1. Gen Info
   1. Sensory Contribution to Mvmt Control
      1. Feedforward: anticipatory sense info to prepare for mvmt
         1. Feedback: sensory info during/after mvmt to make corrections
            1. Somatosensory info = IMPORTANT for motor learning
      2. Well-learned mvmt's = little conscious attention Requires visual, somatosensory, and gravitational info
   2. Motor Syst
      1. 1. Decision in frontal lobe 2. Motor planning areas activated 3. Control circuits regulate mvmt 4. Upper motor neurons (UMN) send signals -> spinal motor neurons -> lower motor neurons (LMN) 5. LMN -> sk. m's -> contraction -> move
      2. Voluntary mvmt = top down
      3. LMN's = info to m's
         1. cell bodies in sp cord/brainstem -> synapse -> sk m.
      4. UMN's = info to motor neurons sp. cord/brainstem
         1. arise in CC/brainstem -> descending tracts -> synapse -> LMN's/interneurons brainstem/sp.cord
         2. TRACTS: Postural/gross (auto sk. m. act.) Fine motor (mvm't limbs/face) Nonspecific (all motor neurons)
         3. Control circuits: adjust activity of UMN's
   3. Skeletal Muscle
      1. Sliding Filament Theory
         1. Subdivision of Sk. M.
      2. Muscle Tone: Resistance to stretch in resting m. Normal = titin + weak actin/myosin bonds Doesn't involve reflexes
         1. Stretch after long immob. = increased resist to stretch
            1. THIS ADDS NEW SARCOMERES
      3. Cocontraction = joint stabilization
2. Spinal Region
   1. spinal interneurons -> cord. m. contracts
      1. Single spinal nerve = myotome
   2. LMN Location: Ventral horn Actions innervate: medial pools = axial/proximal m's anterior pools = extensors posterior pools = flexors
      1. axons grouped by termination
   3. Coord of Mvmt
      1. 1. reciprocal inhibition: inhibition of agonist m's at agonist contraction via interneurons
      2. 2. m. synergies: coord. m. action: activity of m's activated together by NS
      3. 3. proprio body schema: proprio model of body in time and space; plans and adapts mvmts
      4. 4. stepping pattern generators: adaptable networks of spinal interneurons that activate LMN's -> flex/ext of hip/knee
         1. signals in anterior commisure
         2. cortical control also needed for ankle dorsi
      5. GTO: tendon tension -> interneurons -> excite/inhibit LMN's -> synergists/muscle *adjusts m. contraction
   4. Reflexes: M. Spindles
      1. Phasic
         1. brief stimulus response
      2. Tonic
         1. long stimulus response
            1. Parasympathetic inhibition prevents LMN firing; damage = no inhibition
      3. Cutaneous/Withdrawal Reflex
      4. H Reflex: monosynaptic reflex caused by electrically stimulating a nerve
         1. quantify AMN inhib/facili
         2. Afferent Fiber activity -> H Reflex
3. LMN's
   1. A and G Coactivation: depends on sensory info spinal circuitry descending commands
      1. Convey info to extra and intrafusal m. fibers
      2. A: large myelinated; extrafusal G: med myelinated; intrafusal
      3. Henemman's Size Principle: SO -> FOG -> FG
      4. Motor Unit: 1 AMN and m. fibers it innervates
   2. LMN Disorders
      1. CAUSES: trauma degen/vascular disorders tumors
         1. RESULTS IN: reflex loss atrophy flaccid paralysis fibrillaiton
            1. PREVENTS M CONTRACTION
      2. Polio: invades/destroys LMN's
4. Disorders
   1. MN Lesion Signs
      1. Paresis/Paralysis
         1. decreased ability to generate m. force and m, bulk
         2. Complete lesion of peripheral nerve
      2. M. Atrophy
         1. loss of m. bulk
         2. LMN's don't provide stimulation *UMN atrophy is slower b/c LMN are still stimulating m's
      3. Invol M Contractions
         1. spasms cramps fasciculations (quick twitches) myoclonus (brief invol contr) resting/intention tremors fibrillation
         2. UMN/LMN disorders
      4. Abn M Tone
         1. resist to stretch in resting m
         2. Hypotonia (velocity dep and rigid) Flaccidity (lack of resist to passive stretch)
         3. LMN lesions acute UMN lesions dec disorders chronic UMN lesions basal ganglia disorders
      5. Abn Reflexes
         1. Subtopic 1
      6. Disturbances of Mvm't Efficiency and Speed
         1. Subtopic 1
      7. Impaired Postural Control
         1. Subtopic 1
   2. Spasticity
      1. Developmental Spasticity: UMN overactivity affecting vestibulo/resticulospinal tracts
5. UMN's
   1. All motor signals from: brain -> sp. cord cerebrum -> cranial nerve LMN's in brainstem
   2. Classified by synapse location
      1. Medial: postural/girdle muscles
         1. coord. automatic gross mvmt's
         2. Signal Initiation: brainstem
         3. Axons Loc: medial white matter
         4. Tracts:
            1. Reticulospinal
            2. Bilateral postural m's and neck responses to visual/auditory input
            3. Flexion Synergy: unwanted combo of mvm'ts
            4. Originates: reticular formation
            5. Medial Vestibulospinal
            6. Neck
            7. Originates: medial vestib nuclei
            8. Lateral Vestibulospinal
            9. lateral vestibular nuclei responds to gravity info
            10. Postural M's
            11. Medial Corticospinal
            12. medial cortico cortex internal capsule anterior brainstem
            13. neck, shoulder and trunk muscles
      2. Lateral: m's for fractioned mvmt's and face/neck m's
         1. Fractionation: ability to use indiv m's independently of others
         2. Descend in LSC synapse LMN pools
         3. Lateral Corticospinal Tract
            1. fractionate mvmt of distal limbs
            2. Originate: primary motor premotor supplementary motor cortex
            3. Prepare Areas: lateral premotor supplementary premotor
         4. Rubrospinal Tract
            1. extend wrist and fingers
      3. Corticobrainstem Tract
         1. Innervates m's: face tongue pharynx larynx trapezius sternocleidomastoid
         2. Originates: motor areas of CC
      4. Throughout: local reflex arcs
         1. Cerulospinal
            1. interneuron/motor neuron activity enhancement t/out sp. cord
            2. Originates: Locus coeruleus in brainstem
         2. Raphespinal
            1. Same
            2. Originates: Raphe nucleus in brainstem
   3. UMN Syndromes
      1. CAUSES SCI MS trauma stroke/CVA
         1. RESULTS IN: paresis/lysis fractionation loss abn reflexes velocity dep hypertonia abn cocontraction abn hypertonia
      2. PARA's
         1. Paresis: UMN lesions -> m. disuse/2ndary changes in NS/atrophy
         2. Paralysis LMN loss due to lesion
      3. ABN REFLEXES
         1. Abn Cutaneous Resp: m spasms due to stimuli SCI in adults (SPINAL SHOCK)
         2. Hyperreflexia: loss of inhibitory input (CORTICOSPINAL) excessive LMN response of afferent input
         3. Clonus: involuntary, repetitive, rhythmic single contractions lack of UMN control
         4. Clasp Knife Resp: resist drops at certain ROM if passively stretched
      4. VD HYPERTONIA
         1. Myoplasticity: adaptive changes in response to prolonged positioning
         2. Spasticity: neuromuscular overactivity post UMN lesion
            1. Hyperreflexia: no corticospinal inhibition to LMNs excessive LMN resp to muscle spindle output
            2. Brainstem UMN: extra reticulo/vestibulospinal tract signals to LMN's
   4. UMN Lesions
      1. Spastic CP: lesion affects corticospinal/brainstem tracts in perinatal period
         1. TREATMENT: task oriented gait training constraint mvmt therapy (hemi CP) Botox medications
      2. Stroke Middle Cerebral Artery: (Adult Onset Spasticity) CVA affects corticospinal/reticular tracts -> brainstem reticulospinal tract -> extra muscle contraction *RETICULOSPINAL TRACT = VOLUNTARY CONTROL OF PARETIC M'S POST-STROKE
         1. contractures: m's stay in shortened position
         2. ^ weak binding of actin/myosin
         3. TREATMENT: hand/finger mvmt against resistance upper limb robotic therapy botox cycling task oriented gait training (w/ treadmill?)
      3. SCI: (Spinal Spasticity) UMN tracts severed -> interneuron/LMN excitability -> hyperreflexia
         1. RESULTS: excessive stretch reflex cross-bridge binding ^ resist to m. stretch
         2. iSCI RESULTS: paresis hyperreflexia contractures
         3. TREATMENT: activity based therapy Neuromuscular activation below lesion somatosensory input to SC
      4. ALS: destruction of somatic upper, brainstem and SC motor neurons