Neuroscience for the SLP

Speech
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Terms in this set (150)
Speech
Motor output of phonemes
-how you move structures
-speech sound issue, fluency, voice/resonance
Systems
Respiration - phrenic nerve lies in the cervical spine
Phonation - vagus nerve closes cords for speech production
Resonance - regulated by soft palate (velum)
Articulation - move airstream, constrict to produce sound
Language
Phonemes
Morphemes
Syntax
Semantics
Pragmatics

*not motor, all inside head
-receptive/expressive language
-social communication (kids)
-AAC
Communication
Prosody, pragmatics (adults), nonverbal, figurative language
Cognition
Way we process info
Memory
Problem solving
Executive function
Spatial awareness

(Hearing)
Apraxia: Location of lesion
Pre-motor cortex
- problem with planning or programming motor movements
Dysarthria
M1 issue
- speech execution issue
T/F Neurons firing in brain completely determine behavior and our subjective experiences
True
CNS
Brain and spinal cord (UMNs)
Cranial nerves innervate:
Head, neck, internal organs
PNSCranial and spinal nerves (LMNs)Spinal nerves innervate:Upper and lower extremitiesSomatic NSVoluntary control -skeletalAutonomic NSInvoluntary control -smooth musclesWhen does neuronal development begin in utero?Week 3 -no selectivity, overabundanceApoptosisCell death after pruning Kids lose about 20 billion synapses a dayPosterior vs Anterior brainPosterior is sensory, anterior is motorCerebrumEach side receives sensory information and controls motor movements on contralateral side of the bodyMeningesDura Mater Arachnoid mater Pia materMeningitisInflammation of the meningesHematomaBruiseHemorrhageBleed that causes brain to shift, so ICP increases. Neurons become disruptedDecompressions/EvacuationsCleans out blood from a bleed, repairs vesselsHydrocephalusIncrease of CSF, increase ICP (need VP shunt)TALLTongue, arm, lip, legsAnterior Cerebral Artery (ACA)To anterior frontal lobe -PFC, motor to legs contralaterally -right ACA controls left legsDamage to ACALegs contralaterally Cognitive issues from PFC damage Sensory contralaterallyMiddle Cerebral Artery (MCA)Posterior frontal love, lateral temporoparietal lobes -motor, sensation to TALL, speechDamage to left MCASpeech, language dysfunction Right TALL issues (speech and motor) -nonfluent aphasia -spastic dysarthriaPCAPosterior temporal/parietal lobes, occipital, thalamus, brainstem - vision, visual field processing, brainstemDamage to right PCAvision issues on left sideLeft brainAnalytic thoughts, logical, language, science/math, literate, motor speechRight brainHolistic thought, intuition, creativity, art/music, design, visual/spatial, nonverbal communication, figurative languagePre-frontal cortexOrganize and plan to sequence complex movements to complete tasks - decision making - personality -behavior suppression - tied to amygdalaPre-motor cortexGives info to M1 Left: Broca's and insulaDamage to PFCLack of initiation Can't organize tasks Disregulation of personality Emotions Poor judgementDamage to PremotorLeft: Apraxia right TALL, nonfluent aphasia Right: Apraxia left TALL, limbs affected, no speech affectedPrimary motor cortex (M1)Execute and fire pathway -UMNs -motor contralaterally for TALL -bilateral to all other structuresM1 damageHemiparesis, paralysis, spastic dysarthria -left TALLDamage to right MCAAgnosia Left TALLParietal lobe: S1Where we feel things -temperature, pain, discrete touch on contralateral bodyRight parietal lobeNavigate visual space -integrating visual space -knowing where your body parts areLeft parietal lobeLanguageAngular gyrusSemantic integration in reading and writing, naming - left right orientation, identification of fingers and numbersSupra marginal gyrusPhonological integration in reading/writing, proprioceptionRight parietal lobe lesion- Impaired perceptions, especially integrating sensory information - Agnosia - Visual neglect - Loss of spatial awareness - visuospatial problems Ex: right parietal lobe lesion: left weakness, so using right hand. Patient has agnosia (impaired ability to recognize objects as a whole and in space) *child with right parietal lobe lesion might not read, but that's not a language issue. It is a cognition issue.Left parietal lobe lesionReading and writing (visual language domain)Somatosensory cortexSensation -big representation of tongue and mouth -MCA stroke can cause sensory problems for TALL -impaired touch to contralateral side of bodyRight glioblastoma in right parietal lobeIssues: - cognition, understanding where they are in space, left TALL issues, left neglect, reading and writing because of cognitive issues, math, emotional situations, nonverbal communication Ex: say "I love you" without emotionTemporal lobeA1, Hechl's gyrus, primary auditory cortex -recognizes elements of frequency and intensityDamage to temporal lobeImpaired auditory system -cortical deafness, auditory agnosia, word deafnessTemporal association areasMemory formation (lexical and semantics) -understanding people's mental statesLesion in temporal association areaImpaired understanding of other people's mental states and moods -impairment in reading emotional intonation and affect -Hyperacusis -auditory illusions/hallucinations (schizophrenia)Temporal: Wernicke'sMeaning comprehensionDamage to Wernicke'sFluent aphasia -receptive language problems, phonological and lexical semantic processing -impaired auditory memoryRight side of temporal lobeUnderstanding emotional intonation/others' mental states -environmental stimuliDamage to right side of temporal lobeUnderstanding emotional intonation/others' mental states (environmental stimuli) -impaired memory for faces and objectsLeft MCA stroke in temporoparietal lobeParietal: language reading, writing Temporal: receptive language damage -sensory speech disorderV1 - primary visual cortexVisual perceptionV1 - visual/occipital association areasInterprets and integratesV1 - between occipital and temporal lobesWhat things areV1 - between occipital and parietal lobesWhere things areSummary of cerebrumBottom section of premotor: larynx, lips, tongue Apraxia occurs on PMC Association areas - sensory, visual Temporal lobe - sound processing Occipital lobe - vision Left: meaning out of language (words) Right: visual space, nonverbal communicationThalamusRelay Damage: subtle issues but less severe than cortex lesion (subtle, varied)HippocampusExplicit memories -damage: Alzheimers Left: trouble storing new words Right: visual (remember new faces)AmygdalaRaw emotional processing/fear Damage: anxiety, autism Left: understand fear through words Right: fear in someone's toneBasal gangliaInhibitory movement, regulates movementsDamage to basal gangliaNO PARALYSIS -Parkinson's, Tourette's, tremor, Huntington's, dyskinesia, hyper (resting tremors), hypokinetic dysarthria (shuffling, too much braking, rigidity)CerebellumSkilled movements - more sensory fibers than efferent -timing and accuracy of motor movements -indirect pathway -no paralysisDamage to cerebellumIntentional tremor Drunk walk/talk (ataxic dysarthria)MidbrainReflexes related to integration of sensesDamage to midbrainSensory integration problems, eye movement disordersPonsMotivation for basic human needsDamage to ponsLocked in syndrome, coma Pica Sleep/appetite disturbances Sexual/sensory dysfunctionMedulla oblongataLife sustaining function, swallowing, HR, breathingDamage to medullaLoss of gag, swallow and cough reflex -balance problems Vent dependentIs there more of a chance to get better if damage happens in cortex or brainstem?The brainstem, IF you survive (more of a chance you will not survive)Spinal cordCarries reflexive and voluntary signals -communicates with organs and muscles below the level of the head -spinal nerves come down and out -sensory: posterior, motor: anterior -innervates the body superiorly to inferiorly in sections called dermatomes -ipsilateral sensory and motor innervation, contralateral pain and temperatureC1 to C4Phrenic nerve damaged so these patients are on vents -no passive breathing -paralysis on all muscles of respiration -speech and swallowing issuesC5 to T5Voluntary inspiratory muscles damaged -diaphragm spared but paralysis of intercostals/abdominals, may need some form of respiratory support -breathing takes a lot of workT6-T12Diaphragm and most inspiratory muscles are spared -abdominal muscles paralyzed -swallowing evals b/c cough might be absentDifference in swallowing bet a medulla injury and spinal cord injuryMedulla: affects safety of swallowing SC injury: patients might not be able to protect their airwayExplain the process of neurons and synapsesDendrites receive sensory information (mechanoreceptors, cones/rods, hair cells), pass it through the body through the axon to the terminal which will communicate with cell or muscle tissue Sensory goes in to UMNs, interneurons in the cortex talk to the PFC, UMNs talk to the LMNs which talk to the muscles After interneurons talk to PFC, UMNs in M1 send signals to LMNs then back down to a muscleTwo functions of myelin1) prevents cross talk (neurons shouldn't spark other neurons, it should be focused neuron that cases something specific) 2) speeding the signal (sodium rushes into a cell which fires it, myelin speeds up that transmission)The synapseNeuron fires, its an all or nothing thing - signal travels down to terminal where neurotransmitters are -neurotransmitters talk to other neurons or muscles -of there are more excitatory signals than inhibitory signals then the signal will go forwardInhibitory signals in the BGInhibitory signals fire, and they tell the neurons not to reactPNSSensory and motor tracks Pathway: sensory nerves, interneurons, then outputHead, tongue, neck, tongue controlled by what?Cranial nerves (housed in brainstem)Arms and legs controlled by what?Spinal nerves (housed in spinal cord)Final common pathwayLMNs UMNs live in M1 and synapse with LMNs -the only way to talk to muscles is through LMNs -the muscle can only do what LMNs tell it to do, so the signals from the UMNs are very importantDamage to LMNsFlaccid dysarthria (limp, muscle just hangs there) -atrophy -weakness -decreased reflexesDamage to the UMNsSpastic dysarthria - no atrophy -weakness -increased reflexesWhere does most of decussation happen?BrainstemAre cranial nerves ipsilateral or contralateral?Ipsilateral - 12 pairs left and right -innervate head, neck, internal organs -housed in brainstem 1-4: midbrain 5-8: pons 9-12: medullaCN IOlfactory -important to us because of swallowing -sensory for smell only -does not pass through thalamus, connects to pons Lesion: failure to thriveCN IIOptic -sensory for vision only -reading, writing issues, social, AACCN IIIOculomotor -eyelid droop (ptosis) when eye is opened -deals with convergence and accommodation -keeps eyelid open, reactive pupils -double vision if damaged, rolling outwardCN IVTrochlear -Motor, downward - damage causes eye to roll up which results in diplopia (double vision) - chin tuck and head tilt to compensateCN VIAbducens - III and VI work to keep eyes central (need to have equal force) -damage causes eyes to roll inward to the nose - internal strabismus (cross eyes)CN VGross sensation: face, mouth and mandible Fine sensation: nasal cavity, teeth, lips, gums, auricle, EAM, cheeks, mandible Touch: anterior 2/3 of tongue Motor: soft palate, jaw, suprahyoid muscles (lift larynx during swallowing), mandibular depressors and elevators, tensor tympani, tensor veli palatini (opens Eustachian tube) *important for both speech and swallowing *weakness of jaw: jaw always deviated to the side of lesionDamage to CN VJaw deviates to left or right, ipsilaterally -Jaw is not a part of TALL, so if you see jaw deviation, think trigeminal -ipsilateral numbness -loss of muscle tone on flow of mouth -neuralgia/pain in the facial region -hyperacusis (sounds are loud cause tensor tympani doesn't work) -middle ear pressure/fluid buildup -jaw deviates to side of lesionWhy doesn't jaw deviate in a UMN lesion but does with CN V damage?There is BILATERAL innervationVIIFacial nerve -sensory and motor, important for both speech and swallowing -taste to the anterior 2/3 of tongue -Motor: to the muscles of the face including the forehead, eyebrows, eyelids, cheeks, lips and chin -Motor: stapedius, lacrimation and salivary productionFacial nerve damageBell's palsy (ipsilateral weakness) Can't raise or lower forehead Cant't close eyelid or blink Cant't hold material in oral cavity or puff out cheeks Can't pucker/hold seal or retract lips Hyperacusis Dry mouth, lack of taste, dry eyes, reduced tearsHow to distinguish UMN lesion in face to facial nerve damage?UMN lesion would cause contralateral weakness in the lips LMN lesion would cause ipsilateral weakness Lesion in facial nerve - whole face affected Lesion in supranuclear region - wont see anything in upper side of faceVIII Vestibulocochlear NerveSensory for balance and hearingVIII damageLoss of hearing, vertigo, nystagmus - impacted speech perception - might speak loudly - when you're young it would impact speech - distortions in high frequency soundsHow to distinguish LMN from UMN for VIIILMN lesion would cause deafness of ipsilateral ear UMN would cause diminished function but not absentPatient comes in with garbled or slurred speech. What is the likely speech disorder?We don't know! Do an assessmentIX GlossopharyngealTouch taste to the posterior 1/3 of the tongue Touch/pain to upper pharynx (gag sensation) Motor to the pharyngeal constrictors Motor to salivary glands - important for swallowingDamage to IXLoss of taste and touch on posterior tongue Touch and pain problems in upper pharynx, ear and ET Loss of gag sensation Loss of salivary productionDistinguish UMN from LMN for IXLMN is ipsilateral pharyngeal weakness UMN more limited overall impact because of bilateral innervationX VagusSensation to larynx and esophagus Motor to GI system (smooth muscle) Motor to muscles of the soft palate, intrinsic larynx, pharyngeal constrictor, important for VP closure, abducts/adducts vocal folds, cricopharyngeus (sphincter between pharynx and esophagus) Important for swallowingX damageSoft palate doesn't raise, loss of gag reflex Aphonia, dysphonia, monopitch, monointensity Poor pharyngeal constriction Fainting Pain in GI tractLMN vs UMN lesion for XLMN ipsilateral paralysis of the soft palate, lower pharynx, GI structures UMN lesion would have little impact due to bilateral innervationPatient comes in with his uvula deviated. See which arch is lower, that is the one that has an issue. Uvula deviates to rightLeft vagus nerve damage Also test swallow, gag reflex, phonation time, pitch sweep, hypernasal speech, rough sounding voiceXI Accessoryneck and shoulder movement Important for speech and swallowingXI damageInability to turn head to side of lesion Weakness in neck Inability to shrug shoulders Secondary dysphoniaPatient's right shoulder is droopingRight accessory nerve damageXII HypoglossalFine and gross tongue movements Important for speech and swallowingXII damageImpaired tongue movements in all directions Deviation to weak side on protrusion Poor tongue cupping Atrophy FasciculationsHow to distinguish LMN vs UMN for tonguesLMN ipsilateral paralysis of the tongue with atrophy/fasciculations UMN: contralateral weaknessRight side tongue is paralyzedLook at left UMN - Right TALL symptoms and see if they have spastic dysarthria and language. If those symptoms are present, then its probably a cortical injuryAngioedemaLips are swollenJaw deviation meansCN VWhat would you see in a right UMN lesion?Left lip weakness, left TALL, nonverbal communication issues, visuospatial, figurative languageTreacher CollinsHearing problemsWilliams syndromeVisuospatial deficits, agnosia, linguistically advanced, heart problemsHow would tonsil stones affect speech?Make it sound hypernasal (cleft palate would also do this)What structures are regulatory and come from the indirect motor pathway?Basal ganglia CerebellumPatient comes in with tongue deviation to right, labial deviation to rightLeft UMN Check for: right TALL, language, swallowing, spasticityPatient comes in with tongue atrophy on the right sideLeft Hypoglossal nerve damage Fasciculations Lips look symmetrical AtrophyWhat might happen with angioedema?Need intubation or a feeding tube, or AACEdentulous meansNo teethIschemic stroke80% Blockage - could have thrombosis or embolusHemorrhagic20% Bleeding occurs inside or around brain tissue Better outcomes if you survive Aneurysm or AVMMini-stroke (TIA)Blockage is temporary then resolves Sign of something biggerTPAbreaks down blood clots, reduces effects of ischemic stroke Improvements in 1 out of 3 patients Need to get it within first 3 hours Risky in patients with diabetes as this increases risk of hemorrhagePlasticity after brain damageSurviving brain areas increase or reorganize their activity Diaschisis: decreased activity of surviving neurons after damage to other neurons - provide clients with accurate labels for things so they don't practice errorsTBI symptomsLoss of consciousness Amnesia surrounding event Neuro deficits Any alteration in mental status at time of injuryWhat is the center for breathing?Brainstem (medulla)Path of speech signals starting from cortexM1, then brainstem then CN XI M1 then spinal cord then diaphragm M1 then spinal cord then superior thoracic and abdominal musclesResonanceWhat's happening with the soft palate M1 to brainstem (medulla) to CN X (velum) Articulation is what happening with the other articulatorsSpeech production is motorWe use biofeedback to update our movementsSpeech production modelConceptual system, linguistic system, phonological system, muscle movement systemApraxia of Speech (left brain)Planning/programming of sensorimotor movements for speech -imprecise, error filled articulations which is variable/inconsistent -groping for articulatory postures -absence of neuromuscular weakness -errors increase with increasing length and complexity -very likely co-occurs with M1DysarthriaMotor speech disorder characterized as slurred speech resulting from either weakness or dysregulation of the execution of motor speech - error patterns are more consistentSpasmodic dysphoniaRare neurological disorder affecting the intrinsic laryngeal muscles Uncontrollable muscle contractions Happens in speech not involuntary vocalizations More common in women (30-50 years old) Linked to basal ganglia Adductor and abductor typesDevelopmental (Persistent Stuttering)Developmental speech disorders caused by disruption of fluency, timing and rhythm of speech - more prevalent in boys - many recover in childhood - can cause anxiety - disruption in white matter connectivity, reduced white matterHow long can normal speech development take?Upwards of 7-8 years for all phonemes - requires hundreds of muscles -precision in timing and space of contraction -relies on perception for refinement - we develop well rehearsed sound and word maps - sounds are difficult for adult second language learners