Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

57 Cards in this Set

  • Front
  • Back
in the discussion of motor behavior. what are the two looped types of behavior?
Closed loop- maximize accuracy, continuous CNS and peripheral feedback

open loop- maximize speed, no feedback, behavior is pre-programmed, ballistic mvmnts.
mammals have 3 types of muscles. THEY ARE
Skeletal muscles are attached to _____________ and help us _________.
bone; move.
sensory receptor that is sensitive to the position and / or
movement of a part of the body (joints, ligaments, muscles,
or tendons)
4 kinds of proprioceptors
1. located in fibous joint capsule, continous discharge with limb position.

2. located in the fibrous joint capsule, adapt readily and activated by movement

3. located along ligaments, high threshold, slow adaptation, PROTECTIVE REFLEXES.

4. along the joints, believed to signal pain and joint movement extremes.
Muscle spindles are found _______________ they respond to __________________ not ____________________.
muscle length;
not muscle tension
Extrafusal muscle fibers are served by ________________ which results in _______________.
Alpha motor neuron; Contraction.
Intrafusal muscles fibers are connected to ________ for sensory info and ____________ for motor movement.
afferent neurons;
gamma motor neurons.
What is the monosynaptic stretch reflex?
An example is the knee-jerk response.

Another is the response to having added weight on the arm. When weight is added to the arm, the arm falls and the muscle lengthens causing an increase in muscle spindle afferent neurons.
golgi tendon organs are found in _________. respond to increases in muscle ________ not _______. Sensory nerves feed ____________ ________ which inhibits _______________. this system is made up of ____ # of synapses and is faster/slower than Monosynaptic reflex.

tension not length

inhibitory interneurons (spinal cord)

alpha motor neuron

two; slower
skeletal muscles are made of many ________________; which are made up of many ____________________; which are composed of many __________ and ___________ molecules
muscle fibers


actin and myosin molecules.
motor unit is
the smallest unit of motor activity. it includes an alpha motor neuron and all its extrafusal connections.
What is the general rule about number of connectivities in a motor unit.
The smaller the number of connectivities the more precise it is.
(Face = 3 vs bicep = >100)
synapse between terminal of motor neuron
and membrane of muscle fiber
neuromuscular junction
point on muscle fiber at which synapse
motor end plate
As it relates to end plate potentials:

-What is the NT released?
- does it cause de/hyper polarization?
-relative size of potential
causes depolarization;
much larger than normal neuronal firings and therefore ALWAYS causes action potential.
how does the firing of the endplate potential result in extension or contraction.
The firing causes Ca chaels to be open allowing Ca into the cell where it acts as a cofactor to break down ATP in order for myosin to move up and down along actin fibers to cause contraction/extension.
What are antagonistic muscles?
How do muscles reverse their contraction/extension?
How many ways can muscles move?
Those muscular systems that are setup to opppose eachother (Bicep/Tricep).

They dont. When one muscle contracts the other extends. In order to reverse the 1st step the other muscle must contract.

Flexors vs Extensors?
Flexor- muscle whose contraction causes muscles to flex (bend).

Extensors- muscles whose contractions cause extension (straightening).
what is the most common example of a flexor? extensor?
Bicep; Tricep.
Reciprocal innervation. Like hand on a stove or finger to thumb tack. What happens?
1.) pain causes burst of firing in sensory neurons.
2.) Excitation of EXCITATORY neurons causing the bicep to contact.
3.) Excitation of INHIBITORY neurons to inhibit tricep movement. (relaxation)
Coordinated activity requires
Alternating flexions and extensions.
Prefrontal cortex

-what information does it recieve?
-responsible for...
Frontal lobe;

Sensory Information from the parietal and temporal.

planning complex behaviors
premotor cortex is found where? what does it do?
Just rostral (in front of) the primary motor cortex. it passes info about moving to the primary motor.
When an individual chooses to move what are the information pathways in the brain.
Plans or movement originate in the frontal lobe. Information is sent to the premotor cortex and supplementary motor cortex. From there information is sent to the primary motor cortex, where movement messsages are sent.
in the planning of movements, the premotor cortex and supplementary motor cortex recieve information as the whats, wheres and hows from which two areas of the brain.
What- temporal

where and how- parietal

Recall the vental and dorsal streams of vision terminated in these locations.
The areas of importance within the primary motor cortex are the:
-frontal cortex
-precentral gyrus
The largest part of the primary motor cortex has been dedicated to what two body features.
Fingers and any muscles involved in speech.
Neurons in the primary cortex control movements of two descending pathways.. they are...
Lateral group- corticospinal, corticobulbar, and rubrospinal tracts.

Ventromedial group- vestibulospinal, tectospinal, reticulospina, and the ventral corticospinal tract.
The hummunculus as part of the primary motor cortex serves what function?
gross motor instruction of movement.
The lateral descending pathway engage in what kind of limb movement?
Lateral tracts of the spinal cord support INDEPENDENT limb movement
the ventromedial descending pathway engages in what kind of limb movement? also it recieves input from...?
Coordinated movement.
amygdala, hypothalamus, and basal ganglia
if a corticospinal tract lesion were made (to the lateral group) What would be the result?
(independent behaviors)
manual dexterity.

Non impaired
(coordinated behaviors)
-Bar climbing,
-releasing grasp
if a lesion were made to the ventromedial group, the result would be
impaired posture, impaired gait, upper arms hung at sides when reaching up.
Basal ganglia also involved in movement.

- what are the three components of the basal ganglia?
- what are the inputs?
-what are the outputs of the basal ganglia?
-what is its function?
-some control over...
Caudate nucleus, putamen, globus pallidus.

INputs: substancia nigra, primary motor, somatosensory cortices.

Output: Primary motor, supplementary motor, premortal cortices (via thamlamus)

influence primary motor fxn

some control over the ventromedial system

Important in... (3 things)
what kind of info does it recieve?
what controls what?
Important in ballistic movements, somato-sensory integration, and in learning new motor programs.

Recieves sensory information from all modalities.

The medial cerebellum controls the ventromedial group; while the lateral cerebellum, controls the lateral group.
Cerebellar cortex is highly organized it consists of what two types of cells. Where are the outputs going?
Purkinje cells and parallel cells at right angles to one another.

Outputs go to the thalamus and brainstem.
VERY IMPORTANT: In class it was said that the cerebellum had very high what?
NEURAL PLASTICITY... can be fine tuned to protect motor behavior (pitching, dancing, playing instrument).
As mentioned before the cerebellum is important in sensory-motor integration.

-recieves what inputs from where?
-outputs to where?
-what makes cerbellar neurons active?
auditory and visual from tectum and cutaneous and kinesthetic inputs from spine

Outputs-various cerebral nuclei, cortex, lateral and ventromedial groups.

When just walking cerebellar neurons are silent but in the case of any new stimuli (ex a rock and you trip) cerebellar activity spikes.

Highly organized structure of neurons allows for new synaptic connections necessary for learning.
a condition where one moves the wrong limb, part of limb or moves the correct limb in the wrong directions or wrong order.
Limb apraxia.
What form of limb apraxia is a result of damage to the left parietal lobe.
Left parietal apraxia
What form of limb apraxia results from damage to the anterior corpus collosum?
Collosal apraxia
What form of limb apraxia is a reuslt of damage to the anterior left frontal lobe?
sympathetic apraxia
What are the results of the three apraxias:
1.) collosal apraxia- left hand can function right cannot.

2.) Sympathetic apraxia- left hand can function right cannot.

3.) left parietal apraxia- neither limb can be used.
Difficulty in drawing pictures or diagrams or geometric constructions caused by damage to the RIGHT PARIETAL LOBE?
Constructional apraxia
what condition is caused by damage to the parietal lobe and results in specific writing defecits?
Apraxic agraphia
What condition is cause by damage to the PRECENTRAL GYRUS of insular cortex and causes defecits in the ability to produce sounds.
Speech or ORAL apraxia.

-disease of what?
-destroys what?
-development of what
-thought to be caused?
the CNS
myelin sheaths
sclerosis (hard tissue)
Autoimmune disease

weakness, tremors, urine incontinance, numbness, visual disturbances, ataxia (loss of motor coordination).

- cases/yr
- prognosis?
- what is mostly hardly hit?
- what is spared?
atrophy of motor neurons in brain and spine.

40 - 70 YO

5000 new U.S cases/yr

death in 2-5 yrs

corticospinal tract, brain stem

eyes, bladder

weakness, paralysis, wasting, loss of speech, swallowing, breathing
What causes ALS?
Not totally sure. But it has genetic and non-genetic components.

Genetic abnormality in dismutase gene causing superoxides.

toxins, immune response, endocrine dysfunction.
Parkinson's disease

-caused by destructiion of..
- symptoms begin after what
- cause
- symptoms
destruction of DOPAMENERGIC NEURONS from the substancia nigra and caudate nucleus.

-After 70% of all dopamanergid neurons have been killed.

-cause: unknown (toxins?)

-Tremor, rigidity, postural instability, akinesia/bradykinesia,
ultimately loss of voluntary behavior, death
briefly outline what symptoms are common in each of the 5 stages of parkinsons.
Stage 1:
-Mild symptoms (not deblitiating)
-tremor in one limb

Stage 2:
-bilateral symptoms
-minimally diabling
-posture and gait affected

Stage 3:
-Significant slowing
- Early walking impairment
-generalized dysfunction

Stage 4:
-Severe symptoms
-may still be able to walk
-should not live alone
-decrease in tremors

Stage 5:
-Cannot stand or walk
-Cachetic stage
-requires 24 hour attention
Parkinson's treatments

-levodopa + carbidopa
1.) precursor to dopamine- a process completed in the brain.

2.) D2 agonists. Increases release of dopamine from dopamenergic class # 2.

3.) increases dopamine release; reduces uptake and may inhibit acetylcholine release.

4.) MAO inhibitor- decreases the rate of dopamenergic breakdown. reduces superoxide formation.

5.) (benadryl)- antagonize muscarininc cholinergic receptors. may also reduce reuptake.
Parkinsons patients surgical options
Fetal nigral cell grafts

pallidotomy- lesion in the globus pallidus.
Huntingtons disease

- inheritance
- age of incidence
- atrophy of the
- causes reduction in NT..
- symptoms
Automsomally dominant genetic disorder


caudate nucleus

GABA and substance P

choreoid movements and intellectual deterioration.
Huntingtons disease

- effects on brain structure
- genetic cause (what specifically??)
- onset
- psychiatric disturbances
- motor disturbances
Box car ventricles

repeats of 3 base sequence "CAG" on chromosome 4.

Onset is incidious

wide ranging- personality changes, irratibility, manic-depressive, schizophrenic episodes.

Loss of control- flicking, gait, facial grimmacing, ataxia, dystonia, eventual choreoid movements.
Huntington's disease

very progressive, no treatment.

Medication given to deal with psychiatric changes including resperine, phenylthiazine (chlorpramine), and the neuroleptic haloperidol.

Genetic counseling... 50% of offspring will have Huntingtons disease.