More Motor Pathways Flashcards
axonal degeneration occurring distal to the site of injury
orthograde degeneration
what happens with orthograde degeneration
result in the Schwann cells reorganizing into Schwann tubes that can play a critical role in regeneration
If no regeneration after 1 yr, Schwann cells are replaced with fibroblasts
numbness after surgery or injury
has year with schwann tube still there to replace and if not, gets fibroblasts = scar tissue
instead of open channel road, you have a road block that hinders regeneration and that is this scar tissue
accompanies orthograde, axonal degeneration occurs proximal to the site of injury.
retrograde degeneration
what happens with retrograde degeneration
Loss of neurotrophic factors coming from the axon to the cell body via retrograde axoplasmic flow
Soma becomes swollen
loses communication with its end so cell body starts to change
Injury potentials from depolarization at the site of the lesion evoke spontaneous action potentials that travel to the muscle, causing a twitch
stage 1, fasciculations
injury potentials that lead to uncoordinated contractions of the muscle known as fibrillations
Small contractions, not visible on the surface
stage 2 of denervated muscle stages
after the distal axon has degenerated, the muscle begins to show denervation atrophy
stage 3
Denervated muscle develops a large number of ________ sites that are targets for regenerating axons
These can be maintained for about 2 years and will be lost if no reinnervation occurs
acetylcholine receptor
cell body reorganizes, they want to grow a new sprout, produces material and grows this
regeneration
describe the process of regeneration
nerve is cut and nerve degenerates, so now cell body creates more production and creates a growth cone and sends out sprouts., if it finds the schwann tube, it gets all the nutrients and regrows and reinnervates the muscle and the other sprouts dont go anywhere
the one with the right channel grows and the others do not
can regenerate nerves in the periphery
referred to as the vestibulocerebellum
flocculonodular lobe
Receives vestibular, spinal and cortical inputs
cerebellum
what is medulloblastoma
occurring in the roof of 4th ventricle in young children
Damage to flocculonodular lobe
in cerebellum
symptoms of medulloblastoma
Loss of equilibrium, sway side to side, staggering, wide-based gait, falling over, problems with eye movements, can also have noncommunicating hydrocephalus
these cells give the arbor vitae appearance
Purkinje cells
what can we see with damage to the cerebellum?
general incoordination or ataxia (“lack of order”), often in leg movements
changes in muscle tone (hypotonia), reflexes (hyporeflexia) and coordination of voluntary movements ipsi to side of lesion
how is coordination affected with cerebellar disorders?
Voluntary movements may take longer than normal to initiate
Problems stopping or changing direction of movement (overshoot or undershoot of targets = dysmetria)
overshooting or undershooting of targets
dysmetria
difficulty with rapid alternating movements
Dysdiadochokinesia
the largest and it emerges from the basal pons
mainly contains afferents from contra and pontine nuclei
middle cerebellar peduncle
has many decussations and mainly efferent pathways from cerebellum to red nucleus and thalamus
superior cerebellar peduncles
major portion of inferior cerebellar peduncle (“ropelike”) with fibers from spinal cord and brainstem
restiform body
additional fibers of the ICP (inferior cerebellar peduncle) connecting cerebellum and vestibular nuclei
juxstarestiform body
Where is there a better prognosis for regeneration?
better prognosis in peripheral ns than in the cns and for it to occur accurately
if damage is cns, so tightly packed with a bunch of cells that it has more odds against it to have an effective regeneration
what are the Cortical Motor Areas
come from a multitude of areas that add information regarding what muscles we want to move, how fast and where
Primary Motor Area (M-I), Brodmann’s area 4
Supplementary Motor Area (SMA), Brodmann’s area 6
Premotor Area (PMA), Brodmann’s area 6
where do we have connections for movement?
from areas that also assist in the coordination of our movements
Motor areas of cortex receive info from cerebellum, basal ganglia, and peripheral sensory systems (all via the thalamic nuclei) (proprioception)
Provides the most direct cortical control of the motor neurons
M1
facilitate specific sets of neurons in M-I
Serves to prepare M-I , not completely understood
PMA
facilitates coordinated motor acts (complex movements)—SMA is not necessary for simple repetitive tasks
SMA
precursor to the actual motor command
PMA
Set of nuclei at the base of the cerebral hemispheres
Basal ganglia
what consists of the basal ganglia
Putamen, caudate nucleus, globus pallidus, nucleus accumbens, and diencephalic subthalamic nuclei and substantia nigra
striped appearance on sagittal slices not at midline
caudate nucleus, nucleus accumbens and putamen
striatum
refers to the putamen and globus pallidus grouped together
lenticular nucleus
where are bg in relation to the thalamus?
nearby it
bg make constant connection with thalamus and send info to modulate the motor commands in the cortex
what is the importance of the bg?
tie together movement, cognition and emotion
how do we have emotions tied to motor commands?
through some limbic connections
characterized by excessive movement
Hyperkinetic
characterized by diminished or slow movement
Hypokinetic
spasms, involuntary movements of limbs or facial muscles, with possible hypotonia (loss of muscle tone)
choreo
without position”; slow writhing movements (pronounced in hands and fingers); patient may have difficulty holding a limb in a fixed position
athetosis
“jumping about”; wild flailing movements of one arm and leg
ballismus
increased or abnormal tone in muscles or tissue resulting in a somewhat fixed posture
dystonia
lack of movement and are stuck
dystonia
loss of muscle tone
more rigid
hypotonia
tone increase in flexors & extensors
rigidity
decreased or slow movements
Bradykinesia
Neuronal degeneration that is severe in the striatum and especially the caudate nucleus
huntingdon’s disease
What are symptom’s we see with Huntingdon’s disease
Symptoms between age 30-50 years
Involuntary movements (chorea) and alteration of mood or cognitive function
Movements become more pronounced with worsening dementia & personality changes
what disease is an autosomal dominant inheritance (chromosome 4)
huntingdon’s disease
Are we able to do genetic testing for Huntingdon’s?
YES able to do genetic testing to see if they have passed it on
Most well known hypokinetic disorder
parkinson’s disease
Biochemical disease of basal ganglia (evident in substantia nigra pigmented cells that should produce dopamine and transport it to the striatum)
parkinson’s disease
what are treatments for PD
L-dopa, precursor of dopamine that is needed (dopamine does not cross the blood-brain barrier)
Has helped many patients, but also side effects
Thalamotomy or pallidotomy to disrupt the loop (Last resort due to risk of damaging the nearby internal capsule)
Recent implantation of electrodes in globus pallidus (high freq bursts)
Wide spread choice for advanced Parkinson’s
what is a positive sign? (may be involved in basal ganglia)
something new that showed up that didn’t use to be there
tremor for example
what is a negative sign
something that was there and is now diminishing
used to have the ability to do something and now they don’t
what would be a positive and negative sign of PD?
rigidity = positive
bradykinesia = negative
what are examples of PD signs
decreased blinking, expressionless face, lack of arm movements while walking
Resting tremor, generally of the hand and diminishing with voluntary movement
what is rigidity and cog wheel rigidity
(uniform)
tremor or brief relaxations and rigidity superimposed)
