Apraxia

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Apraxia
Apraxia 001.jpg
Apraxia is characterized by loss of the ability to execute or carry out learned purposeful movements.
Specialty Neurology, psychiatry
Treatment Occupational therapy, physical therapy

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex or corpus callosum [1] ), which causes difficulty with motor planning to perform tasks or movements. The nature of the damage determines the disorder's severity, and the absence of sensory loss or paralysis helps to explain the level of difficulty. [2] Children may be born with apraxia; its cause is unknown, and symptoms are usually noticed in the early stages of development. Apraxia occurring later in life, known as acquired apraxia, is typically caused by traumatic brain injury, stroke, dementia, Alzheimer's disease, brain tumor, or other neurodegenerative disorders. [3] The multiple types of apraxia are categorized by the specific ability and/or body part affected.

Contents

The term "apraxia" comes from Ancient Greek ἀ- (a-) 'without'andπρᾶξις (praxis) 'action'. [4]

Types

The several types of apraxia include:

Causes

Apraxia is most often due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimer's disease or other dementias, Parkinson's disease, or Huntington's disease. Also, apraxia possibly may be caused by lesions in other areas of the brain. [11]

Ideomotor apraxia is typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas. It is frequently seen in patients with corticobasal degeneration. [11]

Ideational apraxia has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia, but more research is needed on ideational apraxia due to brain lesions. The localization of lesions in areas of the frontal and temporal lobes would provide explanation for the difficulty in motor planning seen in ideational apraxia, as well as its difficulty to distinguish it from certain aphasias. [14]

Constructional apraxia is often caused by lesions of the inferior nondominant parietal lobe, and can be caused by brain injury, illness, tumor, or other condition that can result in a brain lesion. [14]

Diagnosis

Although qualitative and quantitative studies exist, little consensus exists on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties and research-specific designs that translate poorly to nonresearch use. [15]

The Test to Measure Upper Limb Apraxia (TULIA) is one method of determining upper limb apraxia through the qualitative and quantitative assessment of gesture production. In contrast to previous publications on apraxic assessment, the reliability and validity of TULIA was thoroughly investigated. [16] The TULIA consists of subtests for the imitation and pantomime of nonsymbolic ("put your index finger on top of your nose"), intransitive ("wave goodbye"), and transitive ("show me how to use a hammer") gestures. [15] Discrimination (differentiating between well- and poorly performed tasks) and recognition (indicating which object corresponds to a pantomimed gesture) tasks are also often tested for a full apraxia evaluation. [15]

However, a strong correlation may not be seen between formal test results and actual performance in everyday functioning or activities of daily living (ADLs). A comprehensive assessment of apraxia should include formal testing, standardized measurements of ADLs, observation of daily routines, self-report questionnaires, and targeted interviews with the patients and their relatives. [15]

As stated above, apraxia should not be confused with aphasia (the inability to understand language); however, they frequently occur together. Apraxia is so often accompanied by aphasia that many believe that if a person displays AOS, then the patient also having some level of aphasia should be assumed. [17]

Treatment

Treatment for individuals with apraxia includes speech therapy, occupational therapy, and physical therapy. [18] Currently, no medications are indicated for the treatment of apraxia, only therapy treatments. [19] Generally, treatments for apraxia have received little attention for several reasons, including the tendency for the condition to resolve spontaneously in acute cases. Additionally, the very nature of the automatic-voluntary dissociation of motor abilities that defines apraxia means that patients may still be able to automatically perform activities if cued to do so in daily life. Nevertheless, patients experiencing apraxia have less functional independence in their daily lives, [20] and that evidence for the treatment of apraxia is scarce. [21] However, a literature review of apraxia treatment to date reveals that although the field is in its early stages of treatment design, certain aspects can be included to treat apraxia. [22]

One method is through rehabilitative treatment, which has been found to positively impact apraxia, as well as ADLs. [22] In this review, rehabilitative treatment consisted of 12 different contextual cues, which were used to teach patients how to produce the same gesture under different contextual situations. [22] Additional studies have also recommended varying forms of gesture therapy, whereby the patient is instructed to make gestures (either using objects or symbolically meaningful and nonmeaningful gestures) with progressively less cuing from the therapist. [23] Patients with apraxia may need to use a form of alternative and augmentative communication depending on the severity of the disorder. In addition to using gestures as mentioned, patients can also use communication boards or more sophisticated electronic devices if needed. [24]

No single type of therapy or approach has been proven as the best way to treat a patient with apraxia, since each patient's case varies. One-on-one sessions usually work the best, though, with the support of family members and friends. Since everyone responds to therapy differently, some patients will make significant improvements, while others will make less progress. [25] The overall goal for treatment of apraxia is to treat the motor plans for speech, not treating at the phoneme (sound) level. Individuals with apraxia of speech should receive treatment that focuses on the repetition of target words and rate of speech. The overall goal for treatment of apraxia should be to improve speech intelligibility, rate of speech, and articulation of targeted words. [26]

See also

Related Research Articles

<span class="mw-page-title-main">Aphasia</span> Inability to comprehend or formulate language

In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine, but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases, brain infections, or neurodegenerative diseases.

<span class="mw-page-title-main">Expressive aphasia</span> Language disorder involving inability to produce language

Expressive aphasia is a type of aphasia characterized by partial loss of the ability to produce language, although comprehension generally remains intact. A person with expressive aphasia will exhibit effortful speech. Speech generally includes important content words but leaves out function words that have more grammatical significance than physical meaning, such as prepositions and articles. This is known as "telegraphic speech". The person's intended message may still be understood, but their sentence will not be grammatically correct. In very severe forms of expressive aphasia, a person may only speak using single word utterances. Typically, comprehension is mildly to moderately impaired in expressive aphasia due to difficulty understanding complex grammar.

<span class="mw-page-title-main">Receptive aphasia</span> Language disorder involving inability to understand language

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, fluent aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernicke's aphasia often suffer of anosognosia – they are unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.

Agraphia is an acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell. The loss of writing ability may present with other language or neurological disorders; disorders appearing commonly with agraphia are alexia, aphasia, dysarthria, agnosia, acalculia and apraxia. The study of individuals with agraphia may provide more information about the pathways involved in writing, both language related and motoric. Agraphia cannot be directly treated, but individuals can learn techniques to help regain and rehabilitate some of their previous writing abilities. These techniques differ depending on the type of agraphia.

<span class="mw-page-title-main">Anomic aphasia</span> Medical condition

Anomic aphasia is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say. By contrast, anomia is a deficit of expressive language, and a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.

<span class="mw-page-title-main">Global aphasia</span> Medical condition

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

The primary goals of stroke management are to reduce brain injury and promote maximum patient recovery. Rapid detection and appropriate emergency medical care are essential for optimizing health outcomes. When available, patients are admitted to an acute stroke unit for treatment. These units specialize in providing medical and surgical care aimed at stabilizing the patient's medical status. Standardized assessments are also performed to aid in the development of an appropriate care plan. Current research suggests that stroke units may be effective in reducing in-hospital fatality rates and the length of hospital stays.

<span class="mw-page-title-main">Bálint's syndrome</span> Visual perception disorder

Bálint's syndrome is an uncommon and incompletely understood triad of severe neuropsychological impairments: inability to perceive the visual field as a whole (simultanagnosia), difficulty in fixating the eyes, and inability to move the hand to a specific object by using vision. It was named in 1909 for the Austro-Hungarian neurologist and psychiatrist Rezső Bálint who first identified it.

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

Transcortical motor aphasia (TMoA), also known as commissural dysphasia or white matter dysphasia, results from damage in the anterior superior frontal lobe of the language-dominant hemisphere. This damage is typically due to cerebrovascular accident (CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation.

<span class="mw-page-title-main">Corticobasal degeneration</span> Rare neurodegenerative disease

Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. CBD symptoms typically begin in people from 50 to 70 years of age, and typical survival before death is eight years. It is characterized by marked disorders in movement and cognition, and is classified as one of the Parkinson plus syndromes. Diagnosis is difficult, as symptoms are often similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and dementia with Lewy bodies, and a definitive diagnosis of CBD can only be made upon neuropathologic examination.

<span class="mw-page-title-main">Foix–Chavany–Marie syndrome</span> Medical condition

Foix–Chavany–Marie syndrome (FCMS), also known as bilateral opercular syndrome, is a neuropathological disorder characterized by paralysis of the facial, tongue, pharynx, and masticatory muscles of the mouth that aid in chewing. The disorder is primarily caused by thrombotic and embolic strokes, which cause a deficiency of oxygen in the brain. As a result, bilateral lesions may form in the junctions between the frontal lobe and temporal lobe, the parietal lobe and cortical lobe, or the subcortical region of the brain. FCMS may also arise from defects existing at birth that may be inherited or nonhereditary. Symptoms of FCMS can be present in a person of any age and it is diagnosed using automatic-voluntary dissociation assessment, psycholinguistic testing, neuropsychological testing, and brain scanning. Treatment for FCMS depends on the onset, as well as on the severity of symptoms, and it involves a multidisciplinary approach.

Autotopagnosia from the Greek a and gnosis, meaning "without knowledge", topos meaning "place", and auto meaning "oneself", autotopagnosia virtually translates to the "lack of knowledge about one's own space," and is clinically described as such.

Ideomotor Apraxia, often IMA, is a neurological disorder characterized by the inability to correctly imitate hand gestures and voluntarily mime tool use, e.g. pretend to brush one's hair. The ability to spontaneously use tools, such as brushing one's hair in the morning without being instructed to do so, may remain intact, but is often lost. The general concept of apraxia and the classification of ideomotor apraxia were developed in Germany in the late 19th and early 20th centuries by the work of Hugo Liepmann, Adolph Kussmaul, Arnold Pick, Paul Flechsig, Hermann Munk, Carl Nothnagel, Theodor Meynert, and linguist Heymann Steinthal, among others. Ideomotor apraxia was classified as "ideo-kinetic apraxia" by Liepmann due to the apparent dissociation of the idea of the action with its execution. The classifications of the various subtypes are not well defined at present, however, owing to issues of diagnosis and pathophysiology. Ideomotor apraxia is hypothesized to result from a disruption of the system that relates stored tool use and gesture information with the state of the body to produce the proper motor output. This system is thought to be related to the areas of the brain most often seen to be damaged when ideomotor apraxia is present: the left parietal lobe and the premotor cortex. Little can be done at present to reverse the motor deficit seen in ideomotor apraxia, although the extent of dysfunction it induces is not entirely clear.

Apraxia of speech (AOS), also called verbal apraxia, is a speech sound disorder affecting an individual's ability to translate conscious speech plans into motor plans, which results in limited and difficult speech ability. By the definition of apraxia, AOS affects volitional movement pattern. However, AOS usually also affects automatic speech.

Ideational apraxia (IA) is a neurological disorder which explains the loss of ability to conceptualize, plan, and execute the complex sequences of motor actions involved in the use of tools or otherwise interacting with objects in everyday life. Ideational apraxia is a condition in which an individual is unable to plan movements related to interaction with objects, because they have lost the perception of the object's purpose. Characteristics of this disorder include a disturbance in the concept of the sequential organization of voluntary actions. The patient appears to have lost the knowledge or thought of what an object represents. This disorder was first seen 100 years ago by Doctor Arnold Pick, who described a patient who appeared to have lost their ability to use objects. The patient would make errors such as combing their hair with the wrong side of the comb or placing a pistol in his mouth. From that point on, several other researchers and doctors have stumbled upon this unique disorder. IA has been described under several names such as, agnosia of utilization, conceptual apraxia or loss of knowledge about the use of tools, or Semantic amnesia of tool usage. The term apraxia was first created by Steinthal in 1871 and was then applied by Gogol, Kusmaul, Star, and Pick to patients who failed to pantomime the use of tools. It was not until the 1900s, when Liepmann refined the definition, that it specifically described disorders that involved motor planning, rather than disturbances in the patient’s visual perception, language, or symbolism.

<span class="mw-page-title-main">Gerstmann syndrome</span> Neuropsychological disorder caused by damage to the inferior parietal lobule

Gerstmann syndrome is a neurological disorder that is characterized by a constellation of symptoms that suggests the presence of a lesion usually near the junction of the temporal and parietal lobes at or near the angular gyrus. Gerstmann syndrome is typically associated with damage to the inferior parietal lobule of the dominant hemisphere. It is classically considered a left-hemisphere disorder, although right-hemisphere damage has also been associated with components of the syndrome.

Constructional apraxia is a neurological disorder in which people are unable to perform tasks or movements even though they understand the task, are willing to complete it, and have the physical ability to perform the movements. It is characterized by an inability or difficulty to build, assemble, or draw objects. Constructional apraxia may be caused by lesions in the parietal lobe following stroke or it may serve as an indicator for Alzheimer's disease.

Body part as object (BPO) mime gestures occurs when an individual substitutes a part of their body - usually arms, fingers, or hands - to be part of an object they are miming. Miming uses representational gestures, meaning they are used to convey a message to others without the use of speech. A commonly used example of BPO miming is demonstrated by an individual using their finger to represent a toothbrush while acting out brushing their teeth.

<span class="mw-page-title-main">Disconnection syndrome</span> Collection of neurological symptoms

Disconnection syndrome is a general term for a collection of neurological symptoms caused – via lesions to associational or commissural nerve fibres – by damage to the white matter axons of communication pathways in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

References

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  2. ↑ ASHA
  3. ↑ "Apraxia: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 2019-08-07.
  4. ↑ "Definition of APRAXIA". www.merriam-webster.com. Retrieved 2017-05-02.
  5. ↑ Heilman KM, Watson RT, Gonzalez-Rothi LJ. Praxis. In: Goetz CG. Goetz: Textbook of Clinical Neurology. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2007:chap 4.
  6. ↑ Duffy, Joseph R. (2013). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management. St. Louis, MO: Elsevier. p. 269. ISBN   978-0-323-07200-7.
  7. 1 2 "Apraxia". NORD (National Organization for Rare Disorders). Retrieved 2019-08-02.
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  9. ↑ Nadeau SE (2007). "Gait apraxia: further clues to localization". Eur. Neurol. 58 (3): 142–5. doi:10.1159/000104714. PMID   17622719. S2CID   40700537.
  10. 1 2 Sathian, K; et al. (Jun 2011). "Neurological principles and rehabilitation of action disorders: common clinical deficits". Neurorehabilitation and Neural Repair. 25 (5): 21S–32S. doi:10.1177/1545968311410941. PMC   4139495 . PMID   21613535.
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  12. ↑ Treatment Resource Manual for Speech Pathology 5th edition
  13. ↑ Foundas, Anne L. (2013-01-01), Barnes, Michael P.; Good, David C. (eds.), "Chapter 28 - Apraxia: neural mechanisms and functional recovery", Handbook of Clinical Neurology, Neurological Rehabilitation, 110, Elsevier: 335–345, doi:10.1016/B978-0-444-52901-5.00028-9, PMID   23312653 , retrieved 2019-08-07
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  15. 1 2 3 4 Vanbellingen, T.; Bohlhalter, S. (2011). "Apraxia in neurorehabilitation: Classification, assessment and treatment". NeuroRehabilitation. 28 (2): 91–98. doi:10.3233/NRE-2011-0637. PMID   21447909.
  16. ↑ Vanbellingen, T.; Kersten, B.; Van Hemelrijk, B.; Van de Winckel, A.L.J.; Bertschi, M.; Muri, R.; De Weerdt, W.; Bohlhalter, S. (2010). "Comprehensive assessment of gesture production: a new test to measure upper limb apraxia". European Journal of Neurology. 17 (1): 59–66. doi:10.1111/j.1468-1331.2009.02741.x. PMID   19614961. S2CID   13328067.
  17. ↑ (Manasco, 2014)
  18. ↑ "NINDS Apraxia Information Page" . Retrieved 8 March 2012.
  19. ↑ Worthington, Andrew (2016). "Treatments and technologies in the rehabilitation of apraxia and action disorganisation syndrome: A review". NeuroRehabilitation. 39 (1): 163–174. doi:10.3233/NRE-161348. ISSN   1053-8135. PMC   4942853 . PMID   27314872.
  20. ↑ Hanna-Pladdy, B; Heilman, K.M.; Foundas, A.L. (Feb 2003). "Ecological implications of ideomotor apraxia: evidence from physical activities of daily living". Neurology. 60 (3): 487–490. doi:10.1212/wnl.60.3.487. PMID   12578932. S2CID   23836106.
  21. ↑ West, C; Bowen, A.; Hesketh, A.; Vail, A. (Jan 2008). "Interventions for motor apraxia following stroke". Cochrane Database of Systematic Reviews. 23 (1): CD004132. doi:10.1002/14651858.CD004132.pub2. PMC   6464830 . PMID   18254038.
  22. 1 2 3 Buxbaum LJ, Haaland KY, Hallett M, et al. (February 2008). "Treatment of limb apraxia: moving forward to improved action" (PDF). Am J Phys Med Rehabil. 87 (2): 149–61. doi:10.1097/PHM.0b013e31815e6727. PMID   18209511.
  23. ↑ Smania, N; et al. (Dec 2006). "Rehabilitation of limb apraxia improves daily life activities in patients with stroke". Neurology. 67 (11): 2050–2052. doi:10.1212/01.wnl.0000247279.63483.1f. PMID   17159119. S2CID   4456810.
  24. ↑ "ASHA, Apraxia of Speech in Adults".
  25. ↑ Dovern, A.; Fink, GR.; Weiss, PH. (Jul 2012). "Diagnosis and treatment of upper limb apraxia". J Neurol. 259 (7): 1269–83. doi:10.1007/s00415-011-6336-y. PMC   3390701 . PMID   22215235.
  26. ↑ Wambaugh, JL; Nessler, C; Cameron, R; Mauszycki, SC (2012). "Acquired apraxia of speech: the effects of repeated practice and rate/rhythm control treatments on sound production accuracy". American Journal of Speech-Language Pathology. 21 (2): S5–S27. doi:10.1044/1058-0360(2011/11-0102). PMID   22230177.

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