Aphasia
Neurologically based language disorder, distinct from neurologically based speech disorders such as apraxia of speech and dysarthria.
Ischemic strokes
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.
Thrombus
Collection of blood material that blocks the flow of blood.
Embolus
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.
Hemorrhagic Strokes
Caused by bleeding in the brain due to ruptured blood vessels.
Intracerebral
Within the brain.
Extracerebral
Within the meninges, resulting in subarachnoid, subdural, and epidural varieties.
Nonfluent aphasias
Characterized by limited, agrammatic, effortful, halting, and slow speech with impaired prosody.
Broca's aphasia
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,
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
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 pati
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 behavior
TMA damage
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 co
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.
MTA damage
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.
Global aphasia
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 compreh
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 t
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 mi
Fluent aphasias
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.
Wernicke's aphasia
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-findin
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 psychiatr
Wernicke's damage
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 po
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 w
Conduction aphasia
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 apha
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
Conduction damage
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.
Anomic aphasia
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
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.
Anomic damage
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
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
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 c
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)
Bil
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 differen
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
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.
Dysarthria
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 paral
Dysarthria
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
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
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. Articula
Ataxic dysarthria
Characterized by gait disturbances, movement disorders, articulation disorders, prosodic disorders, phonatory disordes, speech quality.
Ataxic damage
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.
Flaccid dysarthria
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 i
Flaccid damage
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, demyeli
Hyperkinetic dysarthria
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 sev
Hyperkinetic damage
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 invo
Hypokinetic dysarthria
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
Hypokinetic damage
Results from damage to the basal ganglia, extrapyramidal system.
Spastic dysarthria
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.
Spastic damage
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
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 ri
UUMN damage
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-hemi
Dysarthria Assessment
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
Dysarthria treatment targets
Modifcation of respiration, phonation, resonance, articulation, speech rate, prosody, pitch, and vocal intensity.