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Neural Bases Exam II

Motor Speech Disorders (Lecture 5)

Cognitive-Linguistic Processes Generate intent,Generate verbal symbols,Organize verbal symbols, Remember it all!
Sensorimotor Planning/Programming Translate verbal symbols into sensorimotor score, Designate muscle activation patterns, Store expected feedback
Neuromuscular Execution Direct activation of motoneurons,Muscle contraction, Movement, SPEECH!!!!
Cognitive-Linguistic Stage Disorders Aphasia: Defect of Language Generation, Word-finding problems, Agrammatism, Neologisms, Auditory comprehension deficits, Reading and writing deficits
Sensorimotor Planning/Programming Defects Apraxia of speech, Difficulty sequencing syllables, Articulatory groping, “know what you want to say but can’t make mouth say it”, No weakness or paralysis
Neuromotor Execution Defects Muscle weakness, paralysis, incoordination, Type of speech pattern depends on the location of the neural damage
Dysarthria neurologic lesion of CNS or PNS, movement disorders classified based on how they sound; and how they sound corresponds with underlying neuropathology
Apraxia of Speech Impairment of sensorimotor programming, not attributable to muscular weakness or language difficulties
Flaccid Dysarthria LMN Lesion; Pattern of deficit depends on site of lesion: Trigeminal nerve?, Facial nerve?, Pharyngeal plexus (glossopharyngeal/vagus)?, Pharyngeal branch?, Superior laryngeal nerve?, Recurrent laryngeal nerve?
Clinical Presentation of Flaccid Dysarthria: Breathiness, Hypernasality, Imprecise articulation, Nasal air emission, monopitch
Conditions associated with Flaccid Dysarthria neoplasms, trauma, infections, CVA, congenital conditions, myasthenia gravis, Bell's palsy
Syptoms of Flaccid Dysarthria include: inability to make a labial seal or elevate tongue for lingual sounds
Spastic Dysarthria UMN lesion (typically bilateral, Patients appear slow, weak, diffusely involved in the face, often hemiparetic
Spastic Dysarthria Etiologies include multiple strokes, TBI, encephalitis, cerebral palsy
Clinical Presentation of Spastic Dysarthria: Imprecise consonants, Strained-strangled voice (vocal stenosis), Slow rate, Monopitch and loudness, Hypernasality, Pitch breaks
Ataxic Dysarthria Lesion to cerebellum or cerebellar circuits; Several possible patterns of deficit including “robotic quality” and “drunken quality”
Ataxtic Dysarthria Etiologies include neoplasms, progressive cerebellar degeneration, trauma, encephalitis, MS, ETOH toxicity, CVA, congenital conditions
Clinical Presentation of Ataxic Dysarthria: Imprecise consonants, Robotic quality (equal and even stress), Irregular articulatory breakdown (drunken quality), Harsh voice
Hypokinetic Dysarthria Lesions of the basal ganglia that create too much inhibition (not enough excitation); Patients appear stiff, masked, reduced movement, gait is slow and shuffling
Hypokinetic Dysarthria Etiologies include Parkinson’s disease (idiopathic PD), and parkinsonism due to drugs, CVAs or other disease processes
Clinical Presentation of Hypokinetic Dysarthria: Monopitch, Reduced loudness, Breathy voice, Short rushes of speech, “slurred” articulation, hypernasality
Hyperkinetic Dysarthria: Dystonia Lesions to the basal ganglia that result in too little inhibition (too much facilitation); Slow hyperkinesia, with a “build up” of involuntary movement activity
Hyperkinetic Dysarthria (Dystonia) Etiologies include: encephalitis, neoplasms, CVAs, toxic effects of drugs, cerebral palsy
Clinical Presentation of Hyperkinetic (dystonic) Dysarthria: Imprecise consonants, Harsh voice, Strained-strangled voice, Monopitch and loudness, Vowel and consonant breakdowns
Hyperkinetic Dysarthria: Chorea BG lesion causing too much facilitation; Quick hyperkinesia results in irregular, unsustained, random, unpatterned, rapid movements
Hyperkinetic Dysarthria (Chorea) Etiologies include: Huntington’s, Sydenham’s chorea, encephalitis, Gilles de la Tourette syndrome
Clinical Presentation of Hyperkinetic (chorea) Dysarthria: Imprecise consonants, variable rate, Harsh voice, Monopitch and excessive loudness variation, Inappropriate silences and prolonged intervals, Distorted vowels
Flaccid dysarthria, possible site of lesion Trigeminal resulting in imprecise articulation
Flaccid dysarthria, possible site of lesion Facial resulting in slurred speech
Flaccid dysarthria, possible site of lesion Pharyngeal plexus glossopharyngeal/vagus; Pharyngeal branch affects levator veli palatine (hypernasality)
Flaccid dysarthria, possible site of lesion Pharyngeal plexus glossopharyngeal/vagus; Superior laryngeal nerve affects cricothyroid (pitch control, so they sound monotone)
Flaccid dysarthria, possible site of lesion Pharyngeal plexus glossopharyngeal/vagus; Recurrent laryngeal nerve affects intrinsic muscles of larynx (hoarse, breathy, weak voice)
Unilateral UMN dysarthria UUMN lesion; weakness, incoordination, usually mild and transient to bilateral innervation
Clinical presentation of Unilateral Upper Motor Neuron Dysarthria imprecise articulation only sometimes present
AOS (apraxia of speech) Lesion to cortical tissue (maybe insula), Sensorimotor planning/programming deficit
Apraxia of Speech Etiologies include CVA, tumor, infection
Clinical presentation of Apraxia of Speech articulatory errors (perseverative, anticipatory, metathetic errors), articulatory groping, slowness, dysprosody, automatic speeech, inability to program sequences of sounds (especially consonants)
Created by: jrschwa1