Exam II Flashcards
Pyramidal system
Drive voluntary movements by activating ventral horn lower motor neurons directly, UMN pathways
Extrapyramidal system
Modulate voluntary movements by regulating the motor neurons indirectly, not part of the UMN pathways, tracts outside of the pyramids
Lateral MTs
innervate distal limb muscles for fine motor control and perform fractionated movements
Medial MTs
innervate axial/proximal girdle muscles to control posture and perform gross movements, involuntary coordinated responses that are mostly initiated in brainstem centers
Non-specific MTs
Do not activate or regulate any specific movements, activate during stress or emotions
Lateral corticospinal tracts
Most important tract controlling voluntary movements, unique ability to generate fractionated movements by using interneurons to inhibit unwanted neighboring muscles
Rubrospinal tracts
Arises in red nucleus in midbrain, decussates and descends to innervate contralateral motor neurons that activate wrist/finger extensors. In humans, it is small and makes minor contribution to control of distal upper limb muscles
Reticulospinal tracts
to regulate muscle activity in trunk and proximal limb muscles, help with gross movements needed during walking, help with automatic anticipatory postural adjustments during movements like reaching, carrying objects, control of autonomic functions
Medial vestibulospinal tract
Receives information about head position in space from vestibular nuclei, Regulates motor neurons bilaterally to control neck and upper back muscles (extensors)
Lateral vestibulospinal tract
Regulates motor neurons ipsilaterally to activate trunk paravertebrals and proximal LE extensors while inhibiting flexors to maintain upright antigravity posture within BOS
Medial/Anterior corticospinal tracts
activate neck, shoulder and trunk muscles, prepare the postural system for intended movements and coordinate posture with the other medial tracts
Nonspecific motor tracts
Facilitate all types of motor neurons across spinal cord, Activated during intense stress and emotions, involved in sending descending pain-regulating information
Corticobulbar (corticobrainstem) tracts
control of muscles in head, activate cranial motor nerve nuclei bilaterally that innervate muscles of face (except lower half muscles), mastication, tongue, pharynx, larynx, and some neck muscle (SCM/traps)
Cortical motor areas
Premotor and supplementary motor area plan for complex movements, in association with M1
Alpha (α MNs) motor neurons
large cell bodies, large myelinated axons – connect to extrafusal muscles
Gamma (γ MNs) motor neurons
medium cells bodies and myelinated axons – connect to intrafusal spindle muscle fibers
Synergy involving muscles at same joint
activate other muscles at same joints
Phasic synergy - modulated in both amplitude and timing
by Ia afferents
monosynaptic
Synergy involving muscles at neighboring joints
activate muscles at other neighboring joints
Tonic synergy - modulated only in amplitude
by II afferents
bisynaptic/polysynaptic
Hemiplegia or -paresis
(lesion of corticospinal tracts high up in the brain, may retain some voluntary control due to intact reticulospinal tracts) – stroke, TBI, CP
Quadriplegia or -paresis
(lesion of MTs in higher spinal levels) - SCI
Paraplegia or -paresis
(lesion of MTs in lower spinal levels) - SCI
Hypertonia
abnormal high resistance to passive stretch
Spasticity
velocity dependent – in UMN pyramidal/extrapyramidal MT lesions (stroke, SCI)
Rigidity
velocity-independent – in basal ganglia lesions (Parkinson’s disease)
Babinski’s sign
due to lack of inhibitory control by corticospinal tracts on withdrawal reflex receptive fields, normal till 6 months age as corticospinal tracts not myelinated by then.
Signs of motor cortex/tract lesions (UMN lesions)
Paresis/paralysis
Abnormally high tone
Abnormally high reflex activity
Loss of fractionated movements
Abnormal synergies
Myoplasticity
Abnormal co-contractions – CP
Signs of motor neuron lesions (LMN lesions)
Paralysis or paresis - flaccidity
Decrease in muscle tone – hypotonia/flaccidity
Decrease or loss of reflexes (hyporeflexia)
Neurogenic atrophy – due to lack of trophic support to muscles
Clonus
Involuntary reflexive repeating contractions of a single muscle group in response to quick stretch – a manifestation of hyper-reflexia
Cause of Clonus
lack of descending MT control, allowing activation of oscillating neural networks in spinal cord
Myoplasticity
Adaptive changes in muscles in response to changes in neuromuscular activity level, occurs due to increased number of weak actin-myosin bonds, contracture.
feedforward mechanism
Anticipatory use of sensory information
feedback mechanism
Use of sensory information during and after movement to make corrections/adjustments
Mechanoreceptors
Touch, pressure, stretch, vibration
Thermoreceptors
respond to heating/cooling
Chemoreceptors
respond to chemicals
Somatosensations from skin (cutaneous)
touch, temperature, nociception