Exam 1 Flashcards
Sound
Waves transmitted through a medium
Communication
Exchange of information with a sender and a receiver
Speech
Acoustic signal, coding, or representation of language
Language
Abstract, agreed upon set of symbols that represent meaning
Rule based
Motor Speech Processes: Message Planning
What do I want to say?
Motor Speech Processes: Message Coding
How do I say it (what words do I use)
Motor Speech Processes: Motor Planning
Choose the movement strategies, taking into account the intended goal
Motor Speech Processes: Motor Programming
What muscles, how much, when, how long
Motor Speech Processes: Execution
Activation of motor neurons, activation of respiratory, resonatory, phonatory, and articulatory systems
Motor Speech Disorders
Acquired neuromotor speech disorders
Neurogenic speech disorders
Due to damage, disease, developmental differences of neural centers and pathways of speech production in the CNS and/or PNS
Disorders of motor programming/planning
Apraxia or dyspraxia
No motor weakness
Disorders of neuromotor execution
Dysarthria
Must be differentiated from other disorders like psychogenic disorders, normal aging, structural differences
Result of disturbance in execution of speech movements
Language generally uneffected
Related to movement
Limb apraxia
Cant perform actions with body on demand
Orofacial apraxia
Cant complete gestures with articulators such as sticking out tongue on demand
Flaccid Dysarthria
Lower Motor Neuron
Spastic Dysarthria
Bilateral upper motor neuron
Ataxic Dysarthria
Cerebellum/cerebellar control circuits
Hypokinetic Dysarthria
Basal Ganglia (substantia nigra) PD
Hyperkinetic Dysarthria
Basal Ganglia
Methods of Studying Motor Speech Disorders
Perceptual (gold standard)
Instrumental
Acoustic
Visual imaging
Dimensions of Motor Speech Disorder: Age of Onset
congenital or acquired acute/subacute/chronic) Acute: Symptoms within minutes Subacute: Happens over days Chronic: Happens over months
Dimensions of Motor Speech Disorder: Cause or Etiology
Genetic, infection, unknown, etc
Dimensions of Motor Speech Disorder: Natural course
Transient: symptoms will resolve
Stationary: remain unchanged after reaching maximum severity
Improving: symptoms reduced in severity but have not resolved
Progressive/degenerative: symptoms continue to get worse over time
Exacerbating/remitting: symptoms may improve or resolve then become exacerbated and possibly worsen, like MS
Dimensions of Motor Speech Disorders
Age of onset Cause/etiology Natural course Site of lesion Neurologic diagnosis Pathopysiology Subsystems involved Severity Perceptual characteristics
Dimensions of Motor Speech Disorder: Pathopysiology
Changes caused by the disorder such as weakness or spacticity
Etiology
Vascular Inflammatory Traumatic/Toxic Anoxic or autoimmune Metabolic Idiopathic (unknown cause) or latrogenic (treatment induced) Neoplastic (tumor) Altered brain morphology Degenerative
Treatment Approaches
AAC
Normalizing pysiological support (reduce nasality, normalize loudness)
Teach Compensatory behaviors
Medical Approaches (surgery, drug, prosthetic)
Eliminate maladaptive behaviors
Interaction enhancement strategies (communication strategies)
Maintain communication skills (encourage continued communication and social interaction)
Strategies to alter negative attitudes of others (educate others)
ICF: Body Function
Physiological functions of body systems
ICF: Body Structures
Anatomical parts of the body, limbs, organs, and their components
ICF: Impairments
Problems in body function or structure such as significant deviation or loss
ICF: Activity
Execution of a task or action by an individual
ICF: Participation
Involvement in life situation
ICF: Activity Limitation
Difficulties an individual may have in executing activities
ICF: Participation Restrictions
Problems an individual may experience in involvement in life situations
ICF: Environmental Factors
Make up physical, social, attitudinal, and environment in which people live and conduct their lives
Source-Filter Theory
Source is what generates sound (VF, stops and fricatives are also a source at the point of closure)
Filter modifies the sound (rest of the vocal tract, can lengthen vocal tract by rounding lips)
Ten Functional Components of Speech
Abdominal muscles Diaphragm Rib Cage Larynx Tongue/pharynx Posterior Tongue Velopharynx Jaw Lips
Four Major Subsystems of Speech
Respiratory (most common issue in motor speech disorders)
Phonatory
Velopharyngeal
Articulatory
Respiratory/Pulmonary System
Breathing
Speech
Three functional components: diaphragm, rib cage, abdominal muscles, needed for subglottal pressure
Major muscles of inspiration
Diaphragm and external intercostals
Tidal volume
Amount inhaled and exhaled during a normal breath cycle
Inspiratory reserve volume
Amount of air that can be inhaled beyond the tidal volume
Expiratory reserve volume
Amount of air that can be exhaled beyond the tidal volume
Residual volume
Amount remaining in lungs after maximum exhale (keeps lungs from collapsing)
Total lung capacity
Tidal volume, inspiratory reserve, expiratory reserve, residual volume
Inspiratory capacity
Maximum volume of air that can be inhaled from the resting expiratory level
Expiratory capacity
Maximum volume of air that can be exhaled from the resting inspiratory position
Vital capacity
Inspiratory reserve, expiratory reserve and tidal volume (maximum amount of air that can be fully exhaled after as deep an inhalation as possible)
Functional residual capacity
Amount of air remaining in lungs after a normal tidal expiration
Rest breathing
40% inhalation 60% exhalation
Speech breathing
10% inhalation 90% exhalation
Subglottal pressure needed for phonation
3-5cm H2O
What is the only bone in the larynx?
Hyoid (all others are cartilage)
Extrinsic laryngeal muscles
Elevate and depress the larynx
Intrinsic laryngeal muscles
Connect cartilages
Posterior cricoarytenoids
Open (abduct) vocal folds
Cricothyroids
Elongate VFs to change pitch
Velopharyngeal mechanism involves….
Velum (soft palate) and nasopharynx
Velopharyngeal closure: Coronal
Velum raises up to meet the back of the pharynx
Velopharyngeal closure: Sagittal
Most movement is in lateral pharyngeal wall, sides close in to meet velum
Velopharyngeal closure: Circular
Equal movement of the velum and lateral pharyngeal wall
Velopharyngeal closure: Circular with Passavant’s ridge
Equal movement of lateral and posterior pharyngeal wall and velum
Intrinsic Muscles of the Tongue
Muscles used to move the tongue
Extrinsic Muscles of the Tongue
Stabilize the tongue
Sensory innervation for anterior 2/3 of tongue
General sensation CNV
Taste CNVII
Posterior innervation for posterior 1/3 of tongue
Taste and temperature CNIX
Necrosis
Cell death
Lesion
Area of damage
Infarct
Area of necrosis due to vascular disturbance, later replaced by scar tissue
Ischemia
Deficiency of blood flow due to obstruction or constriction
Focal
Involving a single area
Multifocal
Involving more than one area
Diffuse
Involving roughly symmetric portions of the nervous system bilaterally
Primary Motor Cortex
Execute movement
Supplementary Motor Cortex
Plan and coordinate complex movement
Premotor Cortex
Integrates sensory information and prepares primary motor cortex for execution
Lower Motor Neurons
Neurons of brainstem and spinal cord whose axons terminate on muscles
Damage to Lower Motor Neurons results in….
Flaccid dysarthria
All motor CNs are….
LMNs
Efferent pathways
Leaving CNS
Afferent pathways
Sensory, returning to CNS
CN V
Trigeminal (Mixed)
Muscles of mastication, sensation to head jaw and forehead
Tactile sensation for anterior 2/3 of tongue
CN VII
Facial nerve (mixed)
Muscles for facial expression
Taste for anterior 2/3 of tongue
Upper part of face is bilaterally innervated
Lower part is contralaterally innervated
Lesion in UMN would affect lower contralateral side
Lesion in LMN would affect upper and lower face
CN IX
Glossopharyngeal (mixed)
Gag reflex
Sensory input from posterior 1/3 of tongue
CN X
Vagus (mixed)
Innervates muscles of larynx, respiration
Raises the velum
CN XI
Spinal Accessory (motor) Levator and uvula
CN XII
Hypoglossal (motor) Innervates Tongue Innervated contralaterally Will deveate toward weaker side LMN damage will lead to fasciculations and atrophy
Pyramidal System
Direct activation pathway
Skilled voluntary movements
Conscious higher level control
Lesions result in: hypotonia, weakness, babinski reflex
Corticobulbar tract
Pyramidal system
Cortex to brainstem/cranial motor systems
Corticospinal Tract
Pyramidal system
Controls distal muscles of limbs
Extrapyramidal System
Indirect Activation Pathway Coordinate basic movements Suppress undesired movements Posture and tone Hypertonia, hyper-reflexia, hyperactive gag
Basal Ganglia
Influences movement generated by primary motor cortex
Contributes to cognitive and affective deficits
Pass signals for intentional movement and inhibit undesired movement
Abnormalities can lead to over or under filtering (PD is over filtering, HC is under filtering)
Cerebellum
Balance, coordination
Compares intended signal to actual movement
Dysdiadochokinesia and dysmetria
TBI
Non Progressive MSD
Ataxia in cerebellar damage
Tremors, dystonic movements
Noisy, disinhibited, confused and disorientation
Post Traumatic Amnesia
60% acutely Dx with dysarthria, 10% chronic dysarthria
Cortical CVAs
Aphasia
Apraxia
Dysarthria
Unilateral lesions most effects articulation, may produce contralateral weakness or transient mild dysarthria
Bilateral lesions: bulbar palsy, locked in syndrome
ALS
Bulbar signs effect speech first, progresses quickly
Spinal/limb is harder to notice at first
Often progress to mixed
Effects CNS and PNS
UMN: Weakness, increased tone, hyper reflexia
LMN: weakness, flaccidity, atrophy
Implement AAC when speaking at 100-125 wpm
Guillan Barre
Similar to MS but myelin in PNS destroyed
Most recover
Parkinson’s Disease
Hypokinetic dysarthria
Substantia nigra of basal ganglia
Hypokinetic, bradykinesia, rigidity, resting tremor
Implement LSVT at stage 2 to recalibrate loudness
Huntington’s Chorea
Excessive movement
Hyperkinetic
Debilitating movement disorders (chorea is hallmark), personality and cognitive changes
Dementia is also a hallmark
MS
Myelin destroyed in the CNS
Impairments vary based on site of lesion
Duchenne Muscular Distrophy
Loss or malfunction of dystrophin protein
Disturbance in gait
Eventually in a wheelchair
High risk of respiratory impairment
Lupus
Inflammation of joints, organs, and tissues
Fever and fatigue
Butterfly rash on face
Memory loss
Chorea, ataxia, dystonia, facial weakness, vocal fold paresis
Not terminal, but chronic, waxes and wanes
Sydenham’s Chorea (St. Vitus’ Dance)
Results from childhood infections
Jerky, explosive speech
Transient breathiness
Harsh or strained-strangled vocal quality
Involuntary movements of mouth and larynx
Infection destroys cells in striatum of basal ganglia
Many acute symptoms spontaneously resolve
Tardive Dyskinesia
May appear similar to PD, HC, CP, Tourettes, stroke
Sudden uncontrollable movements
Tic-like movements in facial muscles
Sometimes symptoms diminish but some are permanent
