Term
| What does the Medial Longitudinal Fasciculus do? |
|
Definition
allows coordination of conjugate eye
movements |
|
|
Term
| what does the ParaPontine Reticular Formation do? |
|
Definition
| fast horizontal saccadic movement |
|
|
Term
| what does the rostral interstitial nucleus do? |
|
Definition
| fast vertical saccadic eye movements. |
|
|
Term
| what centers of the brain are associated with saccadic eye movements? |
|
Definition
| substantia nigra pars reticulata feeds into the superior colliculus which feeds into the PPRF |
|
|
Term
| what centers of the brain are associated with smooth pursuit? |
|
Definition
| these end up feeding into the PPRF as well. |
|
|
Term
| what is the pathway from the retina to the visual cortex? |
|
Definition
Inputs from retina to optic chiasm, to
lateral geniculate
nucleus (thalamic relay)
to visual cortex |
|
|
Term
| how do ocular dominance columns develop? |
|
Definition
when the lateral geniuclate nucleus sends its signals to the visual cortex layer 4 inputs, the signal is very diffuse and nonsegregated.
As you develop, the lateral geniculate nucleus develops the ocular dominance columns, and then over time you start segregating the visual cortex as well.
So at first the neurons have a very large spread with a lot of overlap, and then you prune them until they were very discrete in their connections. |
|
|
Term
| what would happen to the ocular dominance columns if you suture one eye shut? |
|
Definition
| the ocular dominance columns would bias to the active eye. this shows the power of the reorganization of your nervous system. |
|
|
Term
| what happens if you suture one eye shut between 3-7 weeks after birth? |
|
Definition
| you miss the critical period of development and your dominance columns wont reorganize. |
|
|
Term
| what would happen to your ocular dominance columns if you did not have paired movement of your eyes? on that note, what is strabismus? |
|
Definition
the dominance columns would be completely segregated, no binocular vision (because your eyes are looking at different things!)
Strabismus is a disorder in which the two eyes do not line up in the same direction, and therefore do not look at the same object at the same time. The condition is more commonly known as "crossed eyes." |
|
|
Term
|
Definition
Lazy eye! If don’t patch good eye by 6, brain ignores lazy eye and visual
pathway degenerates: eye functionally blind |
|
|
Term
| how do you quantify muscle fatigue? |
|
Definition
| Fatigue is quantified as the decline in the force during a maximum voluntary contraction(MVC) |
|
|
Term
| how do we determine if someone is voluntarily contracting as hard as possible? |
|
Definition
he level of voluntary drive is tested by applying a supramaximal electric
stimulation to the nerve during a maximal voluntary contraction to determine if additional force can be evoked from the muscle. If the stimulation evokes additional force,
then voluntary activation is insufficient. |
|
|
Term
| what is one way to measure neural drive? |
|
Definition
| superimposed stimulation. first you do a control twitch to see how much force the muscle can generate maximally. Then you have the person do an MVIC and stim them on top of that. if they produce more force, you know they dont have 100% neural drive. the formula is 1- (force increase with superimposed stim/control twitch force) x100%. |
|
|
Term
| what is central activation ratio? |
|
Definition
PEAK VOLUNTARY TORQUE / (PEAK
VOLUNTARY TORQUE + superimposed
torque) |
|
|
Term
| what are some neural mechanisms contributing to fatigue? |
|
Definition
Decreased excitation of
motor neurons from
supraspinal sources
Presynaptic inhibitionof
motor neurons
Afferent feedback
• Activation of Group III
and IVafferents
• Decline in muscle spindle
feedback to the alpha
motor neuron
Decreased excitability of
alpha motor neuron |
|
|
Term
| how can afferent feedback contribute to neural fatigue? |
|
Definition
group III and IV (a delta and C) inputs are sensitive to deep pressure, pain, AND metabolic byproducts of fatigue. these fibers send a signal that goes to an inhibitory interneuron, decussates, trabels up the spinothalamic tract to the thalamus., which modifies neural output.
ALSO the III and IV afferents presynaptically inhibit the output of type Ia afferents (:muscle spindle dynamic). normally Ia afferents singal motor neurons to fire, but now the muscle isnt getting that signal as strongly, so you don't contract as hard. |
|
|
Term
| what are the two neural mechanisms of fatigue? |
|
Definition
type III and IV afferents sending information to the thalamus to decrease drive to the motor neuron
AND III and IV afferents inhibit type Ia afferents (which usually excite the motorneuron) so we get less neural drive. |
|
|
Term
|
Definition
when motor neuron disharge is evoke by constant stimulation of the MN cell body, there is a decline in discharge rate.
there is an increase in threshhold due to sodium channel inactivation
the increase in length of afterhyperpolarization is due to calcium |
|
|
Term
| in therapy, do we want to start our patient off with a force based task, or a position based task? |
|
Definition
| in therapy you want to start with a force task first to develop some strength. then move to position tasks. you wouldnt want to start with position tasks because your patient will fatigue faster. |
|
|
Term
| what type of receptors will desensitize to their ligand with repeated exposure? |
|
Definition
|
|
Term
| how would you test for neuromuscular propagation failure? |
|
Definition
you test for it with an M-wave test
A decline in M wave amplitude suggests
impairment in one of the processes
involved in converting the axonal AP
(initiated by the electric shock) into a muscle (sarcolemmal) action potential |
|
|
Term
| what is neuromuscular propagation? |
|
Definition
| the processes involved in converting an axonal AP to a sarcolemmal AP |
|
|
Term
how could Impairments in neuromuscular propagation may contribute to the decline in force
associated with fatigue |
|
Definition
Reduced transmitter release (Ach) from the presynaptic terminal
• neurotransmitter depletion
• decreased sensitivity of the postsynaptic
receptors and membrane |
|
|
Term
| what are some of the mechanical changes associated with muscle fibers during fatigue? (peripheral mechanisms) |
|
Definition
| it takes more time to fire, more time to relax. this is due to calcium dynamics and sodium channel inactivation |
|
|
Term
| what are some metabolic changes that are associated with muscle fibers during fatigue? (peripheral mechanisms) |
|
Definition
increase in sodium ions, inorganic phosphate, ATP, H+, background Ca+2.
decrease in K+, release of Ca+2 from SR, Ca+2 sensitivity, PCr, ATP hydrolysis. |
|
|
Term
| why is the increase in free phosphate a problem with fatigue? |
|
Definition
| the free phosphate inhibits the action of myosin heads on actin! |
|
|
Term
| as fatigue progresses, what happens to calcium release from the SR? |
|
Definition
| reduction in calcium release. |
|
|
Term
| how does caffeine affect fatigue? |
|
Definition
| caffeine acts directly to release Ca+2 from the SR. when this calcium is released, normal force is regained. |
|
|
Term
| how does acid buildup affect fatigue? |
|
Definition
| not much at normal physiological temps. after a 0.5 pH unit acidification, there was a 30% decrease in force output at 12 degreese celsius, but only a 10% decrease in force at 32 degrees celsius. so H+ doesnt matter THAT much. |
|
|
Term
| how do glycogen store affect fatigue? |
|
Definition
During exercise on cycle ergometer
at 70% of maximal aerobic power,
inability to sustain the task was
associated with glycogen depletion
in vastus lateralis |
|
|
Term
| how does motivation affect fatigue? |
|
Definition
| a loud noise activates the startle reflex (due to reticular brainstem activation from the loud noise), and this allows for the person to push harder. |
|
|
Term
| how do metabolic byproducts contribute to muscle soreness? |
|
Definition
| metabolic byproducts don't contribute that much. they get washed away pretty quickly |
|
|
Term
| what causes muscle soreness? |
|
Definition
tearing of muscle contractile elements..
eccentric contractions by naive subjects doing a new tasks. |
|
|
Term
| so after we have torn our sarcomeres, what type of reactions happen? |
|
Definition
Increased inflammatory processes
• inflammatory responses in the muscle
• Complement and cytokine release
• Neutrophil then monocyte attraction
• Free radical generation
• edema/swelling
Some pain at rest, increased pain with
mechanical stimuli (palpation,
contraction, movement)
greater in Type II fibers
repair begins ~3 d post-exercise |
|
|
Term
| how does muscle regeneration occur? |
|
Definition
| satellite cells get turned on by cytokines released by microphages, and they infiltrate the cell to injury site and differentiate into myoblasts which fuse into myotubes |
|
|
Term
|
Definition
painful, involuntary shortening
• Evident with fatigue/heavy exercise, dehydration,
calcium/magnesium
• possibly K/Na, hormonal changes |
|
|
Term
|
Definition
Muscle Strain - tension exceeds the weakest structural element
• usually located .1- 3mm from muscle-tendon junction, can be diffuse
• caused by: sudden over-stretch or contraction and limb deceleration
• failure of GTO previously thought to play a role
• insufficient warm-up
Contributory causes: corticosteroid , previous injury, disease
Grading
• 1
st
degree (mild - “strain”)– minimal damage/strength loss
• 2
nd
degree (moderate – “pulled”) – partial tear, hemorrhage, mod
pain/loss
• 3
rd
degree (severe – “tear”) – complete tear, extensive hemorrhage,
complete loss of strength |
|
|
Term
| how do NSAIDs affect dealing? |
|
Definition
| immediately after the injury NSAIDs may be good (first 1-5 days) but if you take them for an extended period of time, the inflammatory response doesnt initiate enough repair. the results of this is that after 30 days of NASID use after injury, the person is weaker than if they had not taken the NSAID at all. |
|
|
Term
| what other factors affect healing? |
|
Definition
Controlled mobilization duration
-Complete immobilization for 2 days inferior to 5 days immobilization
• Facilitation of granulation tissue/collagen deposition, strengthening
also Weeks after return from initial muscle injury (hamstring, quads, calf)
- 1 week – 7.8-12.6%
- 2 weeks – 4.7-8.1%
- 3 weeks – 3.3-6.8%
- 4-5 weeks – 0-4.7%
- 6-8 weeks – 2.8-3.3%
(% is chance of re-injury) |
|
|
Term
|
Definition
blow to muscle leading to
fiber tearing and hematoma
• sometimes difficult to distinguish from
complete tear
• Intermuscular hematoma - bleeding
between muscle fascia
• characterized by early migration of
ecchymosis to distal part of limb
• heal more quickly than intramuscular
hematomas
• Intramuscular hematoma - bleeding within
a muscle bundle
• hemorrhage is more confined and localized
• inflammatory response is exaggerated
Increase risk of myositis ossificans,
residual scarring, compartment
syndrome |
|
|
Term
| what is compartment syndrome? |
|
Definition
Hemorrhage leads to increased pressure in muscle unit
• Increased pressure, decreased blood flow
• Ischemia, necrosis, gangrene
Causes
• severe intramuscular contusions
• excessive exercise-induced damage
Signs/symptoms
• severe pain
• palpable tightness
• “shiny” skin appearance
• Compression – decreased blood flow/nerve compressions
Treatment -fascial release (surgery) within 12 hrs |
|
|
Term
|
Definition
extensive structural damage/altered permeability
contents of injured muscles cells leak into circulation
Previously known as ‘crush injury syndrome’
• Bruising
• ischemia, altered blood flow
• severe exertion
• Temperature extreme (severe cold or severe heat)
• Deep burns, electrical burns
• Infections/drugs
Electrolyte imbalances/myoglobin release cause
acute renal failure |
|
|
Term
|
Definition
Definition: Periods of excessive
training or emotional stress
• Symptoms similar to clinical
depression
• Decline in physical performance
• Sense of a loss in muscular strength,
coordination, and work capacity
• Change in appetite, weight loss
• Sleep disturbances, irritability,
restlessness, anxiousness, variable pain
• Loss of motivation, lack of mental
concentration, feelings of depression
• Alterations in the nervous,
endocrine, and immune systems
(decrease in testosterone and thyroxine, increase in cortisol, decreased immune function) |
|
|
Term
| what is muscular dystrophy? |
|
Definition
Progressive, spontaneous degeneration of muscle fibers - loss of
ability to resist repeated contraction/respond to stress.
dystrophin attaches the sarcomeres to the sarcolemma |
|
|
Term
| what is the difference between duchenne's muscular dystrophy and becker's? |
|
Definition
X-linked mutation resulting in absence of dystrophin molecule
• Attached sacromere to sarcolemma
• important in cell integrity
• Impaired function and repair, progressive weakness
• Becker’s represents partial integrity of dystrophin
• Survival to middle ages, Duchenne’s into teens/20s |
|
|
Term
| so what are some signs and symptoms of muscular distrophy? |
|
Definition
| lack of dystrophin staining. muscle damage causes an increase in connective tissue deposition. proximal muscle are used more, so they get more damaged. fibrosis, hardening, and atrophy |
|
|
Term
| what is a myotonic dystrophy? |
|
Definition
Persistent contractures of skeletal muscles after
voluntary contraction, following electrical stimulation
• Abnormality in the intracellular ATP system- fails to return
calcium to the SR
• Contractures are not relieved by muscle relaxants/antispastics/deep anesthesia
• Infiltration of LA into skeletal muscle may induce relaxation
Associated disorders
•Mitral valve prolapse – 20% of individuals
•His-Purkinje deterioration: arrhythmias, 1st
degree
AV block
•Restrictive lung disease |
|
|
Term
| what is an inflammatory myopathy? |
|
Definition
Low-grade inflammation with adenopathy
Polymyositis – inflammation of many muscles
(autoimmune?)
• Bilateral, proximal
• Skeletal muscle degeneration/regeneration
Dermatomyositis (skin/muscle)
Inclusion body myositis - progressive
weakness of distal musculature (wrists,
fingers, tibialis anterior, also possibly quads.) |
|
|
Term
| what is a metabolic myopathy? |
|
Definition
Glycogen Storage Myopathies
• Multiple disease processes involved in glycolysis or
glycogen synthesis
• Often X-linked, autosomal recessive
• Signs/symptoms: muscle weakness, rhabdomyolysis,
exercise intolerance, cramps; often liver, renal, heart, lungs
involvement |
|
|
Term
| what are some more metabolic myopathies? |
|
Definition
Glucocorticoids
• Cushing’s disease or iatrogenic corticosteriods
•proximal muscle weakness and wasting
•Selective for Type II fibers
• Conn’s (excessive aldosterone) and Addison’s disease
(hypoadrenalism) - weakness related to hormonal imbalances
Thyroid
• Hyperthyroidisms – moderate weakness, atrophy in 80% untreated
• Hypothyroid – slowness of muscle contraction/relaxation (slower
myosin ATPase activity), also mild proximal weakness
Pituitary (hypo) – severe weakness, reflective of decreased
adrenal/thyroid hormones |
|
|
