Muscles and Reflexes Flashcards
Muscle Spindles v Golgi Tendon Organs
Muscle Spindle
- Parallel w/ fibers; right on fibers
- If stretch muscle —> stretch spindle —> fires more to convey length
- Contains intrafusal fibers
- 1- Nuclear Bag Fibers - thicker w/ nuclei in elastic center
- 2- Nuclear Chain Fibers - small w/ nuclei throughout
Golgi Tendon Organ
- In muscle tendons
- Ib afferents respond to tendon stretch which happens when muscle contracts
- Convey muscle load
Which afferents connect to which parts of muscle spindle?
- Ia afferents wrap around center of nuclear fibers and convey length AND velocity of stretch (PRIMARY)
- II afferents are on end of nuclear fibers and just convey length (SECONDARY)
- Gamma motor neurons also connect to nuclear fibers and control their sensitivity
Gamma Motor Neurons v. Alpha Motor Neurons
Gamma motor neurons also connect to nuclear fibers and control their sensitivity
- If gamma is firing then Ia still fire even when “unloaded”
- Gamma static - innervates bag2 and chain fibers SO controls sensitivity of both primary and secondary afferents
- Gamma dynamic - innervates only bag1 so only control primary afferents (velocity)
Alpha = extrafusal muscle fibers; contraction
Myotatic Reflex
- Ia afferents are monosynpatic —> input directly to motoneuron (FAST); also relay info to motoneurons via pre-motor interneuron which allows descending CNS path to act on that interneuron to adjust reflex intensity or shut it off
- Ia inhibitory neurons also inhibit the antagonist muscle (reciprocal inhibition)
- II - polysynaptic; only small projection to motor column SO little input to reflex
Crossed Extensor Reflex
Delta afferents relay pain signals to SC —> flex ipsilateral side and extend contralateral side (move away from pain source)
Recurrent Inhibition
- Renshaw Cells receives collateral branches from alpha motoneuron —> inhibits this same motoneuron so that you do not have a prolonged contraction
- Can be disabled if you want a prolonged contraction
Reciprocal Inhibition
The same Ia afferent that leads to muscle contraction also causes inhibition of antagonist muscle (so does not require dual innervation); synapses on Ia inhibitory interneuron
Non-reciprocal Inhibition
- Ib afferents - inhibit muscle contraction to dec tension so do NOT dir synapse on motoneuron; through Ib inhibitory interneuron
- ***This is turned off if body wants co-contraction of antagonist muscles for stability/stiffness
Upper Motor Neuron v. Lower Motor Neuron Lesion
- Upper Motor Neuron Lesion
- Hypertonus (inc tone)
- Spasticity - lesion removes inhibition from gamma motoneurons —> exaggerated mitotic reflex (tendon jerks and resistance to stretch esp when rapid b/c Ia tell velocity)
- Rigidity - muscles are constantly stiff due to cont firing of alpha motoneurons (no descending inhibition); does not sep on speed
- Clasped Knife- stretched muscle contracts (spasticity) but contracts so much that it activated golgi tendon organs —> sudden relaxation
- Lower Motor Neuron Lesion
- Hypotonia and atrophy
Fibrillation v. Fasciculation
- Fibrillation - when single de-nervated muscle fibers depolarize spontaneously; not visible; detect via electrode
- Fasciculation- when an entire group of muscle fibers is unstable and depolarizes spontaneously; visible as muscle twitch
Nerve Conduction Test Basics
- Nerve Conduction Test
- Record at muscle but stimulate at nerve
- Latency = speed of conduction of fastest fibers
- Conduction velocity = distance (b/n stim and recording) / time
Axonal Degeneration v. Myelin Degeneration
Axonal
- Starts distally —> proceeds proximally (so longer nerves more susceptible)
- Secondary disruption of myelin —> balls
- Causes - trauma/toxins/DM/genetic
- Normal latency/conduction velocity BUT dec amp (b/c less # axons - lower summation)
- If cell body is intact…remaining axon can sprout to regenerate
Myelin
- Segmented & multifocal (can happen anywhere)
- Causes -dysfunction of Schwann cells OR injury to myelin (including Guillain Barre autoimmune)
- Leads to certain degree of conduction block which determines symptoms
- If thin myelin left than slower conduction…i no myelin left/conduction block then no conduction —> lower amp b/c dec in synchrony for summation
- Schwann cells are constantly re-myelinating so varying degrees of myelin
MG v LEMS
MG
- IgG against Ach receptors (post-synaptic)
- Often eyes, face, jaw, swallowing 1st
- Dec strength throughout day
- Dx - ice pack or edrophonium
- Electric stim —> deplete Ach —> dec amp
- Tx - acetylcholinesterase inhibit and immune
LEMS
Antibodies against Ca++ channels (pre-synaptic)
-Similar to MG + hypo-reflexia, dry mouth (autonomic)
-Improves w/ exercise b/c inc Ca++
-Electro stim —> even greater dec amp than MG
-Reduced safety factor
-Tx - acetylcholinesterase inhibit, immune, 3,4 diaminopyrodine
Important Labs and Tests in Myopathy DX
- Most important lab - CK (creatine kinase - esp MM for muscle membrane)
- Elevated in inflammatory myopathies, dystrophies. metabolic myopathies and hypothyroid
- Electromyography - shows dec MUP - motor unit potential (b/c lose some fibers or have dysfunction so not in sync)
How do myopathies present?
- Normal sensation, normal reflexes, normal bulk, NO FASCICULATIONS (unlike neuropathy), normal nerve conduction
- Weakness (esp proximal)
- May have myotonia, exercise intolerance, aches
ALS
- Anterior Horn Disorder - problem w/ cell in anterior/ventral horn
- Present w/ both upper and lower motor neuron symptoms BUT no major sensory abnormalities
- Inherited OR acquired (complex)
Safety Factor
- more Ach is released at NMJ than is needed for threshold for AP (just in case)
- Safety margin = Actual EPP - EPP needed for threshold
Babinski Sign
- normally this reflex is tonically repressed by corticospinal tract SO If damaged OR baby OR sleeping…corticospinal tract does not inhibit and you get dorsiflexion of big toe in response to noxious rubbing
POS for upper motor neuron lesion
Hoffman Sign
flick middle finger —> flexion of distal thumb (abnormal if unilateral)
POS for upper motor neuron lesion
Clonus
when you hold ankle and dorsiflex foot —> rhythmic flexion/extension at ankle
POS for upper motor neuron lesion
Central v. Peripheral Facial Paresis
- Central facial paresis - forehead is spared because compensation from other side
- Peripheral facial paresis (Bell’s Palsy) - contralateral forehead and lower face are affected b/c no compensation
Decerebrate Rigidity
- Damage to midbrain eliminates—> LVST damage —> inc activity of gamma motoneurons —> Ia fire more —> HUGE extensor contraction (all extremities extended and head arched back)
- Exaggerated myotatic reflex
Decorticate Rigidity
Cortex/internal capsule/thalamus damage —> LVST damage —> inc activity of motoneurons —> Ia fire more —> legs extended BUT rubrospinal tract intact (unlike decerebrate) w/o cortical input —> hyperactive rubrospinal —> arm flexion
