Apraxia

Apraxia
Classification and external resources
Specialty Neurology
ICD-10 R48.2
ICD-9-CM 438.81, 784.69
DiseasesDB 31600
MedlinePlus 007472
eMedicine neuro/438
Patient UK Apraxia
MeSH D001072

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex), in which someone has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task. A person with apraxia cannot move his or her lips or tongue to the right place to say sounds correctly because, even though the muscles are not weak, the message from the brain to the mouth are disrupted. The nature of the brain damage determines the severity.[1] Apraxia is an acquired disorder of motor planning, but is not caused by incoordination, sensory loss, or failure to comprehend simple commands (which can be tested by asking the person to recognize the correct movement from a series). It is caused by damage to specific areas of the cerebrum. Apraxia should not be confused with ataxia, a lack of coordination of movements; aphasia, an inability to produce and/or comprehend language; abulia, the lack of desire to carry out an action; or allochiria, in which patients perceive stimuli to one side of the body as occurring on the other. Developmental coordination disorder is the developmental disorder of motor planning.

Types

There are several types of apraxia including:

Each type may be tested at decreasing levels of complexity; if the person tested fails to execute the commands, you can make the movement yourself and ask that the person mimic it, or you can even give them a real object (like a toothbrush) and ask them to use it.

Apraxia of speech

Main article: Apraxia of speech

Apraxia of speech (AOS) is a neurologic speech disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech.[7] It occurs in both children (childhood apraxia of speech) and adults (acquired apraxia of speech) who have (prior to the onset of apraxia) acquired some level of speaking ability. AOS affects an individual's volitional speech and[8] is typically the result of a stroke, tumor, or other known neurological illness or injury. Apraxia may be accompanied by a language disorder called aphasia.

Symptoms of AOS include inconsistent articulatory errors, groping oral movements to locate the correct articulatory position, and increasing errors with increasing word and phrase length. Individuals with apraxia of speech know what words they want to say, but their brains have difficulty coordinating the muscle movements necessary to say all the sounds in the words.[9] Patients with apraxia find that vowels are easier to produce than consonants. Single consonants are easier than blends. As in stuttering, final consonants are easier than those in the initial position. This may occur because initial consonants are affected by anticipatory errors. Also, perhaps once a person with apraxia begins speech with the production of a vowel, production continues in a more automatic fashion. Fricatives and affricates are the most difficult phonemes for apraxics to produce. AOS often co-occurs with Oral Apraxia, which is the inability to perform volitional tasks with the oral structures not involving speech. Some of these tasks might include coughing, puckering the lips, and smiling.[10] AOS also often co-occurs with Limb Apraxia.

Developmental verbal dyspraxia presents in children who have no evidence of difficulty with strength or range of motion of the articulators, but are unable to execute speech movements because of motor planning and coordination problems.

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. It is also possible for apraxia to be caused by lesions in other areas of the brain including the non-dominant (usually right) hemisphere.[3]

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.[3]

Ideational apraxia often results in functional impairments in activities of daily living (ADLs) similar to those seen with late stage dementia. More recently, it has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia; however, 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.[11]

Constructional apraxia is often caused by lesions of the inferior non-dominant parietal lobe, and can be caused by brain injury, illness, tumor or other condition that can result in a brain lesion.[11]

Diagnosis

Although qualitative and quantitative studies exist, there is little consensus on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties as well as research-specific designs that translate poorly to non-research use.[12]

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.[13] The TULIA consists of subtests for the imitation and pantomime of non-symbolic (“put your index finger on top of your nose”), intransitive (“wave goodbye”) and transitive (“show me how to use a hammer”) gestures.[12] 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.

However, there may not be a strong correlation 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.[12]

As stated above, apraxia should not be confused with aphasia, however they are frequently accompanied with each other. It has been stated that apraxia is so often accompanied by aphasia that many believe that if a person displays AOS; it should be assumed that the patient also has some level of aphasia.[14]

Treatment

Treatment for individuals with apraxia includes speech therapy, occupational therapy, and physical therapy.[15] Yet, 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, research shows that patients experiencing apraxia have less functional independence in their daily lives,[16] and that evidence for the treatment of apraxia is scarce.[17] 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.[18] One method is through rehabilitative treatment, which has been found to positively impact apraxia, as well as activities of daily living.[18] In this review, rehabilitative treatment consisted of 12 different contextual cues, which were used in order to teach patients how to produce the same gesture under different contextual situations.[18] 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 non-meaningful gestures) with progressively less cuing from the therapist.[19] It may be necessary for patients with apraxia 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.[20] 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. However, one-on-one sessions usually work the best, 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.[21] The overall goal for treatment of apraxia is to treat the motor plans for speech, not treating at the phoneme (sound) level.

Prognosis

The prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid. However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.

Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These team members could be work along with the SLP to provide the best therapy for people with apraxia. However, because people with limb apraxia may have trouble directing their motor movements, occupational therapy for stroke or other brain injury can be difficult.

No drug has been shown useful for treating apraxia.

See also

References

  1. ↑ ASHA
  2. 1 2 Sathian, K; et al. (Jun 2011). "Neurological and rehabilitation of action disorders: common clinical deficits". Neurorehabilitation and Neural Repair 25 (5): 21S–32S. doi:10.1177/1545968311410941. PMID 21613535.
  3. 1 2 3 4 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.
  4. ↑ Nadeau SE (2007). "Gait apraxia: further clues to localization". Eur. Neurol. 58 (3): 142–5. doi:10.1159/000104714. PMID 17622719.
  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, MI: Elsevier. p. 269. ISBN 978-0-323-07200-7.
  7. ↑ Duffy, Joseph R. (2013). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management. St. Louis, Missouri: Elsevier Mosby. p. 269. ISBN 978-0-323-07200-7.
  8. ↑ Manasco, Hunter. (2014). Introduction to neurogenic communication disorder. Burlington, Mass.: Jones & Bartlett Learning. p. 132. ISBN 9780763794170. OCLC 808769513.
  9. ↑ "Apraxia of Speech in Adults". www.asha.org. Retrieved 2015-11-15.
  10. ↑ Duffy, Joseph (2013). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management, 3rd Ed. St. Louis: Elsevier. p. 273.
  11. 1 2 Tonkonogy, Joseph & Puente, Antonio (2009). Localization of clinical syndromes in neuropsychology and neuroscience. Springer Publishing Company. pp. 291–323. ISBN 0826119670.
  12. 1 2 3 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.
  13. ↑ 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.
  14. ↑ (Manasco, 2014)
  15. ↑ "NINDS Apraxia Information Page". Retrieved 8 March 2012.
  16. ↑ 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.
  17. ↑ 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. PMID 18254038.
  18. 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.
  19. ↑ 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.
  20. ↑ "ASHA, Apraxia of Speech in Adults".
  21. ↑ 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.

Further reading

  • 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.

External links

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