Alex r- Brain Mechanisms Flashcards

(30 cards)

1
Q

Overview of nervous system

A

Upper motor neurones have motor cortex (planning, voluntary movement) and brain stem- basal ganglia and cerebellum feed into. Goes to local circuit neurones for reflexes (no cortex) and lower motor neurones in spinal and stem (both cns). Pns is sensory inputs and skeletal muscles W lower motor neurones

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2
Q

Basic types of movement

A

Reflexes, posture, locomotion, sensory orientation, species spec action and acquired skills

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3
Q

Voluntary to reflexive

A

Rhythmic movements can be voluntary but timing is from brain stem, produced by local spinal cord circuits called central pattern generators e.g. breathing

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4
Q

Pns and leprosy

A

Bacterial infection, peripheral nerves thicken which disrupt afferent (sensory input to local circuit neurones in spine and stem so no reflex) and efferent (lower motor neurones to skeletal muscles) signals. Thermal sensation goes first then pain and touch, limb damage from this

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5
Q

Muscle and movement

A

Striated/skeletal muscles are connected to bone or tendon apart from face, cardiac or smooth. Striated as sarcomere W actin and myosin. Myosin binds to actin and pulls along. Fibres stim but nerve impulse, AcH released at NMJ. Open ca+ channels to trigger contraction.

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6
Q

How muscles are controlled by neurones

A

Motor neurone sends signals via efferent connections, voluntary contraction from pns. Signal motor neurone will control many fibres (innervation) but a motor unit is the neurone plus fibres it controls. Signals go from upper to lower MN, proximal to distal (closer to centre of spine, the closer the body part it controls) At brain stem is crosses the midline (contralateral control)

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7
Q

AcH disruptions

A

Curare toxin: ach receptor blocked in muscle tissue. Made from plants, means inability of muscle to respond to motor nerve stim- reversible in some doses
Myasthenia gravis: abnormality in ach receptors, ppl are weak as can only activate some fibres, trouble smiling , ranges in extremeness

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8
Q

Sustained movement

A

Ap travels down lower motor neurone, single motor twitch, train is a sequence. If rapid, contractions get bigger. Multiple neurones activate many fibres, called tetanic contractions needed for sustained strong contraction. Motor pool requirement is bigger moment needs more neurones

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9
Q

Motor neuron problems

A

Lower neurones famished in motor neurone disease or trauma where peripheral nerves cut (polio)- hypotonia which is less muscle tone. Damage leads to motor neurone syndrome (paralysis, wasting, no reflexes and fasciculation/ contractions)

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10
Q

Motor programs

A

Set of commands to initiate movement, don’t depend on sensory info/ abstract representations of movements that centrally orgs. No feedback from limb/ equivalence means movements independent of muscle groups

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11
Q

Cortex

A

Supp motor cortex has learned actions, don’t monitor environment. Primary MC has execution of all voluntary. Posterior parietal is planning, attention. Premotor is sequences, intention, modulated pmc.

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12
Q

Somatotropic organisation

A

Body represented in cortex, contra lateral, more space for fine tuned moments (lips, tongue, hands), means phantom limb syndrome, Jacksonian March (seizure across brain affects body in order). Movements and not muscles represented. Brain achieves moments by averaging large pops of neurones

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13
Q

Evidence for cortical map

A

Mri and pet by lotze and graziano- move parts of body, see parts light up. Mushiake: monkeys activate promotors area in visual cue condition and supp motor not active but opposite in prior training condition (shift the more they learn. Apraxia is inability to move due to damage to ppc. Ideomotor is semantic (instruction), ideation all is inappropriate selection but no paralysis

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14
Q

Anticipatory firing

A

Premotor areas have planning. Libet 85: ppl looked at moving light and could make moments, looked at readiness potential in parietal. Expect decision then neural then activity but found RP, then will then action

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15
Q

Sea squirts

A

Larva form is more complex as need to navigate environment to find a new rock, then it becomes sessile, absorbs own brain

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16
Q

Graded and competitive goal selection

A

Roitman and shadlen 2002: monkeys see 2 targets, then shown stim W 0-50% motion coherence, hinting what direction to choose and then select correct target. 5% is enough for to guide monkeys. Activity in posterior parietal cortex has planning, found could tell condition from activity. If got variety of options, part of brain most active wins movement made

17
Q

Sensorimotor transformation- reaching

A

When sensory stim is converted to motor actions. Responsible for trans visual info about object into direction of reaching (visuomotor trans). Everything happens quickly. Like grasping: dorsal cortex W anterior sulcus and ventral premotor - sensorimotor happens in parietal

18
Q

Linking sequences

A

Supplementary motor area for learned movements, premotor cortex has cues moves. When Sam gone, monkeys can’t perform learn moves- tanji.

19
Q

Background to cerebellum

A

Sometimes called the silent area- when run tms coil nothing seems to be effected
Hard to measure due to location in skull so understudied
Coordinates movement, balance, muscle tone and rapid movements

20
Q

Error correction

A

Signals leaving the motor cortex go through cerebellum, also signals from what body is doing from spine
Compares 2 and adjusts what you to
E.g. of sensorimotor trans
Does comparator function with what done and what want to do, correct mistakes and operate smoothly. Motor cortex is planning and initiating, basal gang inhibits until appropriate

21
Q

Motor learning and ballistic moves

A

Cerebellar neuronal circuits learn to make more accurate moves over time. After motor act done many times, steps become more precise. Once perfected, it establishes a spec motor program for each learned moves. Ballistic are rapid moves that can’t mod course by sensory feedback/can’t stop once started like running

22
Q

Structure of cerebellum

A

Frontal motor and parietal cortex goes to pons, crosses midline to cerebellar cortex. Channels enter called inferior olive (vision and hearing), vestibular nucleus (head body and limbs) and spinal cord (body in space and time). If not match, sends info to deep cerebellar nuclei, crosses midline to ventrolatersl complex in thalamus to pmc. E.g. of reentrance circuit.

23
Q

Cerebellar dysfunction

A

Vulnerable to heavy metals and strokes. Cerebellar ataxia (errros I’m direction of moves, uncontrolled eyes, slurred speech, can’t touch top of nose). Hypometria (response delay and moves short fo goal). Dysdiadocho kinesia (can’t do rapid alternating moves like a wavy line), one side of body can be affected

24
Q

Alcohol

A

Cerebellum sensitive to ethanol, disrupts function. Field sobriety test allows to gauge extenet of alc, really tests cerebellum as tests walking in a line, touching tip on nose w eyes closed

25
Basal ganglia
Does making, selecting and inhibition of movement. Basal ganglia loop DRAW OUT. Start W cortex, goes to caudate and putamen, modulated by substantia nigra pars compacta, goes to globus pallidus and substantia nigra pars reticulata, modulated by subthalamic nucleus, then to thalamus which feeds back to cortex.
26
Loop explained - basics of what is excitatory or not
Cortex Activates of the caudate, inhibits glob which inhibits thalamus and its targets from inhibition so net effect is excitat of neurones (direct). In indirect cortex excitates caudate The thalamus’s role is inhibition so when inhibited: it actually excitates. The sub thalamic nucleus is the same. Excitatory- glutamate inhibitory- gaba
27
Direct pathway
Cortex excitates striatum, inhibits Globus pallidus +SNR, means more inhibition of thalamis so stims cortex Cortex then stims the corticalspinal tract via upper motor neurones, then lower motor neurons, then muscles means movement. Hypokinesia is insufficient direct pathway output or excess indirect pathway output
28
Indirect path
Crotex excitates striatum, inhibits GP+Snp (r) so less inhibition of STN which stims Globus pallidus so less inhibition of thalamus so less stim of cortex Means cortex stim less - upper mn, stim less- lower mn, stim less- ,uscles- stop. Hyperkinesia is excess direct pathway output or insufficient indirect pathway output
29
Parkinson’s
Damage to substantia nigra/dopamine system so over inhibition , trouble voluntary moves but when told to step over mark, tremor gone . Resting tremor, muscle rigidity, bradykinesia
30
Huntington’s
Damage to caudate nucleus which releases inhibition so get unwanted actions. . Muscle jerks, intellectual deteoerioation