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psychology - Neuroscience > lecture 5 - movement control > Flashcards

lecture 5 - movement control Flashcards

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1
Q

what region is responsible for planning of voluntary movement

A

-descending systems - neurons descend from cortex to the neurons in the body

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2
Q

what is the brainstem concerned with

A

-concerned with unconscious movement control, things such as movement and posture
-things we don’t put a lot of thought into

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3
Q

-basal ganglia
-cerebellum

A

-basal ganglia : gatekeeping mechanism , responsible for allowing movements we want to make to be made and stopping movements - connects to motor cortex
-cerebellum - more unconscious control, motor coordination and balance etc - connects to brain stem centre

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4
Q

motor cortex

A

-motor cortex descents down to local circuit neurons - connect to motor neurone pools

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5
Q

description
motor cortex
-function

-monkey study

A

-premotor and primary motor cortex in the frontal lobes
-premotor is more responsible for planning than primary motor
-primary cortex responsible for starting off movements
-responsible for planning and more precise control in voluntary movements

-monkey study
-trained monkey to respond with an action when they saw a particular cue
-but there was a delay between seeing the cue and seeing a go signal that indicated for you to do the signal
-so by recording brain activity they found that during the delay period whilst waiting to produce the response , the premotor cortex is active

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6
Q

organisation of the motor cortex
-contralateral control
-type of organisation

A

-contralateral control - (neurons in motor cortex on the left hemisphere are responsible for movements on the right side of the body
-somatotopically organised (penfield 1930). its grouped by body part-
-muscles are disproportionately represented eg hands or digits have more space in motor cortex than arm etc-look at penfie guy who represents what we would look like according to amount of body part represented in cortex

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7
Q

motor mapping
-wilder penfield 1937 and the montreal procedure

A

-montreal procedure developed whilst treating epileptic patients and operating on them

-4 patients suffering from epilepsy: went through some pre surgery process where the patient would be conscious, would stimulate the nerves of the brain in order to record what responses they produced
-identified areas of the brain which caused seizures (have bursts of excess activity)

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8
Q

what does motor map represent/not represent
-whatdo lesions in the motor cortex cause

A

map doesnt represent individual muscles / body parts, but co ordinated groups of muscles

-lesions to motor cortex regions cause deficits in muscle groups (because the muscle groups do actually overlap, not as distinct as thought)

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9
Q

TMS
transcranial magnetic stimulation of motor cortex
-the video

A

-magnetic coil over motor cortex
-when delivers a magnetic pulse part of body moves
-hempisphere activates response in opposite side of body

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10
Q

key motor areas having more representation in the motor cortexin animals

A

in animals
-increased representation of paws in racoons (they have tiny people hands and are dexterous)
-increased representation of whiskers in rats and mice
-increased representations of the nose in the star nose mole

-all innate

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11
Q

if someone learns a skill will we see a change in the motor cortex as a result of their learning

A

-several studies show this
-looking at violinists or string players
-they have larger representation for left hand digit : require extra control (catania and kaas, 1995)

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12
Q

basal ganglia
-functions
-major structures

A

underneath the cortex
-gatekeeper for initiating movements (preparation for movement)
-full of dopaminergic synapses and their receptors- a key part of this region
-striatum (caudate nucleus,putamen)
-pallidum ( globus pallidus, substantiatnigra)
-thalamus
-subthalamic nucleus

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13
Q

the basal ganglia
-what does the pathway do
-things to be aware of

A

-allows the start/initiation of intended movements
-regions are linked in a circuit of inhibitory(reduced change action potential sends) and excitatory impulses
-some regions will be constantly inhibited/activated (tonic)
-others will be inhibited / activated for brief periods of time only (transient)
-correct regulation of this is vital in allowing movement to begin

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14
Q

direct pathway
-and which neurons are tonic and transient

A

-caudate and putamen
-globus pallidus internal - va/vl complex thalamus-frontal cortex
-globus pallidus tonically active

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15
Q

the direct pathway in a situation where no movement is being planned

A

-in this situation no movement is being planned
-when a is at rest (striatum) is currently not firing

-the neuron in the globus pallidus (b) is tonically active , always firing and sending out signals, it has an inhibitory connection with the thalamus,(c) it stopping the thalamus from sending out signals

-thalamus has other inputs from other regions which are excitatory , (but cell has to add al inputs together to get an outcome)
so thalamus isn’t communicating with the moto cortex and no motor actions are starting (no excitation of D -motor cortex)

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16
Q

direct pathway in movement

A

-a is transiently excited (frontal cortex signals to a , the striatum) striatum fires so burst of transient activity

-striatum (a) has a inhibitory connection to the global pallidus so it switches it off (b is transiently is inhibited)

-c is disinhibited so other inputs can excite it (c is va vl complex)

-leading to excitation of D(the motor neuron cortex)

17
Q

dopamine : the nigrostriatal pathway
-what is this

A

-substantia niagra to striatum
involved in the basal ganglia loop and the initiation of movement

18
Q

explain the nigrostriatal pathway

A

-links substantia nigra and striatum (caudate/putamen)
-provides additional excitatory impulses
-more likely to inhibit the globus pallidus
-allows the frontal cortex to initiate movement

19
Q

disorders of basal ganglia : movement initiation, involed in direct pathway

A

-direct pathway: involved in the release of the upper motor neurons from inhibition
-linked to parkinsons disease
-hypokinesis (reduced initiation of movement)

20
Q

parkisons disease (and dopamine)
-what is it
-symptoms

A

-neurodegenerative progressive disorder - described by dr james parkinson in 1817
-the most recognised symtomps are those that affect movement
: tremor
-slowness of movement (bradykinesia)
-rigidity
-postural instability

21
Q

what causes the movement issues in parkinsons disease

A

-issue in the substantia nigra
-substantia nigra gets its name from the melanin in the cells (produce melanin)

-in a healthy individual when you look at the region, the cells will be evident due to shading
-in parkinsons those are the cells that die off, reduced shading in those with parkinsons
-(melanin containing cells die off)

-causes ? unclear _combined genetics and environment?

22
Q

parkinson’s disease direct pathway

A

-death of the dopaminergic neurons in the nigrostriatal pathway
-reduction of activation of the striatum
-the striatum cannot inhibit the globus pallidus
-the thalamus continues to be inhibited
-movement therefore cant be easily initiated

23
Q

treatment of parkinsons disease

A

-l dopa
- L-Dopa

  • Artificial precursor to dopamine, which can cross the blood brain barrier
  • Increases the concentration of dopamine in the synaptic cleft (agonist of dopamine)
  • As the cells continue to die, however, this treatment will gradually become less effective (it doesnt matter that theres extra materials to make dopamine from, theres simply arent the receptors for the dopamine to bind to
  • Also: side effects due to increased dopamine in other pathways
24
Q

the indirect pathway
-what does it do

A

works to stop unwanted movements

25
Q

indirect pathway explained

A

-By increasing the ability of the globus pallidus (internal) to inhibit the thalamus

  • External segment inhibits the internal segment, preventing it from inhibiting the thalamus
  • External segment also inhibits the subthalamic nucleus, which excites the internal segment, further preventing it from inhibiting the thalamus
    to stop movement
    -cerebral cortex/striatum inhibit the external segment and excites subthalamic nucleus
    -so were taking out the inhibito of the internal segments and were boosting the region that boosts the internal segments
    -internal segment can inhibit thalamus
    -thalamus doesnt signal to cortex-movement is not initiatied
26
Q

disorders of the basal ganglia, movement inhibition (involved with indirect pathway)

A

-the indirect pathway: involved in increasing the level of inhibition
-linked to huntingtons disease :hyperkinetic (increased unwwanted movement)

27
Q

huntingtons disease

A

-described by george huntington 1872

-genetic disorder caused by the mutation of the huntington gene on chromosome 4
-symptoms usually begin mid life (30-50 years)
-changes in mood
-problems with co ordination
-decline in both physical and mental capacities
-results in death within 10-20 years

28
Q

huntigtons is ______ dominant

A

autosomal dominant
-if we have a dominant disorder it means that in order for somebody to inherit huntigntons they only need to inherit one copy of the gene from a parent

29
Q

what happens to the brain in huntingtons disease
-and its effects

A

-profound but selective atrophy of the caudate and putamen
-loosing much tissue mass from the regions
-some associated degeneration of the frontal and temporal cortices

-alteration in mood-usually depression
-changes in perosnality - increase in irritability, suspiciousness, eccentric behaviour
motor symptoms:
-rapid, jerky movement with no clear purpose
-can involve a finger of a whole extremetity, speech apparatus

30
Q

what’s happening to the indirect pathway in huntingtins disease

A

-were losing the caudat and putamen because of the atrophy, so its no longer able to inhibit the external segments of the globus pallidus
means that segment is much better able to inhibit the internal segment directly and indirectly by inhibiting the sub thalamic nucleus
-sub thalamic nucleus cant excite the internal segments, thalamus is free to signal to the motor cortex and produce this unwanted extra movemnets

31
Q

treatments of huntingtons disease and side effects

A

-no cure
-drug tetrabenazine is used to treat the chorea (unvoluntary movements) associated with it
-antagonist of dopamine
blocks dopamine receptors and depletes other amines
-side effects include parkinsonism and depression

32
Q

three types of muscle

A

-skeletal/ striate muscles : movement of the bones

-smooth muscle- forms organs such as stomach and bladder

-cardiac muscles (a mix of smooth and striated) contracts the heart

(last two are involuntary control)

33
Q

how are muscles arranged

A

-arranged in antagonistic pairs-each making only one movement

-Contraction of the skeletal muscles is initiated by the lower motor neurons

  • The cell bodies of the LMNs are found in the spinal cord and brainstem
  • Their axons run down to particular muscles ,to form the Neuromuscular Junction
34
Q

the neuromuscular junction
-what happens at this synapse
-motor neuron pool
-moto unit

A

-motor neuron synapses with skeletal muscle fibres
-ACh acts as an excitatory NT at this synapse
-nicotnic receptors

-Each motor neuron innervates several fibres within one muscle
* The motor neuron pool: All the neurons innervating one muscle

  • The motor unit: All the fibres in a muscle innervated by one neuron
35
Q

the lower motor neurons
-size of motor unit relates to…

A

-the size of the motor unit relates to the type of movement that can be produced
-when they innervate many fibres, movements will be coarser
-eg biceps
-when only a few fibres are innervated by one axon, movements are more precise
eg eye movement

36
Q

organisation of lower motor neurons
-spinal cord
-arms and legs

A

-somatotopic organisation of the lmns
-in the spinal cord,the neurons that act on the muscles of the trunk are located medially
-the neurons for the arms and legs are found more laterally

37
Q

amytrophic lateralsclerosis (ALS)
-discovery
-what is it

A

-known as motor neuron disease or lou gehrigs disease
-first link between symptoms and the neurological disorder by jean martin charcot (1874)
-causes unknown in 90% cases

-a degeneration of both upper motor neurons and lower motor neurons

38
Q

what happens in ALS

A

Progressive neurodegenerative disease

  • Neurons in the brain and spinal cord begin to die
  • Begins with weakness in the affected regions which gradually worsens over time as muscles waste
  • Different classifications according to which neurons are affected first
  • Sensory nerves and cognitive abilities are preserved
  • Symptoms and rate of progression vary between people
39
Q

what is augmented/alternative communication
treatment

A

-one of the last muscular groups to be affected are the extraocular muscles (eye movements)

-Augmentative/Alternative Communication (AAC)systems use this to help people with ALS communicate
-Various technologies allow eye movements to be used like a computer mouse
◦ Graphical User Interfaces: Using images to indicate communication goals (e.g. Shravani et al., 2020)
◦ Using smooth-pursuit eye-movements to write with the eyes(Lenglet et al., 2019)

psychology - Neuroscience (10 decks)

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