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Apraxia

From Wikipedia, the free encyclopedia
Apraxia
Apraxia is characterized by loss of the ability to execute or carry out learned purposeful movements.
SpecialtyNeurology, psychiatry
TreatmentOccupational 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.

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

Types

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The several types of apraxia include:

  • Apraxia of speech (AOS) is having difficulty planning and coordinating the movements necessary for speech (e.g. potato=totapo, topato).[5] AOS can independently occur without issues in areas such as verbal comprehension, reading comprehension, writing, articulation, or prosody.[6]
  • Buccofacial or orofacial apraxia, the most common type of apraxia, is the inability to carry out facial movements on demand. For example, an inability to lick one's lips, wink, or whistle when requested to do so. This suggests an inability to carry out volitional movements of the tongue, cheeks, lips, pharynx, or larynx on command.[7][8]
  • Constructional apraxia is the inability to draw, construct, or copy simple configurations, such as intersecting shapes. These patients have difficulty copying a simple diagram or drawing basic shapes.[7]
  • Gait apraxia is the loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions.[9]
  • Ideational/conceptual apraxia is having an inability to conceptualize a task and impaired ability to complete multistep actions. This form of apraxia consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. Also, a loss occurs in the ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, these patients may try to write with it as if it were a pen, or try to comb their hair with a toothbrush.[10][11]
  • Ideomotor apraxia is having deficits in the ability to plan or complete motor actions that rely on semantic memory. These patients are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." When the ability to perform an action automatically when cued remains intact, though, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings.[10][11]
  • Limb-kinetic apraxia is having the inability to perform precise, voluntary movements of extremities. For example, a person affected by limb apraxia may have difficulty waving hello, tying shoes, or typing on a computer.[12][8] This type is common in patients who have experienced a stroke, some type of brain trauma, or have Alzheimer's disease.[13]
  • Oculomotor apraxia is having difficulty moving the eye on command, especially with saccade movements that direct the gaze to targets. This is one of the three major components of Balint's syndrome.[8]

Causes

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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

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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

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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

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References

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  1. ^ Zeidman, Lawrence A. (2020). Brain Science Under the Swastika: Ethical Violations, Resistance, and Victimization of Neuroscientists in Nazi Europe. Oxford University Press. p. 36. ISBN 978-0-19-872863-4.
  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. ^ a b "Apraxia". NORD (National Organization for Rare Disorders). Retrieved 2019-08-02.
  8. ^ a b c "Apraxia Information Page | National Institute of Neurological Disorders and Stroke". www.ninds.nih.gov. 2019. Retrieved 2019-08-01.
  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. ^ a b 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.
  11. ^ a b c d Gross, RG; Grossman, M. (Nov 2008). "Update on apraxia". Current Neurology and Neuroscience Reports. 8 (6): 490–496. doi:10.1007/s11910-008-0078-y. PMC 2696397. PMID 18957186.
  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
  14. ^ a b Tonkonogy, Joseph & Puente, Antonio (2009). Localization of clinical syndromes in neuropsychology and neuroscience. Springer Publishing Company. pp. 291–323. ISBN 978-0826119674.
  15. ^ a b c d 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. ^ a b c 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.

Further reading

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  • Kasper, D.L.; Braunwald, E.; Fauci, A.S.; Hauser, S.L.; Longo, D.L.; Jameson, J.L.. Harrison's Principles of Internal Medicine. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1.
  • Manasco, H. (2014). Introduction to Neurogenic Communication Disorders. Jones & Bartlett Publishers.
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