Australian scientists are confident magnenetic pulse brain stimulation research will help long-term stroke and Parkinson’s disease patients speak again. The approach, being pioneered by Professor Bruce Murdoch, Director of the Centre for Neurogenic Communication Disorders Research from the University of Queensland, uses magnetic pulses to stimulate damaged areas of the brain.
The technique, known as Transcranial Magnetc Stimulation – TMS – was previously used to treat depression and pain management. It’s the first time the therapy has been looked at for language or communication loss due to neurological damage.
The treatment is literally an on off switch for the brain, switching on brain function in Parkinson and off in stroke victims suffering from aphasia. TMS is a non-invasive method to cause depolarization or hyperpolarization in the neurons of the brain. TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field, causing activity in specific or general parts of the brain with minimal discomfort.
Aphasia in stroke victims is a condition where suffers have impaired language abilities, the range of the disorder includes memory difficulties for words, all the way through to a complete inability to speak
This isn’t a first for TMS use in Parkinsons or stroke, in 2009 Dr Jean-Pascal Le faucheur of Physiology department at Hospital Henri Mondor in France successfully used the therapy with pain management and Parkinsons ::::
“We can either switch on parts of the brain, or switch them off” Professor Murdoch said.
Professor Murdoch says the four-year study has had remarkable success in improving speech and tongue movement in patients who have had Parkinson’s and stroke complications for more than five years. “That is unusual and the degree of improvement that we’ve seen over a long period of time, up to 12 months, is also unusual,” he said.
In initial testing, all patients experienced some improvement in communication.
“The actual technology was developed back in the mid 80’s, it sort of sat around for a while,” Professor Murdoch said. ” Now it’s coming to the fore, people are starting to recognise that the brain is much more plastic, it can heal itself much better than we thought it could. This therapy seems to be a way of helping the brain rewire itself”.
There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented. Studies of the use of TMS and rTMS to treat many neurological and psychiatric conditions have to-date shown only modest effects with little confirmation of results.
“There’s up to 20 per cent improvement in some patients… it doesn’t sound a lot, but that’s clinically important,” Professor Murdoch said. It means that their intelligibility levels are sufficient in the Parkinson’s patients, for instance, that they can start to communicate with their family and friends much more freely. It makes them more self-confident so they can get out into public arenas more freely.”
source: expert reviews
Transcranial Magnetic Stimulation – TMS – is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain. TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field, this can cause activity in specific or general parts of the brain with minimal discomfort, allowing the functioning and interconnections of the brain to be studied.
A variant of TMS, Repetitive Transcranial Magnetic Stimulation – rTMS – has been tested as a treatment tool for various neurological and psychiatric disorders includingmigraines, strokes, Parkinson’s disease, dystonia, tinnitus, depression and auditory hallucinations.
The principle of inductive brain stimulation with eddy currents has been noted since the 20th century. The first successful TMS study was performed in 1985 by Anthony Barker and his colleagues in Sheffield, England. Its earliest application demonstrated conduction of nerve impulses from the motor cortex to the spinal cord, stimulating muscle contractions. The use of magnets rather than a direct electric current to the brain reduced the discomfort of the procedure and research and allowed mapping of the cerebral cortex and its connections.
The exact details of how TMS functions are still being explored. The effects of TMS can be divided into two types depending on the mode of stimulation:
- Single or paired pulse TMS causes neurons in the neocortex under the site of stimulation to depolarize and discharge an action potential. If used in the primary motor cortex, it produces muscle activity referred to as a motor evoked potential (MEP) which can be recorded on electromyography. If used on the occipital cortex, ‘phosphenes’ (flashes of light) might be perceived by the subject. In most other areas of the cortex, the participant does not consciously experience any effect, but his or her behaviour may be slightly altered (e.g. slower reaction time on a cognitive task), or changes in brain activity may be detected using sensing equipment.
- Repetitive TMS produces longer-lasting effects which persist past the initial period of stimulation. rTMS can increase or decrease the excitability of the corticospinal tract depending on the intensity of stimulation, coil orientation and frequency. The mechanism of these effects is not clear although it is widely believed to reflect changes in synaptic efficacy akin to long-term potentiation – LTP – and long-term depression – LTD.
Although TMS is often regarded as safe, the greatest acute risk of TMS is the rare occurrence of induced seizures and syncope. More than 16 cases of TMS-related seizure have been reported in the literature, with at least seven reported before the publication of safety guidelines in 1998, and more than nine reported afterwards. The seizures have been associated with single-pulse and rTMS. Reports have stated that in at least some cases, predisposing factors (medication, brain lesions or genetic susceptibility) may have contributed to the seizure. A review of nine seizures associated with rTMS that had been reported after 1998 stated that four seizures were within the safety parameters, four were outside of those parameters, and one had occurred in a healthy volunteer with no predisposing factors. A 2009 international consensus statement on TMS that contained this review concluded that based on the number of studies, subjects and patients involved with TMS research, the risk of seizure with rTMS is considered very low.
Besides seizures, other risks include fainting, minor pains such as headache or local discomfort, minor cognitive changes and psychiatric symptoms (particularly a low risk of mania in depressed patients). Though other side effects are thought to be possibly associated with TMS (alterations to the endocrine system, altered neurotransmitter and immune system activity) they are considered investigational and lacking substantive proof.
Other adverse effects of TMS are:
- Discomfort or pain from the stimulation of the scalp and associated nerves and muscles on the overlying skin; this is more common with rTMS than single pulse TMS.
- Rapid deformation of the TMS coil produces a loud clicking sound which increases with the stimulator intensity that can affect hearing with sufficient exposure, particularly relevant for rTMS (hearing protection may be used to prevent this)
- rTMS in the presence of incompatible EEG electrodes can result in electrode heating and, in severe cases, skin burns. Non-metallic electrodes are used if concurrent EEG data is required.
The uses of TMS and rTMS can be divided into diagnostic and therapeutic uses.
TMS can be used clinically to measure activity and function of specific brain circuits in humans. The most robust and widely-accepted use is in measuring the connection between the primary motor cortex and a muscle to evaluate damage from stroke, multiple sclerosis, amyotrophic lateral sclerosis, movement disorders, motor neuron disease and injuries and other disorders affecting the facial and other cranial nerves and the spinal cord. TMS has been suggested as a means of assessing Short-interval Intracortical Inhibition – SICI – which measures the internal pathways of the motor cortex but this use has not yet been validated.
Studies of the use of TMS and rTMS to treat many neurological and psychiatric conditions have generally shown only modest effects with little confirmation of results.
However, publications reporting the results of reviews and statistical meta-analyses of earlier investigations have stated that rTMS appeared to be effective in the treatment of certain types of major depression under certain specific conditions. rTMS devices are marketed for the treatment of such disorders in Canada, Australia, New Zealand, the European Union, Israel and the United States.
A meta-analysis of 34 studies comparing rTMS to sham treatment for the acute treatment of depression showed an effect size of 0.55 (p<.001). This is comparable to commonly reported effect sizes of pharmacotherapeutic strategies for treatment of depression in the range of 0.17-0.46.
However, that same meta-analysis found that rTMS was significantly worse than electroconvulsive therapy (effect size -0.47), although side effects were significantly better with rTMS. An analysis of one of the studies included in the meta-analysis showed that one extra remission from depression occurs for every 3 patients given electroconvulsive therapy rather than rTMS (number needed to treat 2.36).
There is evidence that rTMS can temporarily reduce chronic pain and change pain-related brain and nerve activity, and TMS has been used to predict the success of surgically implanted electrical brain stimulation for the treatment of pain.
Other areas of research include the rehabilitation of aphasia and motor disability after stroke, tinnitus, Parkinson’s disease, tic disorders and the negative symptoms of schizophrenia. TMS has failed to show effectiveness for the treatment of brain death, coma, and other persistent vegetative states.
It is difficult to establish a convincing form of “sham” TMS to test for placebo effects during controlled trials in consciousindividuals, due to the neck pain, headache and twitching in the scalp or upper face associated with the intervention. “Sham” TMS manipulations can affect cerebral glucose metabolism and MEPs, which may confound results. This problem is exacerbated when using subjective measures of improvement. Depending on the research question asked and the experimental design, matching this discomfort to distinguish true effects from placebo can be an important and challenging issue.
One multicenter trial of rTMS in depression used an active “sham” placebo treatment that appeared to mimic the sound and scalp stimulation associated with active TMS treatment. The investigators reported that the patients and clinical raters were unable to guess the treatment better than chance, suggesting that the sham placebo adequately blinded these people to treatment.
The investigators concluded: “Although the treatment effect was statistically significant on a clinically meaningful variable (remission), the overall number of remitters and responders was less than one would like with a treatment that requires daily intervention for 3 weeks or more, even with a benign adverse effect profile”.
However, a review of the trial’s report has questioned the adequacy of the placebo, noting that treaters were able to guess whether patients were receiving treatment with active or sham TMS, better than chance. In this regard, the trial’s report stated that the confidence ratings for the treaters’ guesses were low.
TMS uses electromagnetic induction to generate an electric current across the scalp and skullwithout physical contact. A plastic-enclosed coil of wire is held next to the skull and when activated, produces a magnetic field oriented orthogonally to the plane of the coil. The magnetic field passes unimpeded through the skin and skull, inducing an oppositely directed current in the brain that activates nearby nerve cells in much the same way as currents applied directly to the cortical surface.
The path of this current is difficult to model because the brain is irregularly shaped and electricity and magnetism are not conducted uniformly throughout its tissues. The magnetic field is about the same strength as an MRI, and the pulse generally reaches no more than 5 centimeters into the brain.
The design of transcranial magnetic stimulation coils used in either treatment or diagnostic/experimental studies may differ in a variety of ways. These differences should be considered in the interpretation of any study result, and the type of coil used should be specified in the study methods for any published reports.
The most important considerations include:
- the type of material used to construct the core of the coil
- the geometry of the coil configuration
- the biophysical characteristics of the pulse produced by the coil.
With regard to coil composition, the core material may be either a magnetically inert substrate (i.e., the so-called ‘air-core’coil design), or possess a solid, ferromagnetically active material (ie, the so-called ‘solid-core’ design).
Solid core coil design result in a more efficient transfer of electrical energy into a magnetic field, with a substantially reduced amount of energy dissipated as heat, and so can be operated under more aggressive duty cycles often mandated in therapeutic protocols, without treatment interruption due to heat accumulation, or the use of an accessory method of cooling the coil during operation.
Varying the geometric shape of the coil itself may also result in variations in the focality, shape, and depth of cortical penetration of the magnetic field. Differences in the coil substance as well as the electronic operation of the power supply to the coil may also result in variations in the biophysical characteristics of the resulting magnetic pulse (e.g., width or duration of the magnetic field pulse). All of these features should be considered when comparing results obtained from different studies, with respect to both safety and efficacy.
A number of different types of coils exist, each of which produce different magnetic field patterns. Some examples:
- round coil: the original type of TMS coil
- figure-eight coil (i.e. butterfly coil): results in a more focal pattern of activation
- double-cone coil: conforms to shape of head, useful for deeper stimulation
- four-leaf coil: for focal stimulation of peripheral nerves
Design variations in the shape of the TMS coils allow much deeper penetration of the brain than the standard depth of 1.5 cm. Circular, H-shaped, double cone coils and other experimental variations can induce excitation or inhibition of neurons deeper in the brain including activation of motor neurons for the cerebellum, legs and pelvic floor. Though able to penetrate deeper in the brain, they are less able to produced a focused, localized response and are relatively non-focal.
- Cranial electrotherapy stimulation
- Transcranial direct current stimulation
- Electroconvulsive therapy
- God helmet
Aphasia ( əˈfeɪʒə/ or /əˈfeɪziə/, from ancient Greek ἀφασία (ἄφατος, ἀ- + φημί), “speechlessness”) is an impairment of language ability. This class of language disorder ranges from having difficulty remembering words to being completely unable to speak, read, or write.
Acute aphasia disorders usually develop quickly as a result of head injuryor stroke, and progressive forms of aphasia develop slowly from a brain tumor, infection, or dementia.
The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. Aphasia types include expressive aphasia, receptive aphasia, conduction aphasia, anomic aphasia, global aphasia, primary progressive aphasias and many others (see Category:Aphasias). Medical evaluations for the disorder range from clinical screenings by a neurologist to extensive tests by a Speech-Language Pathologist.
Most acute aphasia patients can recover some or most skills by working with a Speech-Language Pathologist. This rehabilitation can take two or more years and is most effective when begun quickly. Only a small minority will recover without therapy, such as those suffering a mini-stroke. Improvement varies widely, depending on the aphasia’s cause, type, and severity. Recovery also depends on the patient’s age, health, motivation, handedness, and educational level.
Classifying the different subtypes of aphasia is difficult and has led to disagreements among experts. The localizationist model is the original model, but modern anatomical techniques and analyses have shown that precise connections between brain regions and symptom classification don’t exist.
The neural organization of language is complicated; language is a comprehensive and complex behavior and it makes sense that it isn’t the product of some small, circumscribed region of the brain.
No classification of patients in subtypes and groups of subtypes is adequate. Only about 60% of patients will fit in a classification scheme such as fluent/nonfluent/pure aphasias.
There is a huge variation among patients with the same diagnosis, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colours.
The localizationist model attempts to classify the aphasia by major characteristics and then link these to areas of the brain in which the damage has been caused. The initial two categories here were devised by early neurologists working in the field, namely Paul Broca and Carl Wernicke. Other researchers have added to the model, resulting in it often being referred to as the “Boston-Neoclassical Model”.
- Individuals with expressive aphasia (also called Broca’s aphasia) were once thought to have frontal lobe damage, though more recent work by Dr. Nina Dronkers using imaging and ‘lesion analysis’ has revealed that patients with Expressive aphasia have lesions to the medial insular cortex. Broca missed these lesions because his studies did not dissect the brains of diseased patients, so only the more temporal damage was visible. Dronkers and Dr. Odile Plaisant scanned Broca’s original patients’ brains using a non-invasive MRI scanner to take a closer look. Damage to a region of the motor association cortex in the left frontal lobe (Broca’s area) disrupts the ability to speak. Individuals with Expressive aphasia often have right-sided weakness or paralysis of the arm and leg, because the frontal lobe is also important for body movement. Video clips showing patients with Expressive-type aphasia can be found here.
- In contrast to Expressive aphasia, damage to the temporal lobe may result in a fluent aphasia that is called receptive aphasia (also known as Sensory aphasia and Wernicke’s aphasia). These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. A video clip with a patient exhibiting Receptive aphasia can be found here
- Working from Wernicke’s model of aphasia, Ludwig Lichtheim proposed five other types of aphasia, but these were not tested against real patients until modern imaging made more in-depth studies available. The other five types of aphasia in the localizationist model are:
- Auditory verbal agnosia (also known as Pure Word Deafness)
- Conduction aphasia
- Apraxia of speech (now considered a separate disorder in itself)
- Transcortical motor aphasia (also known as Adynamic aphasia and Extrasylvian motor aphasia)
- Transcortical sensory aphasia
- Anomic aphasia, also known as Anomia, is another type of aphasia proposed under what is commonly known as the Boston-Neoclassical model, which is essentially a difficulty with naming.
- Global aphasia, results from damage to extensive portions of the perisylvian region of the brain. An individual with global aphasia will have difficulty understanding both spoken and written language and will also have difficulty speaking. This is a severe type of aphasia which makes it quite difficult when communicating with the individual.
- Isolation Aphasia, also known as Mixed Transcortical Aphasia, is a type of disturbance in language skill that causes the inability to comprehend what is being said to you or the difficulty in creating speech with meaning without affecting the ability to recite what has been said and to acquire newly presented words. This type of aphasia is caused by brain damage that isolates the parts of the brain from other parts of the brain that are in charge of speech. The brain damages are caused to left temporal/parietal cortex that spares the Wernicke’s area. Isolation aphasia patients can repeat what other people say, thus they do recognize words but they can’t comprehend the meaning of what they hear and repeat themselves. However, they can not produce meaningful speech of their own.
Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex, Motor neuron disease, Progressive supranuclear palsy, and Alzheimer’s disease; which is the gradual process of losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.
Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient’s speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. They will either replace the desired word with another that sounds or looks like the original one, or has some other connection, or they will replace it with sounds. Accordingly, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they can’t find with sounds. Commonly, substitutions involve picking another (actual) word starting with the same sound (e.g. clocktower – colander), picking another semantically related to the first (e.g. letter – scroll), or picking one phonetically similar to the intended one (e.g. lane – late).
Fluent, Non-fluent and Pure Aphasias
The different types of aphasia can be divided into three categories: fluent, non-fluent and “pure” aphasias.
- Receptive aphasias, also called Fluent aphasias, are impairments related mostly to the input or reception of language, with difficulties either in auditory verbal comprehension or in the repetition of words, phrases, or sentences spoken by others. Speech is easy and fluent, but there are difficulties related to the output of language as well, such as paraphasia. Examples of fluent aphasias are: Receptive aphasia, Transcortical sensory aphasia, Conduction aphasia, Anomic aphasia.
- Expressive aphasias, also called Nonfluent aphasias, are difficulties in articulating, but in most cases there is relatively good auditory verbal comprehension. Examples of nonfluent aphasias are: Expressive aphasia, Transcortical motor aphasia, Global aphasia
- “Pure” aphasias are selective impairments in reading, writing, or the recognition of words. These disorders may be quite selective. For example, a person is able to read but not write, or is able to write but not read. Examples of pure aphasias are: Pure alexia, Agraphia, Auditory verbal agnosia
Primary and secondary cognitive processes
Aphasias can be divided into primary and secondary cognitive processes.
- Primary aphasia is due to problems with cognitive language-processing mechanisms, which can include: Transcortical sensory aphasia, Semantic Dementia, Apraxia of speech, Progressive nonfluent aphasia, and Expressive aphasia
- Secondary aphasia is the result of other problems, like memory impairments, attention disorders, or perceptual problems, which can include: Transcortical motor aphasia, Dynamic aphasia, Anomic aphasia, Receptive aphasia, Progressive jargon aphasia, Conduction aphasia, and Dysarthria.
Cognitive neuropsychological model
The cognitive neuropsychological model builds on cognitive neuropsychology. It assumes that language processing can be broken down into a number of modules, each of which has a specific function. Hence there is a module which recognises phonemes as they are spoken and a module which stores formulated phonemes before they are spoken. Use of this model clinically involves conducting a battery of assessments (usually from the PALPA, the “psycholinguistic assessment of language processing in adult acquired aphasia … that can be tailored to the investigation of an individual patient’s impaired and intact abilities” ), each of which tests one or a number of these modules. Once a diagnosis is reached as to where the impairment lies, therapy can proceed to treat the individual module.
People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia.
- inability to comprehend language
- inability to pronounce, not due to muscle paralysis or weakness
- inability to speak spontaneously
- inability to form words
- inability to name objects
- poor enunciation
- excessive creation and use of personal neologisms
- inability to repeat a phrase
- persistent repetition of phrases
- paraphasia (substituting letters, syllables or words)
- agrammatism (inability to speak in a grammatically correct fashion)
- dysprosody (alterations in inflexion, stress, and rhythm)
- incomplete sentences
- inability to read
- inability to write
- limited verbal output
- difficulty in naming
The following table summarizes some major characteristics of different acute of aphasia:
|Type of aphasia||Repetition||Naming||Auditory comprehension||Fluency|
|Receptive aphasia||mild–mod||mild–severe||defective||fluent paraphasic|
|Transcortical sensory aphasia||good||mod–severe||poor||fluent|
|Conduction aphasia||poor||poor||relatively good||fluent|
|Expressive aphasia||mod–severe||mod–severe||mild difficulty||non-fluent, effortful, slow|
|Transcortical motor aphasia||good||mild–severe||mild||non-fluent|
|Mixed transcortical aphasia||moderate||poor||poor||non-fluent|
- Individuals with Receptive aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new “words” (neologisms). For example, someone with Receptive aphasia may say, “You know that smoodle pinkered and that I want to get him round and take care of him like you want before”, meaning “The dog needs to go out so I will take him for a walk”. They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with Receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes.
- Individuals with Transcortical sensory aphasia Similar deficits as in Receptive aphasia, but repetition ability remains intact.
- Individuals with Conduction aphasia is caused by deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernicke’s area and Broca’s area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Repetition ability is poor.
- Individuals with Anomic aphasia is essentially a difficulty with naming. The patient may have difficulties naming certain words, linked by their grammatical type (e.g. difficulty naming verbs and not nouns) or by their semanticcategory (e.g. difficulty naming words relating to photography but nothing else) or a more general naming difficulty. Patients tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved.
- Individuals with Expressive aphasia frequently speak short, meaningful phrases that are produced with great effort. Expressive aphasia is thus characterized as a nonfluent aphasia. Affected people often omit small words such as “is”, “and”, and “the”. For example, a person with Expressive aphasia may say, “Walk dog” which could mean “I will take the dog for a walk”, “You take the dog for a walk” or even “The dog walked out of the yard”. Individuals with Expressive aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. It is associated with right
- Individuals with Transcortical motor aphasia Similar deficits as Expressive aphasia, except repetition ability remains intact. Auditory comprehension is generally fine for simple conversations, but declines rapidly for more complex conversations. It is associated with right hemiparesis, meaning that there can be paralysis of the patient’s right face and arm.
- Individuals with Global aphasia have severe communication difficulties and will be extremely limited in their ability to speak or comprehend language. They may be totally nonverbal, and/or only use facial expressions and gestures to communicate. It is associated with right hemiparesis, meaning that there can be paralysis of the patient’s right face and arm.
- Individuals with Mixed transcortical aphasia have similar deficits as in global aphasia, but repetition ability remains intact.
- Subcortical aphasias Characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia.
Aphasia usually results from lesions to the language-relevant areas of the frontal, temporal and parietal lobes of the brain, such as Broca’s area, Wernicke’s area, and the neural pathways between them. These areas are almost always located in the left hemisphere, and in most people this is where the ability to produce and comprehend language is found. However, in a very small number of people, language ability is found in the right hemisphere. In either case, damage to these language areas can be caused by a stroke, traumatic brain injury, or other brain injury.
Aphasia may also develop slowly, as in the case of a brain tumor or progressive neurological disease, e.g., Alzheimer’sor Parkinson’s disease. It may also be caused by a sudden hemorrhagic event within the brain. Certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.
Aphasia can result from Herpes Simplex virus (HSV) encephalitis. The (HSV) affects the frontal and temporal lobes, subcortical structures and the hippocampal tissue which can trigger aphasia.
Aphasia is also listed as a rare side effect of the fentanyl patch, an opioid used to control chronic pain.
There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that although there isn’t consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes.
A multi-disciplinary team, including doctors (often a physician is involved, but more likely a clinical neuropsychologist will head the treatment team), physiotherapist, occupational therapist, speech-language pathologist, and social worker, works together in treating aphasia. For the most part, treatment relies heavily on repetition and aims to address language performance by working on task-specific skills. The primary goal is to help the individual and those closest to them adjust to changes and limitations in communication.
Treatment techniques mostly fall under two approaches:
- Substitute Skill Model – an approach that uses an aid to help with spoken language, i.e. a writing board
- Direct Treatment Model – an approach which targets deficits with specific exercises.
Several treatment techniques include the following:
- Visual Communication Therapy (VIC) – the use of index cards with symbols to represent various components of speech
- Visual Action Therapy (VAT) – involves training individuals to assign specific gestures for certain objects
- Functional Communication Treatment (FCT) – focuses on improving activities specific to functional tasks, social interaction, and self-expression
- Promoting Aphasic’s Communicative Effectiveness (PACE) – a means of encouraging normal interaction between patients and clinicians. In this kind of therapy the focus is on pragmatic communication rather than treatment itself. Patients are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object.
- Other – i.e. drawing as a way of communicating, trained conversation partners.
More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of 2–3 hours per week has been specified to produce positive results. The main advantage of using computers is that it can greatly increase intensity of therapy.
These programs consist of a large variety of exercises and can be done at home in addition to face-to-face treatment with a therapist. However, since aphasia presents differently among individuals, these programs must be dynamic and flexible in order to adapt to the variability in impairments.
Another barrier is the capability of computer programs to imitate normal speech and keep up with the speed of regular conversation. Therefore, computer technology seems to be limited in a communicative setting, however is effective in producing improvements in communication training.
Several examples of programs used are StepByStep, Linguagraphica, Computer-Based Visual Communication (C-VIC), TouchSpeak (TS), and Sentence Shaper.
Melodic intonation therapy is often used to treat non-fluent aphasia and has proved to be very effective in some cases.
Zolpidem, a drug with the trade name of Ambien, may provide short-lasting but effective improvement in symptoms of aphasia present in some survivors of stroke. The mechanism for improvement in these cases remains unexplained and is the focus of current research by several groups, to explain how a drug which acts as a hypnotic-sedative in people with normal brain function, can paradoxically increase speech ability in people recovering from severe brain injury. Use of zolpidem for this application remains experimental at this time, and is not officially approved by any pharmaceutical manufacturers of zolpidem or medical regulatory agencies worldwide.
- Auditory processing disorder
- Language disorder
- Speech disorder
|Look up aphasia or aphemia in Wiktionary.|
- Academy of Aphasia
- Aphasia at the Open Directory Project
- Luria’s Areas of the Human Cortex Involved in Language Illustrated summary of Luria’s book Traumatic Aphasia