Exam II (Neuro) PDF

Lower Motor Neurons and the Neuromuscular Junction L. Gilchrist DPT 5035 Jan 2020 Objectives: Describe the location, function, and structure of upper and lower motor neurons. Describe the structure and function of the neuromuscular junction (NMJ): Motor...

Lower Motor Neurons and the Neuromuscular Junction L. Gilchrist DPT 5035 Jan 2020 Objectives: Describe the location, function, and structure of upper and lower motor neurons. Describe the structure and function of the neuromuscular junction (NMJ): Motor end plate Excitation-contraction coupling and electro-mechanical delay End plate potentials Describe the structure and function of motor unit types: Components of a motor unit Types of motor units -- SO, FOG, FG Innervation of motor units (MU) Describe motor unit recruitment: Size principle and its exceptions Gradation of muscle force (twitch summation) Firing threshold and rate coding of force Interaction of recruitment and rate coding Readings: Neuroscience Ch. 16, Netter plates 5.6, 5.9 Motor System Organization Activation of muscle Occurs by activation of Lower MNs Lower MNs activated by: Sensory Neurons (reflexes) Upper MNs ~ real workers Local circuit interneurons that ex) Stepping on the sharp or not activate item (complex( & Location of Lower MNs Cell bodies are located in the grey matter of spinal cord ventral horn. Also called: alpha motor neuron LMN cell bodies arranged in clusters 1 to 3 (across SC segments), according to varo which muscle they innervate. Each cluster is called a motor neuron pool. Cell bodies in one pool all send their axons to muscle fibers in the same muscle. growing kids : LMN will only Innervate muscle fixers to one muscle multiple affect abnormal atypical CNS : could muscleswl one innervation Topographic Location on LMN Pools Proximal Axial (Postural) Muscles are located more medially in the SC More distal muscles (Dexterity) located more laterally in SC Remember is d UM dorsal column not ventral  if it wasn't scatter ? Q: What would happen of area A It would : be biased to one Motor Neuron Pathway muscle unequal load ? the - movement of muscle pure Dendrites and Cell Body in the Spinal cord Axon Leaves the SC via the ventral root Axons are carried in bundles, n within a segmental nerve, then a peripheral nerve. Terminal Endings Each motor neuron axon branches synapses to many muscle fibers within the ⑨ same muscle, called a motor unit. The muscle fibers in a motor unit muscles are scattered throughout a whole muscle.  Neuromuscular Junction specialize Synapse between a motor neuron (MN) and its muscle fiber Electrical signal passed on (via a chemical messenger) from the neuron to muscle cells membrane neuron · releases alpha motor releases neurotransmitter similar to any neuron release neurotransmitter  NMJ Motor Neurons release Acetylcholine (Ach) Always excitatory * never inhibitory on muscle synapse Synaptic Cleft Small gap Width is very small (20-30 nm) allowing rapid diffusion neurontransmitPART Motor End Plate BY ENZYMeS At the synapse, muscle cell membrane has synaptic gutter Within the gutter junctional folds NMJ Neurotransmitter receptors are imbedded in the post-synaptic membrane. closest part where NTs release are Located at the apex (peaks) of the folds ACh nicotinic type receptors in muscle Enzyme called acetylcholinesterase (AChE) is also located in muscle cell membrane Breaks down Ach after it has activated the muscle ↓ 1 APS Located in the depths of the junctional folds. ion channel will--twitch remain open enzyme breaks apart Ach activate goal : > - LMNs Nicotinic Ach Receptor Ionotropic direct and innel Na Channel -rushes in membrane - depolarizes Found in NMJ muscle fixers Muscarinic Ach Receptors – not at NMJ! ↑ Metabotropic und menger ion channel 5 different types M1, M3 & M5 are excitatory receptors M2 and M4 are inhibitory ↑ "What receptor on does it open Found in: post synaptic " Brain membrane ! Heart Smooth muscle Parasympathetic nervous system Activation of the Muscle Fiber by Ach ACh binds to receptors on the post-synaptic membrane. Opens chemically-gated cation channels (both Na and K can pass through) End Plate Potentials Graded depolarization of the muscle cell, called end plate potential (EPP). More transmitter released by the MN → larger the EPP more depolarization fibers in muscle Safety Factor Threshold for a muscle cell action potential is generally reached due to large depolarizations by EPP Neuromuscular synapses have a large safety factor, assuring that if the MN fires an action potential, it will activate its muscle fibers Definition of a Motor Unit Motor unit (MU) = one motor neuron (MN) its soma, axon, and all of the muscle fibers that it innervates Muscle fibers are only innervated by 1 MN Each MN may innervate multiple muscle fibers These fibers are generally spread over a wide area of the muscle and not clustered together Each MN innervates only muscle fibers in one muscle CNS can activate one motor neuron → one motor unit but the brain can NOT activate a single muscle fiber When one motor neuron is activated by an AP, ALL the m. fibers in its motor unit contract together Precision of Control Size of the Motor Unit determines precision of muscle control Fine Control: Small motor units provide precise control and small force. For each additional MN that is activated, only a few muscle fibers will contract → gradual increase in muscle contraction force Gross Control: Large motor units -> more muscle fibers activated & more force For each additional MN that is activated, many muscle fibers contract simultaneously → large increase in m. contraction force. Useful for strength, but not for delicate control. Motor Neurons and Muscle Fiber Types Motor Units and Motor Neurons vary in size Small MNs Innervate small motor units composed of small “red” muscle fibers Slow (S) motor units Fatigue resistant – good for sustained contraction Large MNs Innervate larger, pale muscle fibers with few mitochondria Fast, fatigable (FF) motor units Good for fast, strong, but not prolonged mm contraction Medium MNs Properties between the others Fast, fatigue-resistant (FR) motor units Motor Fiber and Unit Types A. Tension Generated - 1 AP B. Tension with multiple APs C. Fatigability Muscle activation Most muscles, S motor units easier to activate S motor units are tonically active during static tasks (ie. standing) If need larger mm force for activity – activate the larger more fatigable motor units Muscles may be specialized Soleus (postural mm) mostly small motor units Gastroc (needed both for posture and power) has both small and large motor units Activation of Alpha Motor Neurons Activation of a motor neuron pool – Size Principle Recruited in fixed order Weak inputs – activate small MNs and small motor units As synaptic inputs become greater – larger motor neurons are recruited → large mm forces AP Frequency within a MN As the number of AP increases and get closer together, mm fibers begin to not fully relax between APs and get summation At highest rates of firing get strongest and fused (tetanic) contractions Motor Unit Identity and Plasticity Who determines the identity of the motor unit? Surgically altering the innervation of a muscle fiber changes slow mm fibers into fast mm fibers The MN determines the characteristics of the muscle fiber Can you change the properties of an established motor unit? If you change the firing pattern of the MN (from a slow firing patter to a fast firing pattern) – the mm will start to have fast characteristics  Exercise and Motor Units Appropriate exercise training can change the firing pattern of a muscle group Before and after dynamic training of ankle DF make faster as it activated · can Muscles of the Head and (some) Neck Innervated by Lower MNs from the brainstem – not SC Cranial nerves – include: Occulomotor, Trochlear, Abducens, Facial, Glossopharyngeal, Spinal Accessory, Hypoglossal tongue Each has a nucleus (cluster of cell bodies) in the brain stem Axons exit the brainstem and run through the cranial nerve before innervating the mm Damage to Lower MNs Damage to LMNs (cell bodies, axons, terminals) Paralysis – weakness Loss of reflexes – areflexia Loss of muscle tone – flaccid mm motor > muscle - atrophy - muscle fiber decreases Atrophy ↓ no tone Diseases of the Lower MNs Polio it enters the cis motors included is-SC When Alpha Poliovirus > - it killsof MNS In about 0.5% of cases, enters CNS where it destroys Lower MNs causing paralysis In 2015 only 100 new cases world-wide Acute Flaccid Myelitis - not a stroke Rare but increasing disease in children Damages MN in SC - immune reaction that causes Sudden onset of arm or leg weakness Amyotrophic Lateral Sclerosis (ALS) mixed neuron Progressive degenerative disease Can impact both Lower motor neurons –causing weakness, atrophy – and Upper motor neurons – causing spasticity Disease of the NMJ are healthy LMN Myasthenia gravis (MG) is the best-known example of a NMJ disease. Symptoms: Weakness and reduced endurance of voluntary muscle. Ptosis : droopy eyelid Patient appears to fatigue abnormally easily. Cause OF MG: An auto-immune disease function isn't Antibodies to the muscle ACh ion channel receptor proteins E primary there Therefore, the number of functioning receptors is reduced. *ACh release occurs at synapse, but can't bind to muscle cell for AP Muscle Spindles and Proprioception L. Gilchrist DPT 5035 Objectives Describe the structure and function of joint receptor types Describe the structure and function of muscle and tendon receptors: Muscle spindle (group Ia and II endings) Golgi tendon organ (group Ib ending) Describe the structure and function of gamma motor neurons: Gamma static and gamma dynamic endings Effect on spindle's stretch response Effects on spindle's contraction response Describe muscle and tendon spinal reflex circuits: Spindle reflexes (phasic stretch, tonic stretch, Hoffman, vibration) GTO reflex (autogenic inhibition) Readings: Neuroscience Ch 16, Netter 6.6 Proprioception INCLUDES static Limb Position and Kinesthesia (ability to detect movement) Usually are lumped together into proprioception, technically different 2 Mediated by receptors in the joints, muscles, and skin  fibers a ope biggerasmuse gets uptic potential Muscle Spindles: Located within belly of muscle Arranged "in parallel" with the skeletal muscle fibers Provide the CNS with information about length - and rate of change in length of muscles Also provide afferent input for muscle stretch reflexes Contain motor efferents that alter the responsiveness of the receptor Vary in number and density as fine motor control is required Axon -1 motor neuron 2 sensory  Muscle Spindle Anatomy Each spindle contains 2 –12 fibers of modified striated muscle Intrafusal muscle fibers (regular striated muscle is extrafusal) Spindles run between the extrafusal mm fibers in parallel Types of intrafusal muscle fibers: Nuclear Bag: longest and largest L Nuclear Chain: shorter and thinner How the nuclei are set up Innervation of Muscle Spindle: Afferents: (Sensory) Ia and II nerve fibers Efferents: (Motor) Gamma motor neurons go into the intrausal **  Sensory Afferent Endings Afferent Innervation: 2 different sensory endings Ia fibers (annulospiral): Wrap around the central region of the intrafusal fiber Responds both phasic (initiation of movement) and tonic (position) Phasic output is maximal during quick stretch (ie: When something changes + give constant info (Kinesernia & position) tendon tap) Tonic is sustained during constant stretch I difference in speed II fibers (flower spray): W End mainly on the nuclear chain fibers Adjacent to the primary endings Only tonic response – position sense Afferent Response to Stretch Initiate passive movement of a joint: During movement (dynamic phase) – Ia fibers active At position (Tonic phase) → both Ia and II fibers active Ia II  Efferent Innervation of Muscle Alpha MNs – largest, innervate extrafusal muscle fibers Can be stimulated monosynaptically by: Ia and II afferents of mm spindles (reflex) Corticospinal tract fibers (voluntary) Brainstem motor reflexes Gamma motor neurons innervate intrafusal muscle fibers DO NOT innervate extrafusal mm fibers Tend to discharge spontaneously Receive input from the reticular formation, vestibular system, cerebellum, and basal ganglia Activity of Muscle spindles during Muscle Contraction Contraction causes shortening of both extrafusal and intrafusal mm fibers If no other input → would decrease Ia afferent activity Gamma MNs activated to keep the mm spindles at same length as the extrafusal mm fibers → prevents slack in receptor eX) Diceps contract Voluntary movements are normally activated by co-activation of alpha and gamma motor neurons. ALPHA GAMMA AKA COACTIVATION Prevents “unloading” of the mm spindle fibers and thus allows for mm spindle to continue to provide information to the CNS  like no stretch Signals of holding eX) think cup a coffee pouowing andsomeone Phasic Stretch Reflex (aka: myotactic, tendon-jerk, deep tendon reflex) Stimulus: Quick stretch to the muscle (usually via tendon tap) Sensory afferent: Muscle spindle, Group Ia (and II) sensory axons Synaptic connection: Monosynaptic, excitatory SC single synapse to Motor: alpha motor neuron to the same muscle During this same stimulus the Ia sensory afferent also: Activates a Ia Inhibitory Interneuron HAMSTRINGS Inhibits alpha MNs to the Antagonist muscle AKA Causes relaxation of the antagonist. Tonic Stretch Reflex ongoing stretch Stimulus: maintained muscle stretch (static m. length). Sensory Afferents: group II (and group Ia) sensory axons. Synapses to: II axons synapse on alpha MNs that innervate the same muscle in which the spindle is located (agonist) Also synapse to synergist motoneurons same actions other muscles that do the Inhibit antagonists ↳ recruit additional APHA This contraction creates resistance to the muscle MOTOR Neurons AND stretch  Golgi Tendon Organs (GTO) Muscle fibers AND TENDON between extrafusal Located at the Musculotendinous junction Arranged in series with muscle fibers Very sensitive to changes in muscle contraction ↳ main focus is stretch on tendon muscle contraction Secondary a way -> we are creating stretch on tindon due to Autogenic Inhibition = Inverse Myotactic activate golgi tendon using a interneuron to inhibit the same muscle that we just contracted Reflex - muscle to extend - do relaxation to transition the other then contraction * Increase ROM by stretching through * facilities the antagonist STIMULUS: Muscle contraction (weak or strong) or muscle stretch (ROM extremes only). RECEPTOR: Golgi tendon organ (GTO) AFFERENT: Group Ib axon CIRCUIT: Disynaptic (one interneuron) RESPONSE: Inhibition of homonymous muscle and its synergists, and facilitation of the antagonist.  Joint Receptors Articular hyaline cartilage is not innervated (= Aneural). And few nerves in fibrocartilage (such as menisci, labrum, etc.) ? ↳ not primary source for contraction Golgi Ligament Endings Thickly encapsulated, profusely branching sensory nerve axon Resembles a Golgi tendon organ (GTO) LOCATION: At ligament/bone junction. Found in all joints, except cervical spine. SENSE: Extreme stretch tension on ligament La"get out of this position" Ruffini Endings Thinly encapsulated, spray-like endings LOCATION: In fibrous capsule & a few extrinsic ligaments. Found mostly at proximal joints, few at distal joints SENSE: Maintained stretch tension on joint capsule at extreme ROM Direction and amount of joint stretch/movement (flex/ext.) Rate/speed of joint stretch Sensitive to distension of joint capsule, as during joint swelling = stretch cross thatex)knee damage section Pacinian Corpuscle vibration sensation Layered capsule, like the Pacinian cutaneous receptor. LOCATION: In fibrous joint capsule, at 3 synovium/fibrous interface, & in bone periosteum. sitive Present at all joints, but distal joints more than proximal SENSE: movement onset & termination Low firing threshold so they respond to very small deformation * newve damage a peripher good at telling us  * respond to Golgi-Mazzoni Corpuscles do w stretch Thin capsule, enclosing multiple nerve endings. LOCATION: In fibrous joint capsule, perpendicular to capsule surface ex) stairwalking down SENSE: compression, not stretch of capsule. Low firing threshold, are very sensitive  receptors X pain Free Nerve Endings Profusely branching bare sensory axon embedded in tissues LOCATION: In ligaments (very high concentration here). Also present in fibrous capsule, synovium, and intra-articular fat pads (as exists in knee). Found in all joints. SENSE: Multiple stimuli (multi-modal): Mechanical deformations (mvmt->capsule stretch) Chemicals released from injured tissues swing anmage Pain (noxious stimuli) Proprioception Integration of information from muscle, joint, and cutaneous receptors Redundant system Important therefore back up system > - Joint movement in Mid-range: Primarily dependent on activation of muscle receptors Muscle Contraction: Muscle spindles maintain same level of activity through alpha-gamma co- activation stretch of flexion out *Pic has no gamma coactivation → no APs GTO activated through stretch on tendon sense active muscle contraction Muscle Passively Stretched Muscle Spindles: activated GTO: Tendon only gets stretched at extreme ROM In mid-range generally quiet Joint Movement at End Range receptor Ligament Joint receptors provide joint position sense at extremes of joint range Serve a protective function, by informing the CNS when we are about to exceed the normal range of the joint, potentially tearing ligs. Stretch of one side of the joint capsule and increased stretch on ligaments activates sensory axons that facilitate motor neurons to muscles whose contraction would relieve that stretch Pathways for Proprioceptive Information Conscious Proprioception: Paths to the Cortex Processed with tactile information via the Dorsal Column Medial Lemniscus Tract same light touch sensation as g Mediates the sense of: Limb position Motion (active and passive) Muscle tension Effort Unconscious Proprioception and cerebellum send to sc moturpan-motor error-learnhow tenter Paths to the cerebellum & what my action From the Lower extremities and Trunk: Ventral Spinocerebellar Tract Dorsal Spinocerebellar Tract From the Upper Extremities: Cuneocerebellar Tract Rostral Spinocerebellar Tract Use of Proprioceptive Information in Central Processing - I Motor Control (Co-ordination) Project up to the cerebellum, which is the site of motor coordination Cerebellum controls performance of learned skills, such as typing & sports. To coordinate movements, the cerebellum needs continuously up- dated information about limb position, to determine which muscles to contract to produce the desired change in limb position (movement). Thus, joint input guides & helps correct on-going movement Use of Proprioceptive Information in Central Processing - II Motor Learning Cerebellum is also responsible for motor learning, Uses proprioceptive input to assess prior movements, to make improvements for the next performance. Stores a "motor memory" of the correct sequence of signals, so that it knows when a movement "feels right". Use of Proprioceptive Information in Central Processing - III Posture & Balance Control Cerebellum also controls posture and balance via reflexes Needs lots of current information from joint receptors about head & limb position, in order to plan balance-correcting movements EXAMPLE: Ankle sway -> trunk flex/ext. to prevent fall Acute vs. Persistent Pain L. Gilchrist DPT 5035  Objectives Describe the processing of pain information by the brain, including the pain neuromatrix. Describe the neurologic changes that can lead to chronic/persistent pain. Describe the difference in pain generators for acute vs. chronic/persistent pain.  Acute vs. Persistent Pain Acute Pain – Function Topotential let body if there is tissue damage or for tissue damage – Lack of acute pain – helpful? Not particularly helpful - some of born with no pain receptors Persistent = Chronic Pain – Function? Non functional pain - something in the peripheral Negative connation with chronic pain  Persistent/Chronic pain History of pain lasting 3 (to 6) or more months Pain lasting longer than tissue healing Is it the same as long-lasting acute pain? Ongoing pain is long lasting Chronic pain = pain is there but tissue is healed  Acute vs. Persistent Pain Acute Pain – Alarm signal of threat (or potential) to system – Based on sensory signals from periphery – Due to actual or potential damage Persistent Pain – Sensory Inputs may not be basis For pain – No longer related to damage to periphery – Not always based on intensity of stimulus from the periphery Changed nervous system processing  Types of Persistent Pain Episodic pain – such as recurrent headaches and migraines Ongoing disease – such as in arthritis and cancer Acute pain that does not resolve – Chronic low back pain, fibromyalgia Nocieceptive Pain View Pain Neuromatrix View  Mechanisms In acute pain that transitions to persistent pain, an injury occurs that activated nociceptors in the normal fashion Often times this is a musculoskeletal insult such as whiplash injury or low back pain When the injury does not heal as early as expected, the dorsal horn neurons become sensitized  Sensitized dorsal horn neurons Synaptic changes at the thalamus, cingulate cortex, insular cortex, and somatosensory cortex Synpatic lvl changes [ Central Sensitization and Morphometric Changes z Change in volume of diffeernt are of the brain that is processing that pain  As sensitization occurs, pain also is interpreted from non-nociceptive mechanoreceptors Light touch that transition to painful stimulus Also reduction in the activation of pain inhibiting centers in the CNS – Anterior cingulate cortex – Medulla  Example of changed pain modulation Malfunctioning pain modulation is thought to be a mechanism of fibromyalgia processing > - Central > - pain - fatigue Exercise interventions issue – Isometric and aerobic exercise activates opioid and adrenergic pain inhibition in normal subjects – Same exercise increases experimental pain ratings in patients with fibromyalgia and chronic fatigue syndrome (Staub et al, 2005; Whiteside et al, 2004)  Changes to the CNS Functional and structural changes to CNS Pain Central Network (Neuromatrix)  Volumetric Changes Changes have been demonstrated in: – Cingulate cortex Sautedge – Thalamus – Basal Ganglia a – Frontal cortex – Insular cortex – Brainstem Changes in CNS structure with chronic pain Chronic back pain - decreased prefrontal cortex - decreased thalamic cortex Migraines - decreased anterior cingulate cortex - decreased anterior insular cortex - decreased temporal lobe cortex  Functional Changes Using functional MRI in patients with chronic pain Asked patient to think about movements  Change in Context Change – cause or consequence? – Multiple studies suggest that morphologic changes are secondary to constant pain – Experience-dependent neuroplasticity ↳ the more you use that area fire Digger brain Permanence? – Studies of hip OA demonstrate that when pain is removed by surgical intervention, structural differences may receed. (May, 2011) & removal in peripheral > - is it a issue ?  Peripheral issue healed For patients with chronic/persistent pain – Treatment of the painful region unlikely to be successful – Unless there is new or ongoing tissue damage at that region beyond pain perception – Education is essential how brain thinks outcome : change of the damage  Context is Important from brain comes - All pain Pain is perception Influenced heavily by: – Environment E moreception – Stress – Meaning assigned  What do patients need to know about pain and the brain? All pain is real – Even if it does not start in the periphery anymore – The brain is trying to understand the signals it is receiving from all areas  Chronic pain patients have enhanced sensitivity of their alarm systems Could be sensitization or disinhibition Thoughts and beliefs are nerve impulses that influence pain (+ or -)  Other than the CNS – who else is involved in maintaining pain? Sympathetic NS: – Releases adrenalin when perceives a threat – Persistent release in chronic pain – Chronic inflammation can increase the adrenalin receptors  Parasympathetic NS: – More active during rest and sleep – Disturbed in chronic pain T PARASYMADHA  Endocrine Response Similar to ANS, but effects last longer Threatening inputs, including memories – Pituitary releases ACTH – Travels to adrenal gland > stress - – Adrenal gland releases cortisol hormone – Persistently high cortisol linked to: delay Poor healing Memory loss Depression 3 Tissueeling  Immune System Long-term stress and pain increases pro-inflammatory cytokines Damaged nerves are particularly reactive to pro-inflammatory cytokines The CNS can activate the immune system to produce cytokines How to spot potential - centralized pain work on brain Multiple diagnoses Persistent pain after tissue healing should occur Spreading – “smudging” Traveling Worsening problem Gentle movement makes it worse - issue Less predictable -persistant Linked to thoughts and feelings emotional ~ cognitive  Misconceptions Link between tissue damage and level of pain – Implies that a person with chronic pain has unhealed tissue damage – Increased injury → Increased pain Result: PT “Chases” the pain Chronic/Persistent pain can be THE diagnosis  Interventions Need to get past the simple pathway and think about pain broadly  I Implications for Persistent Pain How to do that For patients in acute (subacute) pain – Limit the amount of time that patients spend in acute nociceptive barrage – Be especially vigilant with deep tissue injuries as they more often turn into chronic issues – Treat with appropriate therapies targeting the tissues damaged without excessive increase in pain BAD REGRESS "NO PAIN NO GAINK =  Treatment of the painful region unlikely to be successful – Unless there is new or ongoing tissue damage at that region e 2 yo back pain – Realize that their pain responses will be heightened Manual therapies pt can be reliant - – Can reinforce the maladaptive changes to CNS Motor control training – If hypermobile or altered movement patterns Aerobic exercise below painful threshold and without post-exertional symptom increase  Cognitive aspects While persistent pain is primarily biological, it is influenced and reinforced by cognitive factors away – Catastrophizing pain - go won't – Hypervigilance consistently - don't pain (v) Ask area the if its safe don't limit – Avoidance behaviors - – Somatization don't - themlet on the focus area  Some of the inappropriate cognitive patterns may be seen during the subacute phase > - risk for persistant pain Inappropriate cognitive factors appear to be closely related to movement performance Changing pain beliefs has been shown to begin to normalize movement patterns in the absence of motor retraining  References Butler D & Moseley L. Explain Pain, second edition.2014 Nijs J, Van Houdenhove B. From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: application of pain neurophysiology in manual therapy practice. Manual Therapy 2009, 14:3-12 May A. Chronic pain may change the structure of the brain. Pain 2008, 137:7-15. May A. Structural brain imaging: a window into chronic pain. Neuroscientist 2011, 17:209-220 Pain Sensation L. Gilchrist DPT 5035 Objectives Diagram the neural pathways from somato-receptors for pain to the primary somatosensory cortex. Differentiate the function of A-delta and C-fibers in pain processing Describe how interneurons can modulate pain information using inputs from the peripheral and central nervous system. Readings: Purves Ch 10, Netter Plate 9.3 Function of Pain Warning signal Actual or potential tissue damage Lack of pain sensation > - shorter lives due to damagedtissues Note: Temperature will be covered only cursory here Temperature travels in the same pathways as pain pain a Tempraptors along ou run onways came the  Nociceptors Respond to both directly and lot damage indirectly to noxious stimuli Mechanical trauma – direct stimulation acrophage i-from s >↑) > - Chemicals released by traumatized tissues – indirect - free nerve endings not just in skin · responds activate pain receptors can directly pH shift activation of noceptives · localized improvement from bites ex) mosquitoe inflamed us no feeling Nociceptor Types Thermal Nociceptors – activated by extreme temperatures A delta (thinly myelinated) fibers faster pain receptors not as fast aslight toua E Mechanical Nociceptors – activated by intensive pressure to skin A delta fibers Polymodal nociceptors – high intensity mechanical, thermal, and chemical stimuli C fibers – unmyelinated (slower conduction) These three types are widely distributed in the skin, deep tissues, and viscera. Free nerve endings Most nociceptors are Free nerve endings: Bare sensory axon tips, residing within the dermis and epidermis of the skin and in some mucous membranes  Fast pain vs. Slow pain Fast pain relates to the first signals to reach the CNS Those carried by A delta fibers (fast conductivity) chemically Generally felt as a “sharp” pain 3 mechanically Slow Pain related to the later longer lasting signals to the CNS Carried by the C fibers Felt as “burning” pain don't vice perceive versa snarp > - initial pain but something on foot sunroa congongain longrang ex) Step that going to burnung a is Doi split - hurt  ↓ Similar a ch Nociception – 3 neuron path O First Order Neuron: Receptor to Spinal Cord Activated by tissue damage or dorsal potential tissue damage O Axon from the nociceptor to the spinal cord with the cell body Located in the Dorsal Root Ganglion (DRG) ateral Axons terminate in the dorsal horn gray matter Ast synapse Pain fibers terminate in outer layers crossthe of the dorsal horn (more specific to only nociceptive fibers) Referred pain same projection as somatic neuron Convergence of somatic and visceral nociceptors onto the same dorsal horn neurons Ex: Brain interprets this pain signal as coming from the arm not the heart Second Order Neuron ⑨ Spinal cord → Spinothalamic Tract → Thalamus passesa Most axons cross the spinal cord (FYI: via the anterior white commissure) Crossing occurs within same segment where sensory axons entered or within one segment Axons ascend spinal cord in the lateral spinothalamic tract O Terminates in Thalamus O FYI: specifically the ventral posterior lateral nucleus (VPL) Additional Branch off of the ST Tract Branch comes off of the tract in the brainstem → reticular formation (alertness) = Spinoreticular tract - Increases alertness when you are - in pain wakea to reticular o going -goodlifepreservingskilsour the = formation are you of nuclei) in pain (set cat 3 rd Neuron postcentral set gys > - Thalamus → Somatosensory Cortex Axons ascend through the Internal Capsule Then fan out to the cortex through the cortical radiations Cortical Terminations in Primary Sensory Cortex – primitive sensory perception R body L Brain Located laterally in the parietal cortex Conscious perception of localized sensation Opposite side of the body Other cortical areas Limbic System: Processes the emotional components of pain Insular Cortex: Process information on internal status of the body Regulates autonomic functions ) pain L into is ↑ DP or HR Modulation of Pain Information light touch Gate theory of pain: Non- SC it in hid nociceptive inputs inhibit the nociceptive the firing of the spinal cord nociception neurons So if you have pain in an area 2 excitatory neuron n terneuron Inhibitory a (your elbow), when you rub your inhibitary elbow, it doesn’t hurt so much. post on synapti pain receptors Theoretical basis for TENS (Transcutaneous Electrical Nerve Stimulation) Reduce Stimuli of pain information to brain Other Inhibitors From Brainstem: Stimulation of the Periaqueductal gray (surrounds the third ventrical in the midbrain) produces analgesia Endogenous opioids Enkephalins and Endorphins Part of the answer of why “stress-induced analgesia” occurs Released into the blood stream Interacts with receptors at all levels of the nervous system Clinical Pain Syndromes to nerve fibers irritated damage are Allodynia: Pain resulting from normally innocuous stimuli Ex: Brush of clothing after sunburn or Getting out of bed morning after a hard workout (if you are not in shape!) ex) showering Hyperalgesia: Excessive response to a normally noxious stimuli Ex: Recent report that mammograms (normally somewhat painful) are perceived as being more painful in patients with fibromyalgia Mechanism: Possibly a hyper-excitability of the dorsal horn neurons Both peripheral and central mechanisms proposed Occurs after a prolonged or severe injury Nociceptive vs Neuropathic Pain Nociceptive Pain Neurogenic/Neuropathic Pain Pain resulting from the direct Results from direct injury to the activation of nociceptors in the nerve in PNS or CNS skin or soft tissues. Includes: Actual or potential tissue Complex Regional Pain Syndrome damage (CRPS) Post-herpetic Neuralgia Diabetic Neuropathic Pain Cancer Pain Electromyography (EMG) DPT 5035 Laura Gilchrist Objectives Describe the evaluation of nerve integrity based on EMG What are the abnormalities that can be detected and what are the clinical findings on EMG that would indicate Prepare to evaluate the finding from a clinical EMG study  Electromyography Essentially the study of motor unit axon potential (MUAPs) Reminder: a motor unit is the alpha motor neuron and all of the muscle fibers it innervates not listening to just the motor hevron When one motor neuron fires, multiple muscle fibers contract, muscle fibers are distributed through the muscle and not clumped together Images: Medscape: emedicine.medscape.com/article/1846028-overview EMG Recording Electrode placed either over or into the muscle of skin Area error moves SEMG – surface EMG, used for: past muscle Biofeedback training of muscles Nerve conduction velocity tests Kinesiologic investigations understand which exercise would Activate certain Muscle Needle or wire electrodes – used for recording clinical/diagnostic EMG Fine wire electrodes either monopolar or concentric Set-up and Reading Technical Aspects Signal amplification and filtration Signal is amplified as the potentials are very small Filter out extraneous “noise” EMG data from the recording electrode is compared against a reference electrode with subtraction of signals occurring at both electrodes Example: heart contractions also create electrical signal through body, but “seen” at both the recording electrode and the reference electrode so subtracted out Thus – get only activity specific to the recording electrode or the muscle of interest Size of EMG Potentials Factors that impact the size of recorded potentials: Proximity of muscle fibers to electrode Number and size of muscle fibers in the motor unit Distance between fibers in the motor unit Size of the recording electrode hear another muscle contracted can you Cross-talk: Electrodes may record activity from muscles other than the target due to volume conduction. (in LE up to 20%) Need careful electrode placement, also some technical solutions StMG more wi then needle Clinical EMG Examination: Observation of electrical activity in a number of different muscles Choose the muscles based on suspected pathology Also will chose some muscles to rule out other pathology Example: If UE pathology suspected, will also chose opposite UE and some LE muscles to rule out systemic pathology EMG data needs to be interpreted in context of all other clinical data  peripheral nerve besis of 3 is 1. What lois of pathology 11. What primary innervations & Spinal segment 111 Pattern of Emg Normal EMG Signals In each muscle, what should you see? Insertional Activity: Spontaneous burst of activity when needle is inserted Normally lasts less than 300 ms myocitis innervation Increased: in denervated or inflamed muscle lost peripheral its Decreased: in fibrotic muscle - doesn't contract like muscle fibers Normal vs. Abnormal muscle at rest Muscle Activity at Rest: Normally will be electrically silent when muscle is at rest If see: Normal MUAPs: may mean difficulty to relax muscle Either diphasic or triphasic spontaneous potentials significant abnormal finding see below for more details Voluntary Muscle Contraction Weak contraction (“think about contracting…”) Should cause individual motor units to fire Single MUAPs are recorded Look at amplitude, duration, shape (diphasic or polyphasic), sound, and frequency Strong contraction Summation of MUAPs in to an interference pattern Lots of motor units firing and overlapping MUAPs  Abnormal Spontaneous Potentials Abnormal potentials when muscle should be relaxed Fibrillation Potentials should be a never Single Spontaneous depolarization of a single muscle fiber muscle fiber Not visible through the skin Indicates a lower motor neuron disorder such as a peripheral nerve lesion or disease of the alpha motor neurons - Can also be seen in muscle disease such as muscular dystrophy and myasthenia gravis T thinkaccelerate Positive Sharp Waves Diphasic wave form with an initial large deflection followed by a slow second phase Found in denervated muscle or in muscles with disease (MD, MG) Often seen with fibrillation potentials  More Abnormalities at Rest is diphasic or triphasic normal Fasciculations Involuntary asynchronous contraction of entire motor unit Often seen in muscles with irritation or degeneration of alpha motor neuron Often visible as a small twitch Can be seen in normal individuals (stress, caffeine..) Repetitive Discharge Bizarre high frequency discharge Seen with alpha motor neuron disease, peripheral nerve lesions, and muscle diseases  Abnormal Voluntary Potentials Polyphasics Elicited on voluntary contraction Results from asynchronous firing of muscle fibers in a single motor unit Seen in muscle disease or during reinnervation of muscle fibers -u to notice good Fineaglie. have muscle Giant motor units after they demylineated Indicates hypertrophy of a motor unit by collateral sprouting of alpha motor neurons adopt Often seen in regeneration/recovery from LMN disease orphan retract (ie. polio) motorens n Summary Study with EMG recorded from multiple muscles Ask “What Spinal Segmental Nerve and Peripheral Nerve for each” Looking for evidence of LMN or muscle disease Ask “Where are the abnormalities” Evaluates: Insertional activity At rest With slight contraction With strong contraction Nerve Conduction Velocity Testing and Reflexes Laura Gilchrist PT, PhD DPT 5035 Objectives Describe NCV (nerve conduction velocity) tests used to assess PNS disorders Be prepared to analyze a NCV report, based on a paper case, to assist in the determination of diagnosis.  when to nerve What happens compressed ? Il > - Site where APs how Quickly conducting compression less Show out to figure M - I myelinated class 0 ** * ↳Tap # ge Slower NCV Testing A second way to measure health of the peripheral nerves when they continue to innervate the target but have been damaged (demyelinated…) Involves direct stimulation of peripheral nerve and recording from muscle or skin (sensory receptors) Can be done for motor axons or sensory axons within a peripheral nerve stimulate recording > - col electrical contraction muscle reference  Motor Conduction Velocity Stimulating electrode placed over the nerve to be tested Recording electrode over a muscle innervated by the nerve Reference electrode over distal tendon (remove artifacts) neuromuscular sunction When stimulus (electrical depolarization) occurs, triggers oscilloscope and can record latency to beginning of MUAP in muscle recording Called the M-wave motor conduction stane velocity --Latency Perform same test on second portion of the same nerve Calculating Nerve Conduction Velocity (NCV) CV = conduction distance / prox latency – distal latency What are you measuring if you take time from stimulation site to muscle contraction? latency ? Use 2 sites, subtracts out: Interpreted based of normal values, based only on fastest axons in the nerve doesn't test of all axon only fast axon Sensory Nerve Conduction Stimulated by surface skin electrodes over a portion of the nerve distribution Record over nerve trunk SNAP Sensory nerve AP Can also reverse (switch recording and stimulating electrodes) for antidromic conduction (backwards) which should be same speed Measured from stimulus start to peak of signal Interpreting Results Compare results to normal values Decreased velocity when demyelination or remyelination  *Figure is missing synapse between Sensory and Motor Neurons H-Reflex Hoffmann’s Reflex Useful for radiculopathy and peripheral neuropathy Tests the integrity of the sensory and motor pathways Via use of stretch reflex path Example of S1: Stimulate: Tibial Nerve in popliteal fossa Record: medial portion of the soleus muscle Activates IA afferents in the nerve which synapse on the alpha motor neuron, causing a monosynaptic activation of the soleus Because it represents both sensory and motor traveling to and from the spinal cord, can give early indication of spinal segmental nerve compression F-wave In addition to an M-wave in the motor NVC, may also see a later and smaller motor response to external stimulation called the F-wave Antidromic motor response to stimulation followed by an orthodromic stimulation Initial stimulation produces: Orthodromic contraction: M wave Antidromic AP followed by orthodromic AP → contraction: F-wave