Movement and its common disorders
“Life’s aim is an act not a thought”
(ultimate goal of cognition) Sherrington
Anatomy & Physiology
Spring 2016
Stan Misler
<latrotox@gmail.com>
CNS Structure / Function relations for movement
Spinal cord: stretch or withdrawal reflexes, rhythmic limb movements
Brainstem: (1) pons: connects cerebellum to cerebral hemispheres
(2) midbrain: controller of stereotyped movements, balance
Cerebellum: specialized motor movement processor : timing, coordination,
precision (by moderating force and range of motion) + learning of motor skills)
Diencephalon: thalamus: sensorimotor waystation (all sensory input except
olfaction + all motor outputs) synapse here
Cerebrum: premotor cortex = command planning of complex movement ,
primary motor cortex modification of stretch reflex and initiation of voluntary
movement
basal ganglia for precision of motor performance
Fast movement = activation of pyramidal
track vs. slow deliberate movement =
sensory feedback from muscles and
joints, balance from ears and eyes +
extrapyramidal tracts + basal ganglia
and cerebellum which translate “Do it” to
smoothly integrated movements
Tennis: calculate trajectory of ball in
100ms initiate and complete movement
in 400 ms
Extending the reflex to real life situations
Extending Spinal Reflex to brain: 1A fibers project to
the sensory cortex while aMNs receive info from
motor cortex
Projection of branches of sensory
afferent (1A) fibers to CNS (1st to
medulla, then 2nd from medulla to
thalamus, then 3rd from thalamus to
sensory cortex) defines the position of
muscle in space. Fibers project from
sensory cortex to motor cortex whose
axons activate alpha motor neurons to
muscle.
Without this supraspinal innervation, such
as after acute stroke, there is not enough
background excitation of alpha motor
neurons to sustain a reflex. Ultimately the
1A fibers sprout more synaptic knobs so
alpha motor neurons are excited by stretch
alone
Betz cells of motor cortex
1A
a
Note crossing of motor and sensory
pathways from left to right
Motor unit = fibers in a single muscle that
are synapsed on by a single motor neuron
Small motor units contain only a few slow muscle fibers while large motor units
containing many fibers are either fast fatigue resistant or fast fatiguable. When action is
started first motor units containing slow fibers are activated. Later motor units with
many fast fibers are recruited as needed to sustain load
Treadmill Walking in midbrain transected cat =
rhythmic behavior involving stereotyped pattern of limb movement
maintained by central pattern generator (collection of local interneurons
that reciprocally excite and inhibit each other in spinal cord thus
reciprocally activating extensor and flexor muscles) Speeding up
treadmill -> trot. Activity often called a fixed action pattern. No
feedback from excited muscles or input from cerebral cortex needed but
can be modified by afferent fibers or activated by command source in
brain stem.
Note: animal
is suspended
by harness
CNS control for voluntary movement
Pre-motor ad
supplementary motor
cortices
Red nucleus,
reticular
formation,
vestibular nuclei
Includes motor
neurons to face
Corticospinal tract
included pyramidal
tract
Levels below premotor cortex but above
motor neurons work together to produce
motor and postural programs for
individual acts of complex activity
Feedback from muscle receptors to motor cortex
Basal nuclei or ganglia include
substantial nigra
Details of CNS control of movement
including intent and smoothness of action
Parietal cortex (supplemental motor area) integrates sensory info
Pre-motor cortex uses sensory info to formulate and sustain overall command for
activity: selects plan of action from repertoire of possible behaviorally relevant
actions often using info from other cortical regions. Some of its fibers also go to
aMNs.
Cerebellum = predictive control on effectiveness of movement: detects “motor
error” between an intended movement and actual movement (info from 1A
afferent fibers) and through output to upper motor neuron reduces the error.
Long-term reduction of error = motor learning
thalamus: connects brain stem with sensorimotor cortex and receives input from
basal ganglia
brainstem motor neurons: posture and orienting gaze. (e.g., vestibular complex
Reticulo-, tecto- and rubrospinal tracks for backup activation of alpha-motor
neurons even when pyramidal tract is damaged. This sustains motor behavior to
proximal but not distal muscles, so fine motor (finger) behavior is not possible
Stroke (cerebrovascular accident, CVA)
1. 3rd most common cause of death; most common cause of disability
2. Primary motor cortex -> hemiplegia (one sided weakness on side opposite to CVA)
with areflexia and atonia (spinal shock). Later spasticity (hyperreflexia and rigidity),
stiff extended leg & poor use of fingers. Often comes with sudden aphasia (inability to
speak), dysphasia (difficulty saying words) or talking non-sense; new onset unilateral
poor vision. Most often associated with damage to middle cerebral artery.
3. Premotor cortex -> apraxia = inability to link individual acts into complex activity
(e.g.,hit tennis ball)
4. Initial insult or brain attack: artery blocked -> infarction (embolic = clot from wall of
aorta or internal carotid vs. thrombotic = local clot formation) vs. blood vessel rupture
(aneurysm = hemorrhage with worst headache ever + unconsciousness). Blocked
cerebral artery can be treated by “clot busting” drugs (tPA) for first several hours.
5.Transient ischemic attack: stroke of short duration and complete recovery; often due
to small cholesterol emboli slowly wending way through blood vessel to affected region of
brain but not getting stuck.
6. After completed stroke there are affective symptoms of depression, neglect of side
affected by stroke, or unawareness of that side of world in addition to physical disability
7a. Use of neurorehabilitation: in this case to train new areas of brain to take over lost
function. Good for large movements though fine finger movements, for writing, typing, or
buttoning clothes, remain impaired
b. Control of blood glucose, blood pressure and blood cholesterol + smoking cessation +
treatment of cardiac disease to prevent further emboli, all to prevent future CVA
Brain lesions from CVAs
Left leg weakness and
clumsiness and left
alien hand
Talking non-sense
New onset poor vision
Left-sided hemineglect
Cerebellar degeneration due to alcoholism
or tumor derived toxic chemicals
Destruction of cerebellar Purkinje cells exerting inhibitory
effects on excessive movements -> (a) exaggerated
pendular stretch reflexes (limb oscillates like pendulum 6-8
times before coming to rest); (b) truncal ataxia and poor
posture and loss of ability to maintain upright stance unless
its widebased like with intoxication; (c) explosive and
slurred speech; (d) intention tremor; (e) slurred speech; (f)
wandering eye tracking (nystagmus); (f) finger to nose
dysmetria; (g) decomposition of movement; (h) inability to
do rapid alternating movements (paddycakes) =
dysdiadochokinesis; often with dizziness, nausea and
vomiting
Cerebellar lesions
Progressive walking like drunkard
Finger to nose dysmetria
Parkinsonism
Brain, especially basal ganglia, deficient in
neurotransmitter dopamine which is secreted by
cells of the substantia nigra -> limitation of motor
output; use of precursor L-dopa as treatment
Description stooped old man, shuffling, drooling,
shaking and writhing: (a) magnetic gait (stuck to floor
with shuffle); (b) spontaneous tremor; (c) loss of
facial expression (masked facies); and (d) depression.
Interestingly rapid movement possible in emergency
or in response to music.
More complex wiring diagram
SMA = supplemental motor area; PMC = primary motor cortex
Brain Machine Interfaces