APHASIA --------------- OUTLINE What is aphasia? • Communication process Does the patient have aphasia ? • If so, where is the lesion? • What kind of aphasia is this? Is it important to diagnose aphasia? • Localization • Treatment • Prognosis • Functional state of the patient
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APHASIA --------------- OUTLINE
What is aphasia?
• Communication process
Does the patient have aphasia ?
• If so, where is the lesion?• What kind of aphasia is this?• What is the etiology?
Is it important to diagnose aphasia?
• Localization• Treatment• Prognosis• Functional state of the patient
• Aphasia does not include:• Developmental disorders of
language, often called dysphasia in the united states.
• Purely motor speech disorders, limited to articulation of speech via the oral-motor apparatus, referred to as stuttering, dysarthria, and verbal apraxia.
• Disorders of language that are secondary to primary thought disorders, such as schizophrenia.
• Communication is a multidimensional dynamic process that allows human beings to interact with their environment.
• Through communication, people are able to express thoughts, needs, and emotions. Communication is a complex process that involves cerebration, cognition, hearing, speech production, and motor coordination.
• Evaluation of a communication disorder includes consideration of all aspects of the normal communication process
o80% of people are right handed.o 96-99% of right handed people in the left hemi sphere.o 60% of left handed people also lateralize to the left o 25% of left handed shows right dominancy. o the remaining are mixed dominancy.
• Many naturally left-handed children are trained to use the right hand for writing– in determining handedness, one must ask which hand is
preferred for throwing a ball– threading a needle, sewing– using a tennis racket or hammer– which eye is used for sighting a target with a rifle or other
instrument. • Pharmacological methods: injecting anesthetic in left
• Language: complex system of communication symbols and rules for their use.
• Speech: the articulation and phonation of language sounds. • Motor speech disorders:
– Dysarthrias: disorder of articulation of single sounds, consistent. – Dysphonia: voice disorder – Stuttering – Apraxia of speech: misarticulation of phonemes,especially
consonant sounds. inconsistent distortions and substitutions of phonemes.
• Infections of the nervous system– Brain abscesses can mimic tumors and present with aphasia– Chronic infections, such as tuberculosis or syphilis, can result in focal
abnormalities.– Herpes simplex encephalitis has a predilection for the temporal lobe
and orbital frontal cortex, and aphasia can be an early manifestation, along with headache, confusion, fever, and seizures.• Aphasia often is a permanent sequel in survivors of herpes encephalitis.
– AIDS: either the AIDS dementia complex or the opportunistic infections.
• speech pattern:– Effortful, difficulty initiating speech– Non fluent – Hesitant – telegraphic speech. An example is “wife come hospital.”
• deficiency, particularly in the comprehension of complex syntax.• Third alexia: Reading often is impaired• Writing: right hand could be paralyzed, left hand apraxia • Associated neurological deficits
– right hemiparesis, hemisensory loss, – apraxia of the oral apparatus and the nonparalyzed left limbs
• frequent association with depression – Typically they are aware of and frustrated by their deficits.
• speaker of a foreign language would notice nothing a miss, but a listener who shares the patient’s language detects speech empty of meaning, containing verbal paraphasias, neologisms, and jargon productions.
• Naming is deficient, often with bizarre, paraphasic substitutions for the correct name
• patients show greater deficit in one modality than in the other.
• Writing samples are especially useful in the detection of mild Wernicke’s aphasia.
• Associated signs are limited in Wernicke’s aphasia– Most have no elementary motor or sensory deficits– right homonymous hemianopia may be present.
• Depression is less common; many Wernicke’s aphasics seem unaware of or unconcerned about their communicative deficits.
• The lesions – posterior portion of the superior temporal gyrus, sometimes extending into the
inferior parietal lobule.– Damage to Wernicke’s area (Brodmann’s area 22)– Wernicke’s area lies within the territory of the inferior division of the left middle
• repetition is normal• presumably because the causative lesions do not disrupt the perisylvian language
circuit from Wernicke’s area through the arcuate fasciculus to Broca’s area.
• Three types: 1.Isolation syndrome:
• global aphasia in which the patient repeats, often echolalically• occurring predominantly with large Watershed infarctions of the left hemisphere or both
hemispheres that spare the perisylvian cortex, or in advanced dementias.
2. Transcortical motor aphasia:• analog of Broca’s, speech is hesitant or telegraphic, comprehension is relatively spared, but
repetition is fluent.• deep frontal white matter, or in the medial frontal region, in territory of ANTERIOR CEREBRAL
ARTERY.
3. Transcortical sensory aphasia:• analog of Wernicke’s aphasia, repetition intact• occurring with strokes of the left temporo-occipital area and in dementias.
loss of integration among deferent lobes due to lesion affecting the connecting pathways that leads to disorganized normal function.
• Intrahemespheric disconnection1. Conduction (also called "central") aphasia.2. Buccal Lingual and Sympathetic apraxia in Broca's aphasia. Destruction of the link
between left and right motor association cortices causes an apraxia of commanded movements of the left hand and weakness of right brachiofacial weakness, apraxia of tongue and lips.
3. Pure word deafness.
• Interhemespheric disconnection1.alexia without agraphia2.Left side apraxia3.Agenesis of corpus callosum: right and left visual fields can’t
– Onset, Frequency, Duration• Strokes are characterized by the abrupt onset of a neurological deficit in
a patient with vascular risk factors.• precise temporal profile is important
– Most embolic strokes are sudden and maximal at onset, whereas thrombotic strokes typically wax and wane or increase in steps.
– The sudden onset of Wernicke’s aphasia nearly always indicates an embolus to the inferior division of the left middle cerebral artery.
• Global aphasia may be caused by an embolus to the middle cerebral artery stem, thrombosis of the internal carotid artery, or even a hemorrhage into the deep basal ganglia. – deficits tend to worsen gradually over minutes to hours, in contrast with
the sudden or stepwise onset of ischemic strokes.• Cont,,,,,,
Clinical Evaluation of Aphasia ,,,,,,,,, CONTExamination:
• Examination of Other Cortical Functionso Consciousness o Cognitive Function
o Mental Status and MemoryoOrientation o Alertness; Attention and Concentrationo Judgment and reasoning
o Thought Contents o Complete Neurological Exam
o aimed to localize the lesion “ Associated Deficit” o aimed to define the etiology.
– Psychiatric evaluation: acute encephalopathy or delirium• accompanying behavioral disturbances, such as agitation, hallucinations, drowsiness, or excitement, and
cognitive difficulties, such as disorientation, memory loss, or delusional thinking
– language assessment:oBedside Language Examination
Clinical Evaluation of Aphasia ,,,,,,,,, CONTExamination:
– Content of speech– Paraphrasia– telegraphic speech– conjunctions and proposition use, syntax, and morphology of speech. – Neologism– Jargon of speech – Word salad – Assess pragmatism
– Other Useful Tests • For neurologists, the most helpful battery is the Boston Diagnostic Aphasia Examination • the Western Aphasia Battery.
– Both tests provide subtest information analogous to that obtained with the bedside examination, and therefore meaningful to neurologists, as well as aphasia syndrome classification.
– clinical systemic examination• clues to etiology
– AF– Hypertension and DM– Atherosclerosis – Signs increased intra cranial pressure –papilloedema, brain metastasis – AIDS – evidence of trauma– self injury and loss of sphenctric control –epilepsy
• elicited by asking the patient to describe the weather or the reason for coming to the doctor.
• Counting or listing days of the week. • Signs:
– Fluency: Fluent speech flows rapidly and effortlessly; nonfluent speech is uttered in single words or short phrases, with frequent pauses and hesitations.
• asking the patient to name a few items in each of thee following category– objects– Object parts – Colors – Body parts – Pictures – Proper names of persons
• The examiner should ask questions to be sure that the patient recognizes the items or people that he or she cannot name.
• follow a series of commands of one, two, and three steps. • one-step command is “Stick out your tongue”• two-step command is “Hold up your left thumb and close your eyes.”• The responses to nonsense questions (e.g., “Do you vomit every day?”) quickly
establish whether the patient comprehends. – Successful following of commands ensures adequate comprehension, at least at
this simple level.– failure to follow commands does not automatically establish a loss of
comprehension. The patient must hear the command, understand the language the examiner speaks, and possess the motor ability to execute it, including the absence of apraxia. • Because apraxia is difficult to exclude with confidence:
– it is advisable to test comprehension by tasks that do not require a motor act, such as yes/no questions, or by commands that require only a pointing response.
• examiner must have some idea of the patient’s previous reading ability.– Reading should be tested both aloud and for comprehension.– The examiner should carry a few printed commands to facilitate
a rapid comparison of auditory and reading comprehension.
• Spontaneous writing, such as a sentence describing why the patient has come for examination, is especially sensitive for the detection of language difficulty.
writing to dictation and copying should be tested.– A writing specimen may be the most sensitive indicator of mild
aphasia, and it provides a permanent record for future comparison.
• look for spelling errors, structural errors, and apraxia.
RECOVERY AND REHABILITATION OFTHE PATIENT WITH APHASIA
•The sudden onset of aphasia would be expected to cause great apprehension, but except for cases of pure or almost pure motor disorders of speech, most patients show remarkably little concern.
RECOVERY AND REHABILITATION OFTHE PATIENT WITH APHASIA
• After stroke – If symptoms last longer than two or three months, complete recovery is unlikely– People continue to improve over a period of time– Slow process for both patient and FAMILY– Need to learn compensatory strategies for communicating
• Global aphasia recovery occur after 6 months • The aphasia type often changes during recovery: Global aphasia
evolves into Broca’s aphasia, and Wernicke’s aphasia into conduction or anomic aphasia.
• Language recovery may be mediated by shifting of functions to the right hemisphere or to adjacent left hemisphere regions.
RECOVERY AND REHABILITATION OFTHE PATIENT WITH APHASIA
• Whether contemporary methods of speech therapy accomplish more than can be accounted for by spontaneous recovery is still uncertain.
• Most aphasic disorders are caused by vascular disease and trauma, and they are nearly always accompanied by some degree of spontaneous improvement in the days, weeks, and months that follow the stroke or accident.