Chapter 8: Movement Flashcards
three categories of muscle
Smooth
Skeletal/Striated
Cardiac
Smooth Muscle
controls digestive system and other organs
Skeletal/Striated muscle
controls movements of the body in relation to the environment
Cardiac Muscle
between other 2 categories with properties
Need for antagonistic muscles
- important because there is no control to move the muscle in the opposite direction therefore you need another muscles to do that job
ex) flexor and extensor
fast muscles and conditions under which each is most useful
Fast twitch: fast contraction, fast fatigue
-anaerobic no O2 therefore fatigue quickly due to needed O2 for recovery (oxygen debt, sprinting)
slow muscles and conditions under which each is most useful
- slow contraction
- no fatigue
- to not fatigue because they are aerobic (use O2)
Proprioceptor
-receptor that detects position or movement of ta port of the body
Proprioceptor in muscle
-detect stretch and tension of a muscle and sends messages to enable spinal cord to adjust its signals
Muscle spindle
-receptor parallel to muscle that responds to stretch
Golgi tendon organ
- responds to increase in muscle tension
- act as a brake against vigorous contraction
roles of the primary motor cortex in the control of movement.
- elicits movement
- axons extend to brainstem and spinal cord which generate impulses that control muscles
- each spot does not control a specific muscle- they overlap
role of posterior parietal cortex in the control of movement.
- planning movements
- keeps track of body position relative to the world
- controls aim
role of supplementary motor cortex in control of movement
- planning and organizing rapid sequence of movements
- essential for inhibiting a habit when you need to do something else
role of premotor cortex in control of movement
- most active right before a movement
- receives info about target that body is directing its movement towards and info about body’s current position and posture
role of prefrontal cortex in control of movement
- active during a delay before a movement
- stores sensory info relevant to movement
- considers probable outcomes of possible movements
implications of the timing of the readiness potential before the person is aware of making a decision
Readiness potential- produced by motor cortex before any voluntary movement
- on average 500ms before the movement
- brain activity responsible for the movement begins before the person’s conscious decision
functions and cellular organization of the cerebellum
- contains more neurons than the rest of the brain combined
- motor structure (balance, coordination, timing, aim)
- help to tell if objects are same or different when in hands
- any sequence of rapid movements that require timing
- critical for certain aspects of attention
organization of the cerebellum
- receives input from spinal cord + sensory systems from cranial nuclei and cerebral cortex
- neurons arranged in precise geometric pattern with multiple repetitions of same unit
Purkinje Cells
-flat cells in sequential planes parallel to each other
Parallel Fibres
-axons parallel to one another and perpendicular to planes of Purkinje Cells
Action Potential Path in Cerebellum
- Action potential from parallel fibre excites 1 purkinje cell after another
- Purkinje cell transmits inhibitory message to cells in nuclei of cerebellum and vestibular nuclei in brainstem when it sends info to midbrain and thalamus
Action Potential strength and distance in cerebellum
- depending on which and how many parallel fibres are active they might only stimulate 1st few Purkinje fibres or a long series
- more excited Purkinje= increase collective DURATION of response
- only 1st Purkinje= short message to target cells
- more than 1st= longer message to target cells
Output of Purkinje cells
-timing of movement (onset and offset)
Path in Cerebellum to brain
Parallel fibre -> Purkinje Cell (one after another)
l l
V V
inhibitory message . vestibular nuclei in
nuclei of cerebellum brain stem
l l
V V
midbrain thalamus
list the structures that comprise the basal ganglia
Caudate Nucleus
Putamen
Globus Pallidus
Pathway of Basal Ganglia
Cerebral cortex l l V . V caudate . putamen nucleus l V globus pallidus l . l V . V . thalamus . midbrain l . V motor and prefrontal areas of cerebral cortex
know the function of each and the general contribution of the whole system.
- output from globus pallidus to thalamus = inhibitory
- neurons show a lot of spontaneous activity
- caudate nucleus and putamen tell globus pallidus to stop inhibiting
- basal ganglia selects a movement by stopping it being inhibited
- very important for self initiated behaviours
know the function of each and the general contribution of the whole system.
- output from globus pallidus to thalamus = inhibitory
- neurons show a lot of spontaneous activity
- caudate nucleus and putamen tell globus pallidus to stop inhibiting
- basal ganglia selects a movement by stopping it being inhibited
- very important for self initiated behaviours
- have specialized cells for learning to stop and start a voluntary sequence of motions
symptoms of Parkinson’s disease
- rigidity, muscle tremors, slow movements, difficulty initiating physical and mental activity,
- slow on cognitive tasks such as imagining events or actions
- loss of olfactory is early (first symptom)
- depression
- memory loss
- not paralyzed or weak
- difficulty with spontaneous movement
immediate physiological cause of Parkinson’s disease
- gradual progressive death of neurons especially in substantia nigra
- substantia nigra sends dopamine releasing axons to caudate nucleus and putamen
- lose these axons and therefore lose dopamine
genetic of Parkinson’s disease.
-genes have very small link
environmental causes of Parkinson’s disease.
- exposure to toxins
- MPTP chemical that body converts to MPP+ accumulates in and destroys neurons that release dopamine
- exposure to hazardous herbicides and pesticides
- people who smoke cigarettes and drink coffee have less of a chance of developing Parkinson’s disease
most common treatment for Parkinson’s disease and a problem with that treatment
-goal is to restore missing dopamine
-L-dopa=precursor to dopamine is a main treatment for Parkinson’s
Problems with L-dopa
-ineffective for some patients
-does not prevent continued loss of neurons
-unpleasant side effects (nausea, restlessness, sleep problems, low BP, repetitive movements, hallucinations, delusions)
Other potential therapies for Parkinson’s
- antioxidant drug to decrease further damage
- drugs that directly stimulate dopamine receptors
- drugs that inhibit glutamate or adenosine receptors
- gene therapy : using virus to transfer into the brain a gene that increases dopamine synthesis
- neurotrophins to promote survival and growth of remaining neurons
- drugs that decrease apoptosis of remaining neurons
- high frequency electrical stimulation of globus pallidus or subthalamic nucleus
- possibility that transplanting brain tissue from aborted fetus would help
describe the symptoms of Huntington’s disease
- severe neurological disorder
- arm jerks, facial twitches, tremors spread to other parts of body and develop into writhing
- tremors start interfering with walking, speech, and voluntary movements
- limited ability to learn and improve new movements
- depression, sleep disorders, memory impairment, anxiety, hallucinations, delusions, poor judgement, alcoholism, drug abuse, sexual disorders
immediate physiological cause of Huntington’s disease
- gradual and extensive brain damage in caudate nucleus, putamen, globus pallidus, and cerebral cortex
- genetic cause
genetic cause of Huntington’s disease
- results from dominant gene on chromosome #4
- critical area of gene includes sequence of bases CAG which is repeated 11-24 times in most people, that repetition produces 11-24 glutamines
- people with 35 CAG repetitions are considered safe
- 36-38 repetitions might get it (probably not until old age)
- 39+ repetitions are likely to get it
- can predict whether a person will get it and when