Exam 4 Flashcards
UMN tract for cranial nerves
corticobrainstem tracts
UMN tracts that don’t guide movement. Partially depolarize LMN to enable quick action
nonspecific activating tracts
partial loss of muscle strength
paresis
complete loss of muscle strength
paralysis (-plegia)
which motor neurons will have more severe atrophy if damaged
lower motor neurons
the atrophy of denervation is associated with which motor neurons
LMN
short-lived involuntary contraction of muscle tissue often due to metabolic or muscular issues
muscle spasm
a prolonged contraction of muscle tissue often due to metabolic or muscular issues
muscle cramp
involuntary contractions of entire motor units. Generally indicate irritation of motor neuron. Can be benign or pathologic
fasciculations
involuntary contraction of multiple muscles (limb or whole body) that typically occurs between sleep and wake state. No proximate cause
myoclonus
generally indicative of neural damage
can be resting or intention: suggestive of pathology in the cerebellum
tremors
very important diagnostic finding that cannot be observed. The spontaneous contraction of 1 muscle fiber that has lost its nerve. Indicates denervation (muscle fiber has lost it’s nerve)
fibrillations
type of hypertonia where if a muscle is moved slowly, there is no hypertonia. When a muscle is quickly stretched, the muscle overreacts.
velocity dependent
type of hypertonia where speed doesn’t matter, there is always high tone
velocity independent
posturing due to too much activity from the brainstem UMN. Involuntary continuous contraction of extensor muscles in UE and LE
decerebrate
posturing where connection from cortex to brainstem has been severed. Pattern is involuntary hypertonia in flexion of arms and extension of legs.
decorticate
potential sources of damage to LMN
Trauma (sharp or blunt) Infection (e.g., polio) Degenerative disorders (e.g., ALS) Vascular disorders Tumors
a tremor at rest suggests what pathology
Parkinson’s Disease
an intention tremor is suggestive of pathology of the _____
cerebellum
Signs and symptoms of LMN disorder
Loss of reflexes
Atrophy (more likely atrophy of denervation)
Flaccid paralysis: low tone inability to move
Fibrillations
potential sources of damage to UMN
Spinal cord injury Cerebral palsy Multiple sclerosis Degeneration (e.g., Parkinson’s Disease) Trauma Loss of blood supply (e.g., Stroke)
Signs and symptoms of UMN disorder
paresis paralysis loss of "fractionated" movement abnormal cutaneous reflexes (babinski response...limb withdrawal) muscle stretch hyperreflexia clonus clasp-knife response
what does the process of collateral sprouting create
giant motor unit (one axon innervates more muscle fibers than normal)
if a person had a stroke that only damaged the cortex, they would have ___
paresis
Exaggerated reflex response when descending inhibition is missing or much reduced or when UMN is damaged
muscle stretch hyperreflexia
2 ways to help muscle stretch hyperreflexia
don’t stretch quickly and use pharmacology to turn down LMN (act like GABA)
how do you elicit clonus
quick stretch
Rhythmic, repeating (usually involuntary) contraction
A series of hyperreflexia responses when there is a continuing stimulus of stretch
clonus
how to prevent clonus
Pharmacology
Position ankles in extreme dorsiflexion
Lift leg and set it back down slowly
Lean on that leg
when clonus is sustained, this is an indication of what
UMN damage
example of hyperreflexic response to stretch that goes away (UMN damage)
clasp-knife response
what are 2 ways that the muscle changes in response to lack of movement due to UMN injury
atrophy and increased mechanical stiffness/contracture
what are different ways we can have hypertonia or spasticity
hyperreflexia or brainstem UMN overactivity
types of brainstem overractivity
more tonic or resting (i.e. “rigidity” of PD)
more activity dependent (i.e. muscle overactivity of CVA that create abnormal synergies)
where does the basal ganglia motor loop output to
cortical UMN via thalamus and brainstem UMN via pedunculopontine nucleus
predict the effects of various actions, then make and execute action plans
basal ganglia
piece of basal ganglia that malfunctiosn to cause PD
substantia nigra
excitatory neurotransmitter that has input signals from other brain regions to Putamen
glutamate
5 basal ganglia loops
motor oculomotor executive behavior flexibility and control limbic
loop from basal ganglia to pre central gyrus and back. Contains the plan to move
motor
loop from basal ganglia to prefrontal cortex. Decides what to do
executive
As a group, basal ganglia “loops” help with
predicting future events selecting desired behaviors preventing undesired behaviors motor learning (procedural memory) shifting attention spatial working memory
Motor “loop” regulates
Muscle contraction
Muscle force
Multijoint movements
Sequencing of movements
is the basal ganglia motor loop excitatory or inhibitory
inhibitory
pathology where there is death of dopamine producing cells in substantial nigra
akinetic/rigid PD
excitatory and is the neurotransmitter that makes the basal ganglia circuitry work properly to plan movements. Without it, the basal ganglia malfunction
dopamine
with dopamine gone, the output of basal ganglia increases, leading to
Too little activation of voluntary muscles
Too much activation of postural and girdle muscles
Too little activation of midbrain locomotor region
signs and symptoms of akinetic/rigid parkinson’s disease
akinesia/hypokinesia
rigidity
postural instability
resting tremor
hyperkinetic disorder involving the basal ganglia where it doesn’t output enough
Huntington’s disease
degeneration of striatum and cerebral cortex
Huntington’s disease
tremor of movement where you miss the target and correct it
action tremor
inability to rapidly/smoothly alternate the direction of movement
Dysdiadochokinesia
Wide-based, unsteady, staggering, veering gait
ataxic gait
side effects of spinocerebellum damage
ataxic gait
dysdiadochokinesia
dysmetria
action tremor
side effects of vestsbulocerebellum damage
Nystagmus
Dysequilibrium
Balance deficit (truncal ataxia)
side effect of paravermis and hemisphere damage
Dysarthria (“ataxic”):
side effect of cerebrocerebellar damage
Hand ataxia
Incoordination of fine finger movements
side effect of spinocerebellar damage
gait ataxia
strategies to improve function of pt with cerebellar damage
slow down
use vision to guide movement
think about what you’re doing
simplify movements
what is damaged if a person has ataxia whether eyes are open or closed and their sensation tests have normal results
cerebellum
what is damaged if a person has ataxia only when eyes are closed and their sensation tests have abnormal results
somatosensory
all neural structures distal to the spinal nerves
peripheral nervous system
surrounds individual axons
endoneurium
surrounds bundles of axons
perineurium
surrounds bundles of fascicles
epineurium
All peripheral nerves have axons of ___, ____ and ____ (usually SNS) function
motor, sensory, autonomic
A-alpha are
efferent, extrafusal
Ia, Ib, II are
afferent, proprioception
A-beta are
afferent, exteroception
A-gamma are
efferent-intrafusal
A-delta are
afferent- pain, temperature, viscera
B are
efferent- presynaptic autonomic
C are
afferent-pain, temperature, viscera
efferent-postsynaptic autonomic
