Neurologically Based Communication Disorders- ch. 8
needs assessment and treatment information for aphasia, apraxia, and maybe dysarthrias. Stops at dementias.
Terms in this set (61)
Neurologically based language disorder, distinct from neurologically based speech disorders such as apraxia of speech and dysarthria.
Caused by a blocked or interrupted blood supply to the brain. Blockage or interruption may be caused by two kinds of arterial diseases: thrombosis or embolism.
Collection of blood material that blocks the flow of blood.
Travelling mass of arterial debris or a clump of tissue from a tumor that gets lodged in a smalle artery and thus blocks the flow of blood.
Caused by bleeding in the brain due to ruptured blood vessels.
Within the brain.
Within the meninges, resulting in subarachnoid, subdural, and epidural varieties.
Characterized by limited, agrammatic, effortful, halting, and slow speech with impaired prosody.
Characterized by: nonfluent, effortful, slow, halting, and uneven speech. Limited word output, short phrases and sentences. Misarticulated or distorted sounds. Agrammatic or telegraphic speech, often limited to nouns and verbs, with omission of articles, conjunctions, and prepositions. Impaired repetition of words and sentences, especially the grammatical elements of a sentence. Impaired naming, especially confrontation naming. Rarely normal, but better auditory comprehension of spoken language than production. Difficulty in understanding syntactic structures. Poor oral reading and poor comprehension of material that has been read. Writing problems, slow and laborious writing that is full of spelling errors and letter omissions, possibly because patients are forced to use their nonpreferred left hand due to paralysis of the right hand. Monotonous speech.
What Broca's aphasia may exhibit
Apraxia of speech, dysarthria, right-sided paralysis or weakness, depression or react emotionally when confronted with difficult assessment tasks.
Broca's Aphasia Damage
Damage to Broca's area, Brodmann's areas 44 and 45 in the posterior inferior frontal gyrus of the left hemisphere of the brain. Damage to Broca's area is not necessary to produce this type of aphasia, because symptoms characteristic of Broca's aphasia may be observed in patients whose Broca's area is intact.
Transcortical Motor Aphasia
Characterized by speechlessness, echolalia and perseveration, absent or reduced spontaneous speech, nonfluent, paraphasic, agrammatic, and telegraphic speech, intact repetition skill a distinguishing characteristic of TMA, awareness of grammaticality patients may correct a grammatically incorrect model, refusal to repeat nonsense syllables, unfinished sentences, limited word fluency, simple and imprecise syntactic structures, attempts to initate speech with the help of such motor activities as clapping, vigoruous head nodding, and hand waving, generally good comprehension of simple conversation possibly impaired for complex speech, slow and difficult reading aloud, seriously impaired writing.
What TMA may exhibit
Motor disorders as rigidity of upper extremities, absence or poverty of movement akinesia, lowness of movement bradykinesia, buccofacial apraxia, and weakness of the legs, apathy, withdrawal, and little interest in communication may be additional behavioral characteristics.
Caused be lesions in the anterior superior frontal lobe, often below or above Broca's area, which is not affected. Areas supplied by the anterior cerebral artery and the atnerior branch of the middle cerebral artery are affected in TMA.
Mixed Transcortical Aphasia
Characterized by limited spontaneous speech, automatic, unintentional, and involuntary nature of communication, severe echolalia, repetition of an examiner's statement, severely impaired fluency, severely impaired auditory comprehension for even simple conversation, marked naming difficulty and neologism, impaired confrontation naming, mostily unimpaired automatic speech recitation of months in a year or a number series if somehow initated and not interrupted, severely impaired reading, reading comprehension, and writing.
What MTA exhibits
Varied neuroloic symptoms seen acorss patients, may include bilateral upper motor neuron paralysis, spastic paralysis that affects the volitional muscles, weakness of all limbs, quadriparesis, and visual field defects.
Rare variety of nonfluent aphasia caused by lesions in the watershed area or the arterial border zone of the brain, between the areas supplied by the middle cerebral arteries and anterior and posterior arteries.
Characterized by profoundly impaired language skills and no signficant profile of differential skills, greatly reduced fluency, expressions limited to a few words, exclamations, and serial utterances, impaired repetition, impaired naming, auditory comprehension limited to single words at best, perseveration repetition of short utterances, impaired reading and writing.
What global aphasia may exhibit
Verbal and nonverbal apraxia, although technically not a part of aphasia, may be present in patients with global aphasia. Strong neruological symptoms, including right-sided paresis or paralysis, right-sided sensory loss, and neglect of the left side of the body may be observed in many patients.
Global aphasia damage
Most severe form of nonfluent aphasia. Caused by exensive lesions affecting all language areas, the perisylvian region. Widespread destruction of the fronto-temporoparietal regions of the brain is common. More common sites of damage are supplied by the middle cerebral artery.
Characterized by relatively intact fluency but generally less meaningful, or even meaningless speech. Speech is generally flowing, abundant, easily initiated, and well articulated with good prosody and phrase length.
Characterized by incessant, effortlessly produced, flowing speech with normal, or even abnormal, fluency with normal phrase length. Rapid rate of speech with normal prosodic features and good articulation. Intact grammatical structures. Severe word-finding problems. Paraphsic speech containing semantic and literal paraphasias, extra syllables in words, and creating of meanlingless words, neologisms. Circumlocution, talking around words that cannot be recalled. Empty speech, substitution of such general words as this, that, stuff, and thing. Poor auditory comprehension, espcially for sentences and names of common objects, much worse comprehension of speech when there is background noise, movement, or conversation. Impaired conversational turn taking. Impaired repetition skill. Reading comprehension problems, including difficulty recognizing sounds associated with written words and meanings of printed words. Writing problems, including excessive but meaningless writing, frequent misspellings, and neologistic writing. Generally poor communication in spite of fluent speech.
What Wernicke's may exhibit
May sound confused. Because of lack of insight into their language problems, the patients are less frustrated with their failed attempts at communication. May be paranoid, homicidal, suicidal, and depressed. Because of this, may be confused with psychiatric patients. Generally free from obvious neurological symptoms, paresis and paralysis are uncommon.
Common fluent aphasia. Caused by lesions in Wernicke's area, the posterior portion of the superior temporal gyrus in the left hemisphere of the brain. Supplied by the posterior branch of the left middle cerebral artery.
Transcortical Sensory Aphasia
Characterized by fluent speech with normal phrase length, good prosody, normal articulation, and apparently appropriate grammar and syntax. Paraphasic and empty speech. Severe naming problems and pauses due to those problems. Good repetition skills but poor comprehension of repeated words. Echolalia of grammatically inforrect forms, nonsense syllables, and words from foreign languages. Impaired auditory comprehension of spoken language. Difficulty in pointing, obeying commands, or answering simple yes/no questions. Normal automatic speech. Tendency to complete poems and sentences started by the clinician. Good reading (aloud) but poor comprehension of material that has been read. Generally better oral reading skills than other language skills. Writing problesm that parallel those in expressive speech.
What TSA may exhibit
Hemiparesis assocated with the onset of TSA may disappera, leaving the patient with no obvious neurologic impairment. Neglect of one side of the body may be common. Sound similar to those with Wernicke's aphasia, however repetition is intact in patients with TSA, and impaired in patients with Wernicke's.
Characterized by disproportionate impairment in repetition, especially impaired repetition of longer words, function words, and longer phrases and sentences. Variable speech fluency across patients, generally less fluent than patients with Wernicke's aphasia. Paraphasic speech. Marked word-finding problems, especially for content words. Empty speech because of omitted content words. Efforts to correct errors in speech, though not always successful. Good syntax, prosody, and articulation. Severe to mild naming problems. Near-normal auditory comprehension, especially for routine conversational speech. Being better at ponting to a named stimulus than at confrontation naming. Highly variable reading problems, better comprehension of silently read material. Writing problems in most cases. Buccofacial apraxia, difficulty in performing buccofacial movements when requested, in most patients.
What conduction aphasia may exhibit
Symptoms are similar to Wernicke's aphasia. Main difference is that unlike patients with Wernicke's aphasia, those with conduction aphasia have good to normal auditory comprehension. Some patients may have no neurological symptoms, others may have paresis of the right side of the face, limb, or oral apraxia and right sensory impairment. Patients may recover from most of these impairments.
Rare fluent aphasia. Caused by lesions in the region between Broca's area and Wernicke's area, especially in the suprmarginal gyrus and the arcuate fasciculus. Lesion sites of conduction aphasia are controversial.
Characterized by most debilitating and pervasive word-finding difficulty, which is the distinguishing feature. Pointing to named objects is unimpaired. Generally fluent speech. Normal syntax except for pauses, possibly due to word-finding problems. Use of vague and nonspecific words, resulting in empty speech. Verbal paraphasia, word substitutions. Circumlocution. Good auditory comprehension of spoken language. Intact repetition. Unimpaired articulation. Normal oral reading skills and good reading comprehension. Normal writing skills.
What anomic may exhibit
Generally most language functions, except for naming, are relatively unimpaired. Residual symptom may be a persistent naming difficulty in most patients who recover from any type of aphasia.
Controversial and may be caused by lesions in diferent regions of the brain, including the angular gyrus, the second temporal gyrus, and the juncture of the tempoparietal lobes. Anomic aphasia is a syndrome, whereas anomia is a naming difficulty common to most forms of aphasia.
Subcortical aphasia caused by lesions in the basal ganglia and surrounding structures in the left hemisphere
Characaterized by fluent speech, which may include pauses and hesitations. Intact repetition skills. Normal auditory comprehension for routine conversation, may be defective for complex material. Articulation problems similar to those in Broca's. Prosodic problems. Word-finding problems. Semantic paraphasia in some cases. Relatively preserved writing skills. Limb apraxia if the lesions extend posteriorly to deep white matter in the pareital areas.
Subcortical aphasia caused by lesions or hemorrhages in the left thalamus
Characterized by hemiplegia, hemisensory loss, right-visual field problems, and in some cases, coma. Initial mutism, which may improve to paraphasic speech. Severe naming problems. Good auditory comprehension of simple material and poor comprehension of complex material. Good repetition skills. Impaired reading and writing skills.
Aphasia Screening Tests
Aphasia Language Performance Scale (ALPS)
Sklar Aphasia Scale (SAS)
Children's Acquired Aphasia Screening Tests (CAAST)
Bedside Evaluation and Screening Test - Second Edition (BEST-2)
Aphasia Screening Test (AST)
Quick Assessment for Aphasia
Standardized Aphasia Tests
Boston Diagnostic Aphasia Exam - Third Edition (BDAE-3)
Western Aphasia Battery (WAB)
Minnesota Test for Differential Diagnosis of Aphasia (MTDDA)
Neurosensory Center Comprehensive Examination for Aphasia (NCCEA)
Multilingual Aphasia Examination (MAE)
Bilingual Aphasia Test (BAT)
Porch Index of Communicative Ability (PICA)
Aphasia Diagnostic Profiles (ADP)
Apraxia of speech
Neruogenic speech disorder characterized by sensorimotor problems in positioning and sequentially moving muscles for the volitional production of speech. Primarily an articulatory phonologic disorder, although its etiology and characteristics are different from those of similar disorders in children. Adult patients with AOS will have acquired articulation normally. Their current articulatory problems are due to recent neuropathology.
Apraxia of speech
Adults have unimpaired reflex and automatic acts. The difficulty they have is mostly in executing the voluntary movements involved in speech. Is not caued by muscle weakness or neuromuscular slowness. It is thought that a disorder of motor programming for speech causes it.
Neuropathology of AOS
Caused by injury or damage to speech-motor programming areas in the dominant hemisphere, such as areas as Broca's and supplementary motor areas often are involved.
Symptoms of AOS
Include impaired oral sensation in some patients. When dysarthria is a coexisting condition, facial and lingual weakness may also be present. Some patients may have limb apraxia as well.
Communication deficits in AOS
Patients' initiation of speech may be slowed or delayed. May use compensatory strategy of reduced rate. Speech programming and production errors. Prosodic problems.
Neurologically based speech disorders, distinct from similarly based language disorders such as aphasia. Dysarthrias also are distinct from AOS, which is a neurogenic speech disorder of motor planning of speech movements with no muscular weakness or paralysis.
Different types of dysarthrias share certain characteristics. Impaired muscular control of the speech mechanism and peripheral or cerntal nervous system pathology are common to all forms of dysarthria. Oral communication problems that accompany dysarthria include respiratory, articulatory, phonatory, resonatory, and prosodic distrubances that are caused by weakness, incoordination, or paralysis of speech musculature.
Neuropathology of the dysarthrias
Common etiological factors include degenerative neurological diseases such as Parkinson's, Wilson's disease, progressive supranuglear palsy, dystonia, Huntington's disease, ALS, MS, and myasthenia gravis. Can also be caused by nonprogressive neurological conditions including stroke, infections, TBI, surgical trauma, as well as congenital conditions including CP, moebius syndrome, encephalitis, toxic effects from alcohol or durgs. Common sites of lesion include lower motor neuron, unilateral or bilateral upper motor neuron, cerebellum, and basal ganglia, extrapyramidal system. Patholophysiology and neuromuscular problems include muscle weakness, spasticity, incoordination, and rigidity. Usually is a variety of movement disorders, including reduced or variable range and speed of movement, involuntary movements, reduced strength of movement, unsteady or inaccurate movement, and abnormal tone.
Communicative Disorders Associated with Dysarthria
Respiratory problems include forced inspirations or expirations that interrupt speech, audible or breathy inspiration, and grunting at the end of expiration. Phonatory disorders such as pitch disorders, loudness disorders, vocal-quality problems. Articulation disorders include imprecise production of consonants, prolongation and repetion of phonemes, irregular breakdowns in articulation, distortion of vowels, and weak production of pressure consonants. Prosodic disorders, resonance disorders.
Characterized by gait disturbances, movement disorders, articulation disorders, prosodic disorders, phonatory disordes, speech quality.
Results from damage to the cerebellar system. Includes bilateral or generalized cerebellar lesions, degenerative ataxia, cerebellar vascular lesions, tumors, TBI, toxic conditions, and inflammatory conditions.
Characterized by various muscular disorders. Isolated twitches of resting muscles, fasciculations and contractions of individual muslces, fibrillations. Rapid and progressive weakness with the use of a muscle and recovery with rest. Respiratory weakness in combination with cranial nerve weakness. Phonatory disorders, including breathy voice, audible inspiration, and short phrases. Resonance disorders, including hypernasality, imprecise consonants, nasal emission, and short phrases. Phonatory-prosodic disorders, including harsh voice, monopitch, and monoloudness. Articulation disorders which are more pronounced with lesions of CN V, VII, and XII.
Results from damage to the motor units of cranial or spinal nerves that supply speech muscles, lower motor neuron involvement. Neuropathology includes diseases as myasthenia gravis and botulism, vascular diseases and brainstem strokes, infections, demyelinating diseases, degenerative diseases, and surgical trauma during brain, laryngeal, facial, or chest surgery. Specific crainial nerves that may be involved in flaccid dysarthria include the trigeminal V, facial VII, glossopharyngeal IX, vagus X, and hypoglossal XII nerves.
Characterized by movement disorders due to damage to the basal ganglia control circuit, abnormal and involuntary movements of the orofacial muscles. Myoclonus, involuntary jerks of body parts. Tics of the face and shoulders. Tremor. Chorea. Abrupt and severe contractions of the extremities. Writhing, involuntary movements, often in hands, atheotosis. Spasms, sudden and involuntary contractions of a muscle or group of muscles. Dystonia, which results from contractions of antagonistic muscles that cause abnormal postures. Spasmodic torticollis, intermittent dystonia and spasms of the neck muscles. Blepharospasm, forceful and involuntary closure of the eyes due to spasm of the obicularis oculi muscle. Communicative disorders, specific symptoms depending on the dominant neurological condition. Phonatory disorders, resonance disorders, prosodic disorders, respiratory problems, inconsistent articulation problems.
Results from damage to the basal ganglia, extrapyramidal system. Dysarthria is associated with involuntary movement and variable muscle tone. Prosodic distrubances are dominant. Muscles of the face, jaw, tongue, palate, larynx, and respiration may be involved.
Characterized by tremors in the resting facial, mouth, and limb muscles that diminish when moved involuntarily. Mask-like face with infrequent blinking and no smiling. Micrographic writing, small print. Walking disorders. Postural disturbances. Decreased swallowing, accumulation of saliva in the mouth and drooling. Phonatory disorders. Prosodic disorders. Articulation disorders. Respiratory problems.
Results from damage to the basal ganglia, extrapyramidal system.
Characterized by spasticity and weakness. Movement disorders. Hyperactive gag reflex. Hyperadduction of vocal folds and inadequate closure of the velopharyngeal port. Prosodic disorders. Articulation disorders. Phonatory disorders. Resonance disorders.
Results from bilateral damage to the upper motor neurons, direct and indirect motor pathways. Lesions in multiple areas, including the cortical areas, basal ganglia, internal capsule, pons, and medulla are common.
Mixed flaccid-spastic dysarthria associated with ALS
Characterzied by imprecise production of consonants, hypernasality, harsh voice, slow rate, monopitch, short phrases, distorted vowels, low pitch, monoloudness, excess and equal stress or reduced stress, prolonged intervals, prolonged phonemes, a strained and strangled quality, breathiness, audible inspiration, inappropriate silences, and nasal emission.
Mixed ataxic-spastic dysarthria associated with MS
Characterized by impaired loudnesss control, harsh voice quality, imprecise articulation, impaired emphasis, hypernasality, inappropriate pitch levels, and sudden articulatory breakdowns.
Unilateral Upper Motor Neuron Dysarthria
Characterized by unilateral lower face weakness, unilateral tongue weakness, unilateral palatal weakness, and hemiplegia/hemiparesis. Articulation disorders. Phonatory disorders. Prosodic disorders. Resonance disorders. Dysphagia, aphasia, apraxia, and right hemisphere syndrome.
Results from damage to the upper motor neurons that supply cranial and spinal nerves involved in speech production. Dysarthria due to vascular disorders that produce left-hemisphere lesions may coexist with aphasia or apraxia. Dysarthria due to right-hemisphere lesions may coexist with right hemisphere syndrome.
Record an extended conversational speech sample and a reading sample. Use a variety of speech tasks. Assess the diadochokinetic rate or alternating motion rates (AMRs) and sequential motion rates (SMRs). Assess speech production mechanism during nonspeech activities. Assess respiratory problems by observing posture and breathing habits during quiet and speech. Assess phonotory disorders, articulation disorders, prosodic disorders, resonance disorders, speech intelligibility. Use standardized tests such as Assessment of Intelligibility of Dysarthric Speakers (AIDS) and Frenchay Dysarthria Assessment (FDA).
Dysarthria treatment targets
Modifcation of respiration, phonation, resonance, articulation, speech rate, prosody, pitch, and vocal intensity.
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