Lecture 3 Spinal Cord 241001 PDF

Neural Basis of Sensory and Motor Function KINE 3440 School of Health and Human Performance Department of Kinesiology Spinal Cord Outline of the lecture Spinal Cord and Sensations Central Pathways Divergent Pathways Spinal Cord and Movements M...

Neural Basis of Sensory and Motor Function KINE 3440 School of Health and Human Performance Department of Kinesiology Spinal Cord Outline of the lecture Spinal Cord and Sensations Central Pathways Divergent Pathways Spinal Cord and Movements Motor units Segmental/intersegmental control  Central somatosensory pathways Three broad types – Conscious relay (to cortex) – Divergent (brainstem) – Unconscious relay (cerebellum)  Conscious relay pathways Two systems – Dorsal column / medial lemniscus Touch and proprioception – Spinothalamic tract / anterolateral system Pain and temperature  Touch & proprioception 3-neuron system – Primary afferent enters dorsal root Dorsal column system – Ascends ipsilaterally to medulla as: Fasciculus gracilis (lower limb) or fasciculus cuneatus (upper limb) Located in dorsal columns of spinal cord white matter – Synapse at nucleus gracilis or cuneatus – Second neuron decussates, ascends to thalamus as: Medial lemniscus – Third neuron connects thalamus to cortex (postcentral gyrus of parietal lobe)  Key notes Ipsilateral relation to body in spinal cord Somatotopic organization at all levels CN V (Trigeminal) for face Pathway is most ‘spread out’ at post-central gyrus  2. Spinothalamic* / anterolateral system *sometimes called neospinothalamic tract Pain and temperature (fast/conscious) 3-neuron system – Primary afferent: dorsal root – Synapse in spinal grey – Secondary afferent decussates, becomes: neospinothalamic tract – Synapse in VPL of thalamus – Connect to post-central gyrus  Key notes Contralateral connection with body at spinal cord Unusual ipsilateral ‘descending’ trigeminothalamic tract in pons/medulla Divergent pathways “Slow, broad acting pain”  3. Divergent pathways Slow, aching pain Mediates affective/autonomic responses to pain  Peripheral aspects Primary afferent – C fibres from free-endings – Sensitized (to stimuli that are not NORMALLY painful) with repeated stimulation – Sensitized by: Histamines, prostaglandins (tissue damage) Dorsal root ganglion Synapse in spinal grey: substance P neurotransmitter  Central aspects Ascending projection neurons – “Wide-dynamic-range” – Inputs from cutaneous, musculoskeletal and visceral afferents Targets: – Reticular formation of medulla (spinoreticular pathway) – Periaqueductal grey matter in midbrain (spinomesencephalic pathway) – Limbic system via the thalamus (paleospinothalamic / spinolimbic pathway) Limbic system in cerebral cortex Periaqueductal grey matter in midbrain (mesencephalon) Reticular formation / reticular activating system in medulla/pons  Functions Spinoreticular – Arousal, broad activation response to pain Spinomesencephalic – Superior colliculus: eye movements & attention to pain site – Periaqueductal grey matter: pain regulation Paleospinothalamic / spinolimbic – Relay to limbic system of cortex – Emotional responses to pain Unconscious pathways  4. Unconscious relay pathways Target: cerebellum – ipsilateral* Two proprioceptive pathways: sensory – Sensory inputs (spindles, GTO, joint) – Posterior spinocerebellar (lower limb) – Cuneocerebellar (upper limb)  Unconscious relay pathways Two efference copy pathways – Send copy of motor neuron signals (i.e., NOT sensory) to cerebellum – Anterior spinocerebellar (lower limb) * bilateral – Rostrospinocerebellar (upper limb) Functions – Supraspinal reflexes Posture Balance Adjustments to limb movements  Motor systems First, several years ago I placed a very large and bolded statement in my motor control course notes that the classic muscle action charts in anatomy and kinesiology books are partially correct at best, and woefully inaccurate at worst. Much data has been presented in the past 5-10 years or so (e.g., see Herzog's work) on task-specific muscle activation,compartmentalization, and more; all of which suggest that our classic notions of muscle actions need rethinking. Control of movement Reflexive control Reactive (feedback) process Voluntary control Predictive (feedforward) process Flexible Learning  Reflexive control of movement Segmental reflex One (or a small #) sensory receptor One spinal segment One (or a small #) muscle Reflexive control of movement Intersegmental reflex Several sensory receptors Several spinal segments Several muscles Reflexive control of movement Supraspinal reflex Several sensory receptors Afferent pathway Brainstem/cerebellum nucleus Descending pathway Several muscles Voluntary control of movement Motor units From spinal cord to muscle Lower motor neurons Alpha mn Alpha & gamma mns Motor units and motor unit pools Motor unit One alpha motor neuron plus all the muscle fibres that it innervates. Motor unit pool All the alpha motor neurons and associated motor units that innervate a specific muscle. Motor unit types Names Metabolic properties Threshold for firing # of associated myofibrils (AKA innervation ratio) Twitch response Fatigue profile Type I = S Type IIa = FR Type IIb = FF Tension and fatigue Single pulse Unfused tetanic input Note: fibre tension increases only 3-5 fold between single action potential and sustained tetanic input Muscle cells are changed by neural input Key point: myofibril physiological characteristics are determined by the NEURAL INPUT received! Orderly motor unit recruitment Henneman’s size principle Smallest motor neurons recruited first Constant ACh input causes more depolarization in smaller motor neurons These are slow twitch, small force increments Primary means of varying muscle force output Simply increase total neural drive No need to select units Henneman’s size-recruitment principle visualized The final common pathway: alpha motor neurons Lower motor neurons are “the final common pathway” All neural drive to muscle goes through the alpha mn Each alpha mn has many sources of influence This includes voluntary commands, and reflexive influences Some are excitatory, many are inhibitory The firing rate of the alpha mn is based on the simple addition of all sources of influence Primary drivers of the alpha mn 1. Interneurons Interneurons: inhibitory effects Renshaw cells Negative feedback within the same motor neuron pool Helps filter activity: only strongly active neurons survive Renshaw cell inhibition Ia interneurons Inhibition of antagonistic muscle during stretch reflex Ib interneurons GTO inputs mediated by these (homonymous)  Alpha mn Ib interneuron Ia interneuron Renshaw cell *note: black means inhibitory influence Ventral horn of spinal grey matter 2. Afferent input Segmental and intersegmental reflexes Proprioceptors (type I afferents) Muscle spindles: myotatic reflex (stretch) Ia afferents, one synapse Golgi tendon organs: clasp-knife reflex (tension) Ib afferents, two synapses (Ib inhibitory interneuron) Cutaneous inputs (A-beta, A-sigma, C) Typically involve interneurons Withdrawal reflexes: temperature, nociception Crossed-extensor reflex: pressure, vibration 3. Descending influences Descending motor pathways Fractionated movements (voluntary control) Lateral activation systems Lateral corticospinal & rubrospinal Postural/gross movements (supraspinal reflexes) Medial activating systems Medial corticospinal Bulbar tracts: midbrain, pons, medulla Measuring the state of the motor unit pool What is the point? CNS damage Lose descending influences on the motor neuron pool Many of these influences are inhibitory in nature (suppressing activity) Afferent inputs cause alpha MN to fire – reflexes are easily elicited Can show this with stretch reflex testing Or you can use electrical stimulation H-reflex in a nutshell Activate Ia spindle afferent with current Measure EMG in homonymous muscle Latency: how fast (30-40 ms normal)? Amplitude: how much? X The Hoffman reflex (H-reflex) Stimulus Low voltage over sensory nerve Stimulates spindle Ia afferent Pathway Carried to spinal cord Ia afferent synapses on alpha mn Alpha mn fires Output Evoked response in muscle (EMG) H-reflex Alpha mn Low intensity stimulation site EMG recording site (large response) Details Most nerves are ‘mixed’ Motor nerves + various afferents Ia afferents have lowest threshold to be activated Use low voltage to isolate Ia afferent 30-40 ms latency for EMG = H-reflex If voltage is too high Motor nerve will be activated Creates direct activation of muscle This is the M-wave (5-8 ms, very large) Clinical uses of H-reflex Latency Time to see H-wave: myelination status Threshold Magnitude of electrical pulse required Lower threshold: higher excitability in motor unit pool (e.g., UMN disorder) Size of evoked response Small response: alpha mn death, muscle death Large response: hyperreflexia (spasticity!) Disorders of motor neurons Disorders of lower motor neurons Common etiologies Peripheral lesions (trauma, compressive, polyneuropathies) * not selective for motor Infectious – can be selective for motor Degenerative disorders – can be selective for motor Types of nerve damage Death of cells (loss of signal) Demyelination (delayed signal) LMN: history/examination Weakness Voluntary and reflexive conditions (final common pathway) Non-specific to LMN pathology Atrophy Disuse Non-specific to LMN Tone Flaccid muscles (hypotonia) Resting state Fibrillations and fasciculations LMN: clinical investigation NCV/EMG: M-wave Demyelinating disorder: latency increases Motor neuron death: amplitude decreases LMN: clinical investigation NCV/EMG: H-reflex Demyelinating: increased latency Death of cells: reduced** amplitude LMN: clinical investigation Muscle biopsy Muscle fibre atrophy (disuse) Fibre type clustering (motor unit remodelling) -Motor neuron dies -Acute: muscle cells inactive -Chronic: surviving motor neurons branch to muscle cells -those muscle cells take on characteristics of new motor unit -nearby muscle cells become similar type Common LMN disorders Poliomyelitis (polio) Etiology: infectious (viral: poliovirus) Pathophysiology: virus attacks and destroys anterior horn cells S&S: weakness, cramps, flaccid paralysis Vaccine: Salk and Sabin (two varieties) *extremely effective Variable timecourse: Acute: weakness (few neurons die) Chronic: regain strength (motor unit remodeling) Much later: lose strength very quickly (lose large motor units when neurons die) – this is post-polio syndrome  Post-polio syndrome Poliomyelitis  Spinal muscular atrophy (SMA) Etiology: degenerative (mutated gene for Survivor Motor Neuron 1 protein) Pathophysiology: death of LMN in spinal cord and brainstem Incidence: 1/60K live births Prognosis: 50% survival past 2 years of age (cause of death: respiratory failure) Combined UMN/LMN disorders Amyotrophic lateral sclerosis (ALS) AKA Lou Gherig’s disease Etymology: “A” (no) “myo” (muscle) “trophic” (nourishment), lateral (region of spinal cord affected), sclerosis (hardening) Etiology: degenerative, cause unknown Pathophysiology: death of upper and lower motor neurons, bilaterally (spinal cord and brainstem) Prognosis: 50% mortality within 3 years, COD respiratory complications Signs and symptoms When LMN are affected: flaccid paralysis When UMN are affected: spastic paralysis When both are affected: ??? Limb and face Speech, eyes Breathing Clinical investigation: NCV/EMG: M-wave? NCV/EMG: H-reflex? Biopsy? Motor unit pools: myotome organization Somatotopic layout of motor units  Upper motor neuron – Influence movement – Synapse on lower motor neurons (not muscles) Direct excitatory connections are rare Most connections are via inhibitory interneurons Role: modulate reflexive actions Limb and head/neck – Spinal and cranial nerve projections  Lateral group pathways Fractionated movements: 3 pathways – Lateral corticospinal – Rubrospinal – Lateral reticulospinal (ipsilateral)  Lateral corticospinal tract (pyramidal tract) Originates: primary motor cortex, premotor cortex, posterior parietal cortex – Somatotopic representation Descending pathway – Corona radiata (cerebrum) – Internal capsule (diencephalon) – Cerebral peduncles (midbrain) – Pyramids (medulla) – decussation point – Spinal cord: lateral column Ends at alpha motor neurons, contralateral  Functions Voluntary control of movement – Individual muscles: fractionated movement – Groups of muscles: synergies Predominant control mode: – Upper limb: extensors – Lower limb: flexors Releases body from reflexive control – Inhibitory influences at alpha motor neuron Cortical origins Descending bundles  Rubrospinal tract Minor role in humans – Predominates with corticospinal injury Originates: red nucleus (midbrain) Decussates: immediately Terminates: cervical, thoracic LMNs Functions: promotes upper limb flexor tone  Lateral reticulospinal tract Originates: reticular formation (medulla) Decussates: **DOES NOT! Function: facilitate flexor tone, inhibit extensor tone  Medial group pathways Postural and gross movements – Medial corticospinal – Tectospinal – Medial reticulospinal – Vestibulospinal (medial and lateral) More subconscious/reflexive in nature  Medial corticospinal tract Originates: primary and premotor cortex Ipsilateral connections Terminates: thoracic segment LMNs (proximal muscles) Function: postural support for voluntary action Right ------ Left Left ------ Right  Medial reticulospinal system Originates: reticular formation (pons) Ipsilateral connections Terminates: thoracic, lumbar LMNs Functions: trunk extensor tone, lower limb extensor tone – (Opposite to lateral reticulospinal system) Right ------ Left Pons Left ------ Right  Tectospinal tract Originates: superior colliculus (optic tectum of midbrain) Decussates: immediately Terminates: cervical segment LMNs Function: rotate head towards interesting visual and auditory events Right ------ Left Superior colliculi Left ------ Right  Vestibulospinal tracts Medial – Originates: medial vestibular nucleus (medulla) – Contralateral – Terminates: cervical, thoracic LMNs – Function: head/neck rotation Lateral – Originates: lateral vestibular nucleus (medulla) – Ipsilateral – Terminates: lumbar LMNs (lower limb) – Function: upright stance (lower limb extensor tone) Right ------ Left Medulla Left ------ Right  Corticobulbar tracts Upper motor neurons for cranial nerve nuclei – CN V: Trigeminal – CN VII: Facial – CN XI: Spinal accessory – CN XII: Hypoglossal Originate: primary motor cortex – Very lateral  Functions V Trigeminal: Jaw movements (chewing) – Masseter muscle VII Facial: Facial expression – Upper face: bilateral UMN innervation – Lower face: contralateral UMN innervation only XI Spinal Accessory: Head rotation – Sternocleidomastoid XII Hypoglossal: Tongue muscles