CHAPTER 3 & 4 MAIN POINTS
CHAPTER 3 CONCEPTS:
An etiology is the underlying medical cause of a symptom or deficit. An idiopathic etiology is one of unknown origin
Neurogenic communication disorders usually result from damage to the CNS, PNS, or both. Such damage can cause communicative, cognitive, language, and behavioral deficits
Etiologies of neurogenic communication disorders are often
stroke,
traumatic brain injury (TBI),
surgical trauma,
degenerative disorders, and
infectious diseases
A stroke occurs when blood flow to a part of the brain is interrupted by a clot or hemorrhage within the brain. A stroke is also known as a cerebrovascular accident (CVA). There are two main categories of stroke:
ischemic
hemorrhagic
Ischemic strokes occur when a blood vessel supplying blood flow to the brain is occluded or blocked. This blockage deprives the brain tissue of blood supply necessary to survive. There are three main forms of ischemic stroke:
thrombotic
embolic
transient ischemic attacks.
A thrombotic stroke is when an occlusion forms within a blood vessel and restricts blood flow to the brain. An occlusion that forms in a cumulative fashion and restricts blood flow to brain tissue is known as a thrombus. A thrombus is usually a result of atherosclerosis.
An embolic stroke is when a mass traveling through the vascular system (an embolus) lodges in a blood vessel usually inside the brain and restricts blood flow to brain tissue. A thrombus can become an embolus if any piece of it breaks off the wall of an artery and travels to lodge elsewhere and create a blockage of blood flow to the brain.
Transient ischemic attacks (TIAs), also known as mini strokes, are when a small ischemia within the brain occurs and is resolved by the body within 24 hours. TIAs do not cause permanent damage; however, recurring TIAs can cause language and cognitive deficits. TIAs can also be a warning sign of a larger oncoming stroke.
Hemorrhagic strokes occur when a blood vessel within the brain ruptures.
Three mechanisms of damage to the brain are possible with hemorrhagic strokes.
First, the blood supply to a portion of the brain is interrupted as a result of the broken or burst blood vessel.
Second, the blood from the hemorrhaged vessel spills outside the circulatory system into the brain and damages the tissue it comes into contact with.
Third, intracranial pressure increases because of the continued release of blood into the brain or between the skull and the cranium.
There are two main forms of hemorrhagic strokes:
subarachnoid
intracerebral
Subarachnoid hemorrhagic strokes occur when there is a bleed between the surface of the brain and the skull in an area known as the subarachnoid space
Intracerebral hemorrhagic strokes occur when a blood vessel bursts within the brain itself.
An aneurysm is the abnormal stretching or ballooning of an arterial wall. Aneurysms can be the result of hypertension, disease, hereditary factors, or atherosclerosis. When an aneurysm ruptures, it becomes a hemorrhagic stroke. Aneurysms often occur within the circle of Willis.
A brain tumor is an abnormal growth of cells in the brain. A brain tumor is also known as a neoplasm.
A primary tumor of the brain is a tumor that originates in the brain.
A secondary tumor of the brain is a cancerous tumor that has spread from another part of the body to the brain.
A secondary tumor is also called a metastatic brain tumor. The deficits produced by a brain tumor depend on the area of the brain the tumor affects and to what degree.
A malignant brain tumor is brain cancer.
Surgical trauma is damage to the delicate tissues of the brain that might occur with the surgical removal of a tumor or the repair of a hemorrhage in the brain to save a person’s life. Those who have surgical trauma can experience acquired language and cognitive deficits.
Infections can also cause damage to the CNS and PNS. Infections can be viral, fungal, bacterial, or parasitic. The deficits caused by infections depend on the site of the infection, the nature of the infection, and the extent of damage done by the infection. A multitude of infections of the nervous system can affect speech, language, and cognition. Some of these infections include encephalitis,
HIV/AIDS, Creutzfeldt-Jakob disease, syphilis, and poliomyelitis.
Encephalitis is a general term for an acute inflammatory infection of the brain or spinal cord. A viral or bacterial infection of the brain or spinal cord causes encephalitis. The symptoms of encephalitis vary depending on the type and location of the infection.
Human immunodeficiency virus (HIV) leads to acquired
immune deficiency syndrome (AIDS). HIV/AIDS can cause
neurologic changes and deficits, which are known as neuro-AIDS, HIV/AIDS dementia, or HIV-associated neurocognitive disorder. Some deficits include inability to learn new information, slow information processing, disfluent speech, impaired recall, and reduced attention ability. Mild to severe deficits in the use of functional language might also occur.
A small infectious protein called a prion causes Creutzfeldt-Jakob disease. Prion diseases, including Creutzfeldt-Jakob disease, attack the CNS. The symptoms include dementia with rapid onset and involuntary movement disturbances called myoclonus. Certain Alzheimer-like neuropathologic changes,
such as amyloid plaques, are present in the brain tissue of
those affected by Creutzfeldt-Jakob disease.
Syphilis is a sexually transmitted disease caused by a
corkscrew-shaped bacterium called a spirochete.
Neurosyphilis is a variation of syphilis that affects the nervous system. Some signs and symptoms of neurosyphilis include meningitis, visual difficulties or abnormalities, facial weakness, cognitive deficits, and motor problems.
Poliomyelitis is caused by a virus that attacks the motor nerve tracks of the PNS. Symptoms of polio include nonsymmetrical paralysis with diminished or absent reflexes. Seizures are sudden, often periodic, abnormal levels of electrical discharge in the brain.
The three primary stages of a seizure are the
aura
ictus
postictus.
The aura is the period immediately before the seizure during which a person might experience warning signs of an upcoming seizure.
The ictus is the main stage of the seizure that can include loss of consciousness and convulsions.
The postictus is the period right after the ictus during which a person can experience confusion, memory loss, weakness, and depression. The time between seizures is called the interictal period.
Status epilepticus is when a person experiences seizures without an interictal period.
There are two main categories of seizures:
partial seizures
generalized seizures.
Partial seizures occur when the abnormal levels of electrical activity are contained within a particular region of the brain.
The two primary forms of partial seizures include simple partial seizures and complex partial seizures.
During a simple partial seizure, the affected individual remains conscious, and the seizure is restricted to a limited region of the brain.
During a complex partial seizure, the individual seizing experiences altered states of consciousness, and larger or multiple regions of seizure activity occur in one single cerebral hemisphere.
Generalized seizures occur when the abnormal levels of electrical activity affect the entire brain. A total loss of consciousness or awareness occurs with generalized seizures.
There are two forms of generalized seizures:
tonic-clonic seizures
petit mal seizures.
During tonic-clonic seizures, the individual loses consciousness, and the body stiffens and convulsed.
During petit mal seizures, an individual loses awareness for a few seconds and might assume the posture of a daydreamer or appear to be staring absently. Petit mal seizures are usually a disorder of childhood.
CHAPTER 4 CONCEPTS:
Aphasia is an acquired deficit in language resulting from brain damage. Aphasia is most often caused by a stroke to the left cerebral hemisphere. Aphasia is not the result of motor, intellectual, cognitive, or psychological impairment
Language deficits are grossly divided into expressive language deficits and receptive language deficits.
Expressive language deficits are characterized by difficulty in formulating or producing language to communicate an intended meaning. Expressive language deficits are usually caused by lesions in the anterior left cerebral hemisphere often at or near Broca’s area
Receptive language deficits are characterized by difficulty
deriving meaning from verbal or written language. Receptive language deficits are usually caused by lesions in the posterior left hemisphere often at or near Wernicke’s area
Signs and symptoms of aphasia include anomia, verbal comprehension deficits, paraphasias, perseveration, agrammiatism, repetition deficits, alexia, and agraphia
Anomia is a word-finding deficit.
Verbal comprehension deficits are the inability to understand verbal language produced by others and are deficits of receptive language.
Paraphasias are errors of expression that occur at the syllable, word, or phrase level and are produced unintentionally.
A phonemic paraphasia is an error made at the phoneme level
A neologistic paraphasia is an error made when the word produced is entirely different from the word intended and is 50% or more indiscernible.
A semantic paraphasia is when one word is substituted for another word that is similar in meaning
An unrelated verbal paraphasia is an error made when one word produced is substituted for another word that is not similar in meaning.
A perseveration is a word that is said repeatedly and inappropriately. A perseverative paraphasia occurs when a word produced earlier is repeatedly and inadvertently produced by an individual with aphasia instead of the intended word.
Agrammatism is the lack of appropriate grammatical construction of language. Agranimatic speech is caused by the omission of function words, which are the in-between words used to frame content words of a sentence. Content words are the words that carry most of the meaning. Agrammatic speech generally sounds telegraphic because few words are used, though the words are usually used with efficiency.
Repetition deficits are caused by lesions along the arcuate fasciculus. The arcuate fasciculus consists of white matter pathways stretching between Broca’s area and Wernicke’s area.
Alexia is an acquired impairment of reading.
Agraphia is an acquired impairment in the ability to form letters or words for written language.
Behaviors related to aphasia include self-repairs, speech disfluencies, struggle in nonfluent aphasias, and preserved or automatic language
Self-repairs occur when a speaker restates or revises a word or phrase to produce it error free or refine a word’s meaning. Individuals with aphasia are unsuccessful at self-repair far more often than unimpaired individuals. Multiple unsuccessful attempts at self-repair often compromise the prosody and speech fluency of individuals with aphasia.
Speech disfluencies produced by those with aphasia consist of sound, word, part-word, or phrase repetitions, prolongations, and interjections. These are normal disfluencies that escalate in frequency to pathologic levels
Individuals with nonfluent aphasia often visibly struggle when attempting to produce expression.
Preserved language is the intact production of rote and overlearned language. This can include the ability to recite days of the week or months of the year or to count to 10.
Automatic language is language that is associated with and produced somewhat reflexively in response to a stimulus
Some cognitive deficits that can co-occur with aphasia include problems with
arousal
attention
short-term memory
problem-solving
inferencing, and
executive functioning skills.
Some motor deficits that occur alongside aphasia and directly concern the speech-language pathologist include the
dysarthria,
apraxia of speech, and
dysphagia.
The cortical aphasias are those aphasias that arise as a result of damage to the cortex. The nonfluent cortical aphasias include
Broca’s aphasia,
transcortical motor aphasia, and
global aphasia.
Broca’s aphasia is the result of damage to the inferior posterior frontal lobe of the left hemisphere. Individuals with Broca’s aphasia have mostly intact receptive language abilities with deficits in repetition and expression.
Transcortical motor aphasia is a result of damage to the supplementary motor cortex or the area just anterior to Broca’s area. Individuals with transcortical motor aphasia display mostly intact receptive language abilities and relatively intact repetition with deficits in expressive language.
Global aphasia is a result of damage to a large area of the zone of language within the left cerebral hemisphere. Global aphasia is characterized by severe to profound deficits in expressive language, receptive language, and repetition.
The fluent cortical aphasias include
Wernicke’s aphasia,
transcortical sensory aphasia,
conduction aphasia, and
anomic aphasia
Wernicke’s aphasia is a result of lesion to the cortex at or around Wernicke’s area. Wernicke’s aphasia is characterized by receptive language deficits, fluent but empty speech, and repetition deficits.
Transcortical sensory aphasia is a result of damage just posterior to Wernicke’s area. Transcortical sensory aphasia presents with deficits in receptive language, relatively intact repetition, and fluent and often empty speech resembling Wernicke’s aphasia.
Conduction aphasia is a result of damage to the supramarginal gyrus of the parietal lobe that is posterior to the sensory cortex above Wernicke’s area. This damages the arcuate fasciculus but leaves Broca’s and Wernicke’s areas intact. Conduction aphasia typically presents with relatively intact receptive and expressive
language but with deficits in repetition.
Anomic aphasia can result from damage anywhere within the language areas of the left hemisphere and is characterized by mild to moderate word finding deficits in absence of other deficits.
The subcortical aphasias are those aphasias that arise as a result of or alongside damage to the subcortex. The subcortical aphasias include thalamic aphasia and striatocapsular aphasia.
Thalamic aphasia is a result of an ischemic stroke to the left side of the thalamus. Some signs include almost fluent speech, significant anomia in spontaneous speech, impaired receptive language, perseverative semantic paraphasias, normal articulation, hypophonic voice, intact repetition, and intact grammar.
Striatocapsular aphasia is language deficits associated with lesion at the striatum of the basal ganglia but that occur as a result of a lack of blood flow to the cortical primary language areas.
Assessment of aphasia usually includes the following: a case history, assessment of functional communication and speech, a standardized aphasia test (or the administration of formal diagnostic tasks), a cognitive evaluation, and at times a quality-of-life assessment.
Screenings for aphasia are useful to quickly determine the presence of aphasia and the need for a comprehensive follow-up assessment.
Aphasia therapy facilitates spontaneous recovery. Spontaneous recovery can occur up to 6 months postonset.
The three categories of aphasia therapy are
restorative,
compensatory, and
social.
Restorative approaches are based on the idea of neuroplasticity.Neuroplasticity is the ability of a part of the brain to change its function to take on a new role.
Restorative approaches include
Schuell’s stimulation therapy,
melodic intonation therapy,
constraint-induced therapy, and
errorless learning.
Schuell’s stimulation therapy reestablishes lost language abilities through the use of auditory stimuli to evoke a response.
Melodic intonation therapy is the use of the intact melodic/ prosodic processing of the right hemisphere to cue word retrieval and production in the left hemisphere.
Constraint-induced therapy constrains a patient’s ability to compensate for deficits and forces the person to use the weakened skills, thereby directly exercising and improving the areas of weakness.
Errorless learning therapy is a technique that focuses on reducing the number of errors produced by patients in therapy by setting the difficulty of therapy tasks very low for the client to succeed.
Compensatory approaches enable patients to increase their level of function despite their deficit.
Compensatory approaches for aphasia usually take the form of augmentative and alternative communication (AAC).
Compensatory approaches can include both low-tech techniques and high-tech AAC devices. Low-tech techniques include gestures, drawings, and pointing to pictures on a communication board. High-tech devices include programmable voice-generating computers such as Lingraphica and apps for the iPhone and iPad.
Social approaches revolve around increasing an individual's self-confidence, opportunities to communicate, and overall sense of value and acceptance as a communicator.
Social approaches include communication partner training and group therapy.
Communication partner training changes the behavior of those in the environment who most interact with those with aphasia to facilitate the communication of the person with aphasia.
Group therapy is a dynamic setting in which hope, psychosocial emotional support, pragmatics, self-confidence, and additional goals are addressed with multiple clients and clinicians present. Group therapy for those with aphasia allows for the targeting of. many goals, such as pragmatics, left unaddressed in individual one-on-one therapy sessions.
CHAPTER 3 CONCEPTS:
An etiology is the underlying medical cause of a symptom or deficit. An idiopathic etiology is one of unknown origin
Neurogenic communication disorders usually result from damage to the CNS, PNS, or both. Such damage can cause communicative, cognitive, language, and behavioral deficits
Etiologies of neurogenic communication disorders are often
stroke,
traumatic brain injury (TBI),
surgical trauma,
degenerative disorders, and
infectious diseases
A stroke occurs when blood flow to a part of the brain is interrupted by a clot or hemorrhage within the brain. A stroke is also known as a cerebrovascular accident (CVA). There are two main categories of stroke:
ischemic
hemorrhagic
Ischemic strokes occur when a blood vessel supplying blood flow to the brain is occluded or blocked. This blockage deprives the brain tissue of blood supply necessary to survive. There are three main forms of ischemic stroke:
thrombotic
embolic
transient ischemic attacks.
A thrombotic stroke is when an occlusion forms within a blood vessel and restricts blood flow to the brain. An occlusion that forms in a cumulative fashion and restricts blood flow to brain tissue is known as a thrombus. A thrombus is usually a result of atherosclerosis.
An embolic stroke is when a mass traveling through the vascular system (an embolus) lodges in a blood vessel usually inside the brain and restricts blood flow to brain tissue. A thrombus can become an embolus if any piece of it breaks off the wall of an artery and travels to lodge elsewhere and create a blockage of blood flow to the brain.
Transient ischemic attacks (TIAs), also known as mini strokes, are when a small ischemia within the brain occurs and is resolved by the body within 24 hours. TIAs do not cause permanent damage; however, recurring TIAs can cause language and cognitive deficits. TIAs can also be a warning sign of a larger oncoming stroke.
Hemorrhagic strokes occur when a blood vessel within the brain ruptures.
Three mechanisms of damage to the brain are possible with hemorrhagic strokes.
First, the blood supply to a portion of the brain is interrupted as a result of the broken or burst blood vessel.
Second, the blood from the hemorrhaged vessel spills outside the circulatory system into the brain and damages the tissue it comes into contact with.
Third, intracranial pressure increases because of the continued release of blood into the brain or between the skull and the cranium.
There are two main forms of hemorrhagic strokes:
subarachnoid
intracerebral
Subarachnoid hemorrhagic strokes occur when there is a bleed between the surface of the brain and the skull in an area known as the subarachnoid space
Intracerebral hemorrhagic strokes occur when a blood vessel bursts within the brain itself.
An aneurysm is the abnormal stretching or ballooning of an arterial wall. Aneurysms can be the result of hypertension, disease, hereditary factors, or atherosclerosis. When an aneurysm ruptures, it becomes a hemorrhagic stroke. Aneurysms often occur within the circle of Willis.
A brain tumor is an abnormal growth of cells in the brain. A brain tumor is also known as a neoplasm.
A primary tumor of the brain is a tumor that originates in the brain.
A secondary tumor of the brain is a cancerous tumor that has spread from another part of the body to the brain.
A secondary tumor is also called a metastatic brain tumor. The deficits produced by a brain tumor depend on the area of the brain the tumor affects and to what degree.
A malignant brain tumor is brain cancer.
Surgical trauma is damage to the delicate tissues of the brain that might occur with the surgical removal of a tumor or the repair of a hemorrhage in the brain to save a person’s life. Those who have surgical trauma can experience acquired language and cognitive deficits.
Infections can also cause damage to the CNS and PNS. Infections can be viral, fungal, bacterial, or parasitic. The deficits caused by infections depend on the site of the infection, the nature of the infection, and the extent of damage done by the infection. A multitude of infections of the nervous system can affect speech, language, and cognition. Some of these infections include encephalitis,
HIV/AIDS, Creutzfeldt-Jakob disease, syphilis, and poliomyelitis.
Encephalitis is a general term for an acute inflammatory infection of the brain or spinal cord. A viral or bacterial infection of the brain or spinal cord causes encephalitis. The symptoms of encephalitis vary depending on the type and location of the infection.
Human immunodeficiency virus (HIV) leads to acquired
immune deficiency syndrome (AIDS). HIV/AIDS can cause
neurologic changes and deficits, which are known as neuro-AIDS, HIV/AIDS dementia, or HIV-associated neurocognitive disorder. Some deficits include inability to learn new information, slow information processing, disfluent speech, impaired recall, and reduced attention ability. Mild to severe deficits in the use of functional language might also occur.
A small infectious protein called a prion causes Creutzfeldt-Jakob disease. Prion diseases, including Creutzfeldt-Jakob disease, attack the CNS. The symptoms include dementia with rapid onset and involuntary movement disturbances called myoclonus. Certain Alzheimer-like neuropathologic changes,
such as amyloid plaques, are present in the brain tissue of
those affected by Creutzfeldt-Jakob disease.
Syphilis is a sexually transmitted disease caused by a
corkscrew-shaped bacterium called a spirochete.
Neurosyphilis is a variation of syphilis that affects the nervous system. Some signs and symptoms of neurosyphilis include meningitis, visual difficulties or abnormalities, facial weakness, cognitive deficits, and motor problems.
Poliomyelitis is caused by a virus that attacks the motor nerve tracks of the PNS. Symptoms of polio include nonsymmetrical paralysis with diminished or absent reflexes. Seizures are sudden, often periodic, abnormal levels of electrical discharge in the brain.
The three primary stages of a seizure are the
aura
ictus
postictus.
The aura is the period immediately before the seizure during which a person might experience warning signs of an upcoming seizure.
The ictus is the main stage of the seizure that can include loss of consciousness and convulsions.
The postictus is the period right after the ictus during which a person can experience confusion, memory loss, weakness, and depression. The time between seizures is called the interictal period.
Status epilepticus is when a person experiences seizures without an interictal period.
There are two main categories of seizures:
partial seizures
generalized seizures.
Partial seizures occur when the abnormal levels of electrical activity are contained within a particular region of the brain.
The two primary forms of partial seizures include simple partial seizures and complex partial seizures.
During a simple partial seizure, the affected individual remains conscious, and the seizure is restricted to a limited region of the brain.
During a complex partial seizure, the individual seizing experiences altered states of consciousness, and larger or multiple regions of seizure activity occur in one single cerebral hemisphere.
Generalized seizures occur when the abnormal levels of electrical activity affect the entire brain. A total loss of consciousness or awareness occurs with generalized seizures.
There are two forms of generalized seizures:
tonic-clonic seizures
petit mal seizures.
During tonic-clonic seizures, the individual loses consciousness, and the body stiffens and convulsed.
During petit mal seizures, an individual loses awareness for a few seconds and might assume the posture of a daydreamer or appear to be staring absently. Petit mal seizures are usually a disorder of childhood.
CHAPTER 4 CONCEPTS:
Aphasia is an acquired deficit in language resulting from brain damage. Aphasia is most often caused by a stroke to the left cerebral hemisphere. Aphasia is not the result of motor, intellectual, cognitive, or psychological impairment
Language deficits are grossly divided into expressive language deficits and receptive language deficits.
Expressive language deficits are characterized by difficulty in formulating or producing language to communicate an intended meaning. Expressive language deficits are usually caused by lesions in the anterior left cerebral hemisphere often at or near Broca’s area
Receptive language deficits are characterized by difficulty
deriving meaning from verbal or written language. Receptive language deficits are usually caused by lesions in the posterior left hemisphere often at or near Wernicke’s area
Signs and symptoms of aphasia include anomia, verbal comprehension deficits, paraphasias, perseveration, agrammiatism, repetition deficits, alexia, and agraphia
Anomia is a word-finding deficit.
Verbal comprehension deficits are the inability to understand verbal language produced by others and are deficits of receptive language.
Paraphasias are errors of expression that occur at the syllable, word, or phrase level and are produced unintentionally.
A phonemic paraphasia is an error made at the phoneme level
A neologistic paraphasia is an error made when the word produced is entirely different from the word intended and is 50% or more indiscernible.
A semantic paraphasia is when one word is substituted for another word that is similar in meaning
An unrelated verbal paraphasia is an error made when one word produced is substituted for another word that is not similar in meaning.
A perseveration is a word that is said repeatedly and inappropriately. A perseverative paraphasia occurs when a word produced earlier is repeatedly and inadvertently produced by an individual with aphasia instead of the intended word.
Agrammatism is the lack of appropriate grammatical construction of language. Agranimatic speech is caused by the omission of function words, which are the in-between words used to frame content words of a sentence. Content words are the words that carry most of the meaning. Agrammatic speech generally sounds telegraphic because few words are used, though the words are usually used with efficiency.
Repetition deficits are caused by lesions along the arcuate fasciculus. The arcuate fasciculus consists of white matter pathways stretching between Broca’s area and Wernicke’s area.
Alexia is an acquired impairment of reading.
Agraphia is an acquired impairment in the ability to form letters or words for written language.
Behaviors related to aphasia include self-repairs, speech disfluencies, struggle in nonfluent aphasias, and preserved or automatic language
Self-repairs occur when a speaker restates or revises a word or phrase to produce it error free or refine a word’s meaning. Individuals with aphasia are unsuccessful at self-repair far more often than unimpaired individuals. Multiple unsuccessful attempts at self-repair often compromise the prosody and speech fluency of individuals with aphasia.
Speech disfluencies produced by those with aphasia consist of sound, word, part-word, or phrase repetitions, prolongations, and interjections. These are normal disfluencies that escalate in frequency to pathologic levels
Individuals with nonfluent aphasia often visibly struggle when attempting to produce expression.
Preserved language is the intact production of rote and overlearned language. This can include the ability to recite days of the week or months of the year or to count to 10.
Automatic language is language that is associated with and produced somewhat reflexively in response to a stimulus
Some cognitive deficits that can co-occur with aphasia include problems with
arousal
attention
short-term memory
problem-solving
inferencing, and
executive functioning skills.
Some motor deficits that occur alongside aphasia and directly concern the speech-language pathologist include the
dysarthria,
apraxia of speech, and
dysphagia.
The cortical aphasias are those aphasias that arise as a result of damage to the cortex. The nonfluent cortical aphasias include
Broca’s aphasia,
transcortical motor aphasia, and
global aphasia.
Broca’s aphasia is the result of damage to the inferior posterior frontal lobe of the left hemisphere. Individuals with Broca’s aphasia have mostly intact receptive language abilities with deficits in repetition and expression.
Transcortical motor aphasia is a result of damage to the supplementary motor cortex or the area just anterior to Broca’s area. Individuals with transcortical motor aphasia display mostly intact receptive language abilities and relatively intact repetition with deficits in expressive language.
Global aphasia is a result of damage to a large area of the zone of language within the left cerebral hemisphere. Global aphasia is characterized by severe to profound deficits in expressive language, receptive language, and repetition.
The fluent cortical aphasias include
Wernicke’s aphasia,
transcortical sensory aphasia,
conduction aphasia, and
anomic aphasia
Wernicke’s aphasia is a result of lesion to the cortex at or around Wernicke’s area. Wernicke’s aphasia is characterized by receptive language deficits, fluent but empty speech, and repetition deficits.
Transcortical sensory aphasia is a result of damage just posterior to Wernicke’s area. Transcortical sensory aphasia presents with deficits in receptive language, relatively intact repetition, and fluent and often empty speech resembling Wernicke’s aphasia.
Conduction aphasia is a result of damage to the supramarginal gyrus of the parietal lobe that is posterior to the sensory cortex above Wernicke’s area. This damages the arcuate fasciculus but leaves Broca’s and Wernicke’s areas intact. Conduction aphasia typically presents with relatively intact receptive and expressive
language but with deficits in repetition.
Anomic aphasia can result from damage anywhere within the language areas of the left hemisphere and is characterized by mild to moderate word finding deficits in absence of other deficits.
The subcortical aphasias are those aphasias that arise as a result of or alongside damage to the subcortex. The subcortical aphasias include thalamic aphasia and striatocapsular aphasia.
Thalamic aphasia is a result of an ischemic stroke to the left side of the thalamus. Some signs include almost fluent speech, significant anomia in spontaneous speech, impaired receptive language, perseverative semantic paraphasias, normal articulation, hypophonic voice, intact repetition, and intact grammar.
Striatocapsular aphasia is language deficits associated with lesion at the striatum of the basal ganglia but that occur as a result of a lack of blood flow to the cortical primary language areas.
Assessment of aphasia usually includes the following: a case history, assessment of functional communication and speech, a standardized aphasia test (or the administration of formal diagnostic tasks), a cognitive evaluation, and at times a quality-of-life assessment.
Screenings for aphasia are useful to quickly determine the presence of aphasia and the need for a comprehensive follow-up assessment.
Aphasia therapy facilitates spontaneous recovery. Spontaneous recovery can occur up to 6 months postonset.
The three categories of aphasia therapy are
restorative,
compensatory, and
social.
Restorative approaches are based on the idea of neuroplasticity.Neuroplasticity is the ability of a part of the brain to change its function to take on a new role.
Restorative approaches include
Schuell’s stimulation therapy,
melodic intonation therapy,
constraint-induced therapy, and
errorless learning.
Schuell’s stimulation therapy reestablishes lost language abilities through the use of auditory stimuli to evoke a response.
Melodic intonation therapy is the use of the intact melodic/ prosodic processing of the right hemisphere to cue word retrieval and production in the left hemisphere.
Constraint-induced therapy constrains a patient’s ability to compensate for deficits and forces the person to use the weakened skills, thereby directly exercising and improving the areas of weakness.
Errorless learning therapy is a technique that focuses on reducing the number of errors produced by patients in therapy by setting the difficulty of therapy tasks very low for the client to succeed.
Compensatory approaches enable patients to increase their level of function despite their deficit.
Compensatory approaches for aphasia usually take the form of augmentative and alternative communication (AAC).
Compensatory approaches can include both low-tech techniques and high-tech AAC devices. Low-tech techniques include gestures, drawings, and pointing to pictures on a communication board. High-tech devices include programmable voice-generating computers such as Lingraphica and apps for the iPhone and iPad.
Social approaches revolve around increasing an individual's self-confidence, opportunities to communicate, and overall sense of value and acceptance as a communicator.
Social approaches include communication partner training and group therapy.
Communication partner training changes the behavior of those in the environment who most interact with those with aphasia to facilitate the communication of the person with aphasia.
Group therapy is a dynamic setting in which hope, psychosocial emotional support, pragmatics, self-confidence, and additional goals are addressed with multiple clients and clinicians present. Group therapy for those with aphasia allows for the targeting of. many goals, such as pragmatics, left unaddressed in individual one-on-one therapy sessions.