Pons to contralateral cerebellum as mossy fibres | Infromation from sensory and sensory association areas
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What is the projection through the inferior cerebellar peduncle? What do the fibres carry?
Ascending spinocerebellar mossy fibres (juncrossed) Somatosensory information (e.g. from Clarke's nucleus, proprioceptors) Also fibres form inferior olive climbing fibres - mediate learning
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Is the representation in the cerebellum ipsi or contralateral?
Ipsilateral
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Do parallel fibres and Purkinje cell fibres run along with the folia or perpendicular to them?
``` Parallel = parallel Purkinje = perpendicular ```
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How do you stain Purkinje cells?
Silver impregnation (the Golgi method) - selects only some neurons and glia
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What can cause upper motoneuron signs? What are they?
Strokes, cerebral palsy, multiple sclerosis Immediate flaccid paralysis, gradually becomes spastic with hyperreflexia, clonus and + Babinski sign, voluntary movement impaired, reflex contraction remains
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What can cause lower motoneuron signs? What are they?
Lesions in spinal cord or peripherally, e.g. poliomyelitis. Muscular weakness, flaccid paralysis, muscle wasting, areflexia
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When can ventromedial corticospinal pathways reorganise to allow recovery of function after a stroke?
Prenatally or in early neonatal life
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What are AVMs?
Arteriovenous malformations congenital vascular anomalies consisting of direct fistulas artery --> vein iwhtout an intervening capillary bed Propensity to bleed/haemorrhage Treat with surgical resection, focused radiotherapy or endovascular embolisation
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What are cavernomas?
Thin dilated vascular channels that don't have a feeding artery and so don't appear on angiograms In brain or spinal cord Some familial Risk of bleeding lower than AVM but if multiple haemorrhages, then surgical resection
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Which corticobulbar fibres provide bilateral innervation to motor nuclei?
V upper VII XII
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Where do you find the cingulated motor areas?
buried medially
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What is Clarke's nucleus?
Part of the spinocerebellar tract (up through inferior cerebellar peduncle) T1-L3/4 Proprioception related Spinal interneurons in lamina VII
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How do you find the caudate nucleus?
Remove the septum pellucidum on a saggital section, can just about see the caudate inside the lateral ventricle Follows the course of the lateral ventricles (ant horn, body, inf horn) Tail of caudate into the temporal lobe
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Which part of the brain is the basal ganglia in?
Forebrain
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What composes the neostriatum?
Caudate and putamen, separated in development by the internal capsule
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Where is the putamen?
Lateral to the internal capsule, medial to the insula
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What are the two major divisions of the substantia nigra?
Pars compacta = dopaminergic, innervates the neostriatum | Pars reticulate = non-dopaminergic control of eye movements
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What is the shape of the caudate?
Large head anteriorly
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Where is the globus pallidus?
More posteriorly, medial to the putamen, inferior to the caudate and internal capsule
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Where is the thalamus?
More posteriorly, either side of the third ventricle so medial to the internal capsule
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What is the counterpart of the corpus callosum more anteriorly? What else can be seen at this level?
Anterior commissure Hypothalamus Caudate, putamen, globus pallidus
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How do the basal ganglia structures appear anteriorly to posteriorly?
Caudate (getting smaller), putamen (getting bigger then smaller), then globus pallidus, then thalamus. Most posteriorly thalamus large but putamen and globus pallidus is not present. Internal capsule now ventral and tightly bundled and form cerebral peduncles
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Where does the caudate input predominantly originate from?
Prefrontal cortex
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Where does the putamen input predominantly originate from?
Sensorimotor cortex
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Where do fibres from the internal globus pallidus terminate?
VL VA thalamus, medial nucleus of the thalamus
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What does the substantia nigra pars compacta look like in fresh and fixed tissue?
Dark pigmented area in midbrain next to the cerebral peduncles In a cross section through the brain where myelin has been stained it appears as a lighter area
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Where is the subthalamic nucleus?
At the junction of the midbrain and diencephalon | Probably unable to find
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Where does the medial dorsal nucleus of the thalamus project to?
Prefrontal cortex, involved in complex executive functions
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What does the internal capsule carry?
Corticospinal tract Other cortical output fibres Thalamocortical input fibres
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What is the clinical significance of the genu?
Where MCA haemorrhage or thrombosis commonly affects the internal capsule
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What is the clinical significance of the genu?
Where MCA haemorrhage or thrombosis commonly affects the internal capsule At the genu there are corticospinal fibres to the the head, neck and part of the upper limb
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Give two examples of thalamocortical fibres
LGN --> runs around lateral ventricle --> post --> visual cortex as optic radiation MGN --> auditory radiation
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What is the blood supply of the striatum and internal capsule?
Small arteries originating from the middle and anterior cerebral arteries End-arteries Termed striate arteries from the MCA
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What is the cause of Hungtington's chorea?
Partly due to death of cells in the neostriatum
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What do lesions of the subthalamic nucleus lead to?
Hemiballismus, violent disorder in which flailing limb movements are produced
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What is Wilson's disease?
Copper deposits in the basal ganglia, kidney, liver, and Kayser-Fleischer rings.
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Which deep nuclei are targeted in deep brain stimulation?
Subthalamic nucleus, globus pallidus internal, ventral anterior thalamus, pedunculopontine nucleus
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What is ETV?
Endoscopic third ventriculostomy Surgical procedure involving placing an endoscope through the frontal lobe into the lateral ventricle, then through the foramen of Munro into the third ventricle. There make a hole (ventriculostomy) in the floor of the third ventricle to allow CSF to drain from the ventricle into the subarachnoid space, then onwards to be absorbed. Diverts CSF from any blockage downstream of the third ventricle, e.g. from a tumour obstructing the aqueduct, so preventing hydrocephalus
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What is stereotaxy?
coordinate based system used to localise brain regions
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Discuss prefrontal damage, and tests for it
Executive function. Inability to inhibit behaviours. Emotional lability. 1. Winsconsin Card Sort Test - perseveration, despite not 'wanting' to 2. Sentence suppression task - give someone a sentence with the last word missing out. Ask to complete with a logical word, and can. If you ask to finish with an illogical word, really struggle. 3. Stroop - colour words written in different colours. Told to say what the colour it is printed in is. Attention - anterior cingulate so dorsomedial and lateral 4. Respond to words with an x - start pressing with non targets after a while. Working memory - tends to be dorsolateral 5. Delayed matching to sample - Monkeys with two choices, one with food, pause, has to hold on line. Prefrontal firing during delay period sustained. Emotion - medial and orbital prefrontal 6. Iowa gambling task - risky or non risky gambles. Can manipulate so certain behaviours are optimal. People should be able to resist the big gambles. Medial prefrontal damage struggle with this Planning - prob lateral (combination of attention, behavioural inhibition etc) 7. Tower of London Task - pegs of different lengths, have to reach a target by moving multiple pegs. Subgoals may be out of keeping with ultimate goals.
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Which areas are involved in attention?
Prefrontal and right parietal generally