speechtherapy ppt

Assignment Work Collected by :CHAMAN LAL;PT; M.P.P.S(PAK)CERT.AFSM&SMAP :1 Assignment Work Collected by :CHAMAN LAL;PT; M.P.P.S(PAK)CERT.AFSM&SMAP


Oral-Motor Assessment and Training in the Treatment of Speech Impairment: Physiologic Evidence and Treatment AlternativesThomas F. Campbell, Ph.D. U of PittsburghSteven M. Barlow, Ph.D. U of KansasChristopher A. Moore, Ph.D. U of WashingtonASHA November 18, 2000 :2 Oral-Motor Assessment and Training in the Treatment of Speech Impairment: Physiologic Evidence and Treatment AlternativesThomas F. Campbell, Ph.D. U of PittsburghSteven M. Barlow, Ph.D. U of KansasChristopher A. Moore, Ph.D. U of WashingtonASHA November 18, 2000


Motor Cortex to Motor Units: Human Neonate :3 Motor Cortex to Motor Units: Human Neonate Steven M. Barlow, Ph.D. Audrey Woerner, B.A. Communication Neuroscience Laboratories Speech-Language-Hearing: Sciences & Disorders University of Kansas


Germinal Isocortex, spinal cord, cerebellum :4 Germinal Isocortex, spinal cord, cerebellum Germinal zones and layers of cerebral isocortex, spinal cord, and cerebellum of mammals. (Jacobsen, 1983)


Human Infant Cortex @ 5 months :5 Human Infant Cortex @ 5 months Camera lucida drawings from Golgi preparations of cerebral cortex in human infant (age 5 months). Layers I, V, VI are recognizable. Scale 100 m. (Marin-Padilla, 1970).


Adult Cortex :6 Adult Cortex (Ranson & Clark, 1959)


Efferent tuning Corticobulbar :7 Efferent tuning Corticobulbar


-Motoneurons :8 -Motoneurons Largest -motoneurons have cell body surface areas of 79,000 to 250,000 m2 w/10,000 synaptic knobs, large number of axonal terminals to innervate a large number of muscle fibers (Large MU), high tension. Smallest -motoneurons have cell body surface areas of 10,000 to 15,000 m2 with fewer synapses, proportionately fewer axonal terminals to form Small MUs, low tension.


Neural Control of the Differentiation of Skeletal Muscle :9 Neural Control of the Differentiation of Skeletal Muscle -MoNu’s induce matching functional characteristics in target muscles (Eccles et al., 1958; Jacobsen, 1978) Slow muscles innervated by small -MoNu’s: lower CVs, longer afterpotential, and lower and more prolonged low-frequency firing rates (5-20 impulses/sec) (Granit et al., 1956; Henneman et al., 1965) Fast muscles are innervated by large -MoNu’s: rapid CVs, brief hyperpolarizing afterpotential, and can fire rapidly (30-100 impulses/sec) Functional properties of MoNu and corresponding CoMoNu Fast muscles excited infrequently & short durations Slow muscles excited frequently & longer periods


Upper/Lower MoNu & MU Genesis :10 Upper/Lower MoNu & MU Genesis Neonates have only ‘slow’ muscles MU collateralization is the rule at birth, specificity follows with activity and ontogenesis Differentiation into ‘fast/slow’ occurs over several weeks Corticomotoneurons continue to differentiate along with intracortical and descending projections Motor units manifest specificity according to slow & fast units, commensurate with changes in size, membrane properties, and driven largely by the firing rate of pyramidal neurons and lower motor neurons.


Neonate vs. Adult MU Collateralization :11 Neonate vs. Adult MU Collateralization Mouse @ 4 days Rat - adult


Polyneuronal vs Single :12 Polyneuronal vs Single (After Purves & Lichtman, 1980; Purves, 1988) Motor Neuron Innervation of Skeletal Muscle


Muscle Fiber Polyneuronal Innervation :13 Muscle Fiber Polyneuronal Innervation Rat soleus m. (Brown et al., 1976)


MU Size vs. Age :14 MU Size vs. Age Postnatal reduction in MU size. Soleus m. in rat. (Brown et al., 1976)


Properties of MUs :15 Properties of MUs The range of forces produced by MUs in different muscles varies widely, but in all muscles the distribution of twitch or tetanic tensions has the form of an exponential curve, with the number of units being inversely related to the tensions they produce. Small MUs are most abundant, red in color, low force output, rich capillary supply, aerobic metabolism, fatigue resistant. Large MUs are very few in number, pale in color, highest force, few or no capillaries, anaerobic metabolism, glycogen-dependent for contraction, fatigue rapidly. Small MUs are necessary for producing finely graded forces. MU recruitment thresholds are highly correlated with axonal conduction velocities, and thus MoNu size.


Efferent tuning Corticobulbar :16 Efferent tuning Corticobulbar


Gastroc MUs :17 Gastroc MUs (adapted from Burke et al., 1974) GASTROC m. TENSION vs MU Type


Slow vs. Fast MoNu :18 Slow vs. Fast MoNu


MU Recruitment & Firing Frequency :19 MU Recruitment & Firing Frequency (adapted from Monster & Chan, 1977) (Muller et al., 1977; Barlow & Muller, 1992) lip operating range estimates


Trophic Effects of Neurons on Their Targets :20 Trophic Effects of Neurons on Their Targets Retrograde: trophic effects dominated by chemical mechanisms Anterograde: trophic effects dominated by activity-dependent mechanisms, synaptic activation of the postsynaptic cell (Harris, 1974; Purves, 1976; Grinnell & Herrara, 1981; Purves & Lichtman, 1985) Unequivocal evidence that muscle activity is capable of regulating virtually all the muscle properties that change in response to denervation (injury).


Muscle Fibers :21 Muscle Fibers Vertebrate muscle fibers are generally categorized according to their contractile, histochemical, antigenic, and metabolic qualities. However, muscle fiber properties can change radically depending upon the type of neuronal innervation, and the pattern of activity. (P 187 Purves & Lichtman, 1985)


Cross-Reinnervation :22 Cross-Reinnervation The experiments on cross-reinnervation add considerable strength to the view that neural activity is a heavy determinant of postsynaptic muscle fiber properties. The properties of target cells depend not only on the presence or absence of innervation, but on the kind of innervation received (entrainment, therapeutic patterned input, behavior motor patterns). These observations are relevant to development and maintenance of motor units, and thus, the effector substrate of fine motor control.


Motoneurons and Cross-Innervation :23 Motoneurons and Cross-Innervation MoNu innervating slow- and fast-twitch muscle fibers tend to fire at different frequencies. If a slow-twitch muscle is denervated and then stimulated directly with the ‘slow’ pattern of impulses, it will maintain its slow properties; however, if it is stimulated with the ‘fast’ pattern, many of its properties will come to resemble those of fast-twitch muscle. Likewise, a denervated fast-twitch muscle stimulated with the ‘fast’ pattern will remain fast, but will come to resemble a slow-twitch muscle if stimulated with the ‘slow’ pattern. Thus the type of use to which a muscle is subjected can influence its biochemical and physiological properties. (Nicholls, Martin, Wallace, 1992) p. 408


Cross-Reinnervation :24 Cross-Reinnervation (Close, 1965)


Cross-Reinnervation Histochemistry :25 Cross-Reinnervation Histochemistry (Salmons & Sreter, 1976) Electrophoretogram of myosins for fast, slow, and a fast muscle stimulated for 20 weeks in a continuous pattern to mimic a slow MoNu discharge.


Muscle Performance Variables :26 Muscle Performance Variables Multidimensionality of the clinical assessment of muscle performance. Patterns of MU recruitment, rate of force change, NRT, MRT Contractile stability throughout recruitment range Force decay ‘fatigue’ Sensorimotor integration: reflex specificity, gain, modulation ‘Physiologic operating range’ and functional behavior Contractile Power should be based not simply on how forceful a maximal contraction is but on the quality of the contraction. Normally, full contraction is accompanied by a smooth, prompt, and steady increase in tension to the maximum of which the subject is capable. Stability is another hallmark of normal tetanus.


Motor Power Paradox :27 Motor Power Paradox Power and bulk may be normal even in neuromuscular disorders. McComas et al. (1971) have shown that normal or nearly normal maximum twitch tension(s) may be maintained in the face of losses of up to 90% of the normal complement of motor units (MUs) in chronic neurogenic disorders. In acute neurogenic disease, there is a better correlation between strength and quantitative MU loss.


McComas et al., 1971 :28 McComas et al., 1971 AMPLITUDE of MU POTENTIAL 20 40 60 80V 0.1 0.2 0.3 0.4 2 mV


McComas et al., 1971 :29 McComas et al., 1971 (McComas et al., 1971)


Universal Newborn Sensorimotor Screening and Habilitation: Premature and Term Infants :30 Universal Newborn Sensorimotor Screening and Habilitation: Premature and Term Infants Supported in part by NIH R01 DC00365-08, NIH M01 RR00750-24S1, and Neuro Logic, Inc.


Research Team :31 Research Team COLLABORATING INVESTIGATORS Kathy Weatherstone, MD KU Medical Center-Neonatology & Perinatal Medicine Connie Freeman, ARNP KU Medical Center-Neonatology Michael Mosier, PhD KU Medical Center-Biostatistics Anna Dusick, MD Indiana University School of Medicine - Neonatology Shirley Coltart, MSRN Indiana University School of Medicine - Neonatology Don S. Finan, PhD University of South Carolina - Neuroscience Esther Thelen, PhD Indiana University - Developmental Psychology Preston Garraghty, PhD Indiana University - Neural Plasticity Carol Boliek, PhD University of Arizona - Chest Wall Kinematics Amitava Biswas, PhD University of Texas-El Paso - Engineering/Neuroscience Rick Konopacki, MSEE University of Wisconsin - Servo Dynamics/Engineering


Born Too Soon :32 Born Too Soon ~ 450,000 babies are born prematurely in the U.S. each year


Incidence and Cost :33 Incidence and Cost ~ 25,000 babies are born each year as extremely premature - micropremies (27 weeks GA or less) Medical care costs approach $750,000 for a single micropremie in the NICU Translates to more than $15 Billion annually for the micropremies (~$65,000 per week during 1st month) Preterm babies combined = Upwards of $200+ Billion annually and rising.


Residual Effects :34 Residual Effects Post term costs are much higher for premies during the 1st three years compared to babies born at term Many neurological problems are not discovered using traditional diagnostic tools until toddler-preschool-elementary school years ~ 20% of the premies will manifest profound impairments


Residual – Long Term Effects :35 Residual – Long Term Effects Translates to ~80,000 babies/year or nearly 500,000 children pre-K with severe-profound impairments learning disability developmental delay sensory perception & integration disorders sensorimotor dysfunction cognitive impairments literacy, language, & speech disorders The number of children with mild-moderate impairments is presumed to be much greater


Early Identification :36 Early Identification Historically, a ‘wait’ and ‘see’ approach Quantitative methods are generally lacking for assessing brain-behavior relations in NICU babies Risky Critical periods or sequencing in neural development Salient forms of stimulation endogenous activity-dependent mechanisms some forms of neural delay/defect may be resolved through optimization of neuroplasticity


Immediate Goals :37 Immediate Goals DIAGNOSTIC TOOLS: To develop objective, physiologic methods for assessing the functional status of neural systems involved in control of orofacial, respiratory, and spinal muscle systems in premature and term infants. TREATMENT: To develop physiologically-based intervention techniques for use in the NICU that ‘stimulate’ development of brain circuits involved in motor control.


Baby’s Face ? :38 Baby’s Face ? Standard equipment Sensory systems operational 1st (precocious) Facial sensorimotor specialization begins in utero Fetal ‘sensory face’ remarkably similar to the adult Human neonate is relatively helpless in motor capabilities Suckling, maintaining the airway, and responding to tactual stimuli are 'mature' neonatal oral functions that are modified by local sensory experience and integrated with the whole of the organism (Bosma, 1970).


Facial Skin Mechanoreceptors :39 Facial Skin Mechanoreceptors


Baby R1 setup :40 Baby R1 setup Going After R1’s in Neonates (Barlow, 1991)


Infant R1’s :41 Infant R1’s INFANT


Adult R1’s :42 Adult R1’s Adult: age 22 ADULT


Developmental Issues :43 Developmental Issues Appropriate oral experiences are critical in the final weeks of gestation. Interruption of these experiences may impair fragile syntheses of how the brain maps these functions. For many premature babies, the NICU environment rate limits sensorimotor development, essentially a model of sensory deprivation for orofacial systems, and quite possibly aversive for other sensory systems (auditory, cutaneous).


Oromotor Dysfunction :44 Oromotor Dysfunction 35 week GA 1770 gm oromotor dysfunction tongue thrust Premature and brain- damaged infants’ ability to adapt oromotor skills is frequently compromised. Unsuccessful initiation of oral feeding has significant clinical consequences. SUCK1.AVI


Development of Oral Function :45 Development of Oral Function Facial (Perioral) reflexes and oromotor responses in the infant are dependent on post-conceptual maturation and experience.


Methods :46 Methods Study patients: 16 uncomplicated preterm infants - NICU (Indiana University School of Medicine) 7 intubated (1-6 days) Mean gestational age: 30 weeks (29-33) Mean birth weight: 1521 gms (SD=330) Mean age at first testing: 34 weeks (31-36) All infants had normal VS, SO2, and neurologic exam including ability to NNS


Methods :47 Methods Testing @ bedside before a feeding Brief examination, positioned and settled SUCK testing EMG testing of Trigeminofacial Reflex Brain stem and cortical interactions


Actifier :48 Actifier


Actifier - top view :49 Actifier - top view


ACTIFIER Orofacial Recordings in the NICU Isolette :50 ACTIFIER Orofacial Recordings in the NICU Isolette


NICU Isolette - NNS Dynamics :51 NICU Isolette - NNS Dynamics


NNS 34 & 38 wks :52 NNS 34 & 38 wks 0 15 30 45 60 60 45 30 15 0 15 10 5 TIME (seconds) Baglet Pressure (cmH2O) Baglet Pressure (cmH2O)


NNS Burst Length Ontogenesis :53 NNS Burst Length Ontogenesis


Modulation of Neural Pathways in the Brain Stem :54 Modulation of Neural Pathways in the Brain Stem “Can I modulate your newborn’s trigeminofacial pathway? Great! Just sign here please.”


Actifier and Stimulation :55 Actifier and Stimulation SUCK1.AVI


Preterm R1 surface :56 Preterm R1 surface


Adult/neo R1 surfaces :57 Adult/neo R1 surfaces


R1 Latency Function :58 R1 Latency Function Barlow, Dusick, Finan, Coltart, & Biswas (2001) Brain Research


Entrainment :59 Entrainment of Rhythmic Motor Outputs is a powerful experimental approach for revealing moment-to-moment influences of mechanosensory inputs on motor control. Entrainment is defined as the synchronization of an endogenous oscillator to external periodic events (Pavlidis, 1973; Glass & Mackey, 1988; Kriellaars, Brownstone, Noga & Jordan, 1994). For a given stimulus with fixed amplitude and period, a stable phase relationship between the stimulus and oscillator must exist to satisfy the conditions for entrainment. Entrainment


Entrain :60 Entrain NNS Mechanosensory Entrainment: 2.5 Hz external input (Finan & Barlow, 1996, 1999)


Plasticity :61 Plasticity The role of ‘early oromotor experience’ will be tested in future studies as a formal test of plasticity in the neural substrate subserving functional oromotor behaviors.


Neuroplasticity :62 Neuroplasticity The pattern of electrical activity and competitive interaction between adjacent nerve terminals are primary determinants of development and stability of synaptic connections (Garraghty, Kaas & Florence, 1994). In essence, 'neurons wire together, if they fire together' (Sporns, 1994). ENTRAINMENT is used to ‘jump start’ circuits in the brain, which in turn, stimulates desired patterns of activity and development. Huge potential in human premies and traumatic brain injury.


Synapse Formation& Activity-Dependent Growth :63 Synapse Formation& Activity-Dependent Growth Gan & Macagno (1995)J. Neuroscience 15(5): 3243-3253.


Intraventricular Hemorrhage - IVH :64 Intraventricular Hemorrhage - IVH Born 27 Weeks GA BW = 1047 gms Neurologic exam: spasticity, no functional oromotor skills Early ultrasound revealed Grade III IVH blood in ventricles


IVH - CT scan :65 IVH - CT scan frontal atrophy ventriculomegaly dolichocephaly microcephalic ventriculoperitoneal shunt


Slide 66 :66 Time (seconds) (cmH2O) 15 30 45 60 0 5 10 15


IVH vs CONTROL Pressure Histograms :67 ANOVA Source DF SS MS F P Level N Mean StDev Factor 1 50621.5 50621.5 585.28 0.000 IVH 38 13.38 10.00 Error 114 9860.0 86.5 CONTROL 78 57.90 8.94 Total 115 60481 Pooled StDev = 9.300 IVH vs CONTROL Pressure Histograms IVH P0008_S.DAT 42 week GA CONTROL P0011_S.DAT


Premie Findings :68 Premie Findings ACTIFIER technology permits non-invasive assessment of functional brain-behavior relations and biomechanics during SUCK in the premature infant (32 wks GA). FAST, < 5 minutes of sampling ROBUST DEVELOPMENTAL TRENDS Suck Dynamics changes as a function of maturation (age & experience) including longer, stronger, and more uniform suck burst patterns. The speed and local sign of neural transmission shows strong developmental trends in the normal baby. H.R. 4365 Children’s Health Act


Future Directions :69 Future Directions Miniaturized ACTIFIER technology will be used to map the dynamics of neural modulation between brain stem and cerebral systems in the premies. Outcome studies will be developed to identify links between early neuro insult & later appearing impairments (communication, cognitive, learning, and sensorimotor including speech, locomotion & manipulation. Entrainment and remodeling (Barlow & Thelen, 2000) ROBOBABY


Early Human Development = Amazing :70 Early Human Development = Amazing