Sandbox:nou
Dr Norina Usma
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Historical Perspective
Classification
Apraxia may be classified into different subtypes based on it's clinical features:
- Ideomotor apraxia: The most commonly known type of apraxia is Ideomotor apraxia, or decreased performance of skilled motor performances despite integral language, sensory and motor function[1]</ref>. Ideomotor apraxia is classically demonstrated when a patient questioned verbally to make a motion with a limb. Patients with Ideomotor apraxia display spatial and temporal errors, inconvenient timing, amplitude, sequencing, configuration, limb position in space. It is an inability to carry out, learned motor acts, command, adequate motor, and sensory abilities. Ideomotor apraxia can be due to cerebral damage in numerous areas, including the left parietal lobe, the intrahemispheric association fibers, the dominant hemisphere motor association cortex, and the anterior corpus callosum. In the last two, ideomotor apraxia is usually restricted to the left arm. They often use their arm as an object relatively than indicating how to use the object . Patients are frequently able to achieve the same acts without struggle in their daily lives. This process has been called the "voluntary-automatic dissociation"[2][3]</ref>.These patients have a deficiency in their skill to plan or ample motor actions that depend on semantic memory. They can describe how to achieve a response, but incapable to "imagine" or do the movement. Though the capability to perform an act inevitably when cued remains complete, this is recognized as automatic-voluntary dissociation[4].
- Constructional apraxia: It is a condition resulting from neurological damage, which is demonstrated by the inability to construct and copy to command two- and three-dimensional stimuli. Constructional apraxia has been a classic sign of a parietal lobe lesion, and as a valuable tool to escalate the spatial abilities functioned by this lobe. It has become gradually clear that Constructional Apraxia is a complex construct that can be observed with very different tasks that are only slightly interrelated, and hit various kinds of visuospatial, attentional, perceptual, planning, and motor mechanisms[5].The patient with constructional apraxia is unable to construct, draw, or copy simple configurations; for example, intersecting shapes; they have trouble drawing basic shapes or copying a simple diagram[6].
- Buccofacial or orofacial apraxia: This is the most common type of apraxia; patients cannot convey facial movements on requests, such as voluntary movements of the tongue, cheeks, lips, pharynx, or larynx on command, for example, include licking lips, whistling, coughing, or winking)[7]</ref>.
- Gait apraxia: Apraxia of gait is a rare locomotion syndrome categorized by the incapability of lifting the feet from the floor regardless of discontinuous stepping action. The accountable site of lesions is in the basal ganglia and frontal lobe[8]</ref>.
- Limb-kinetic apraxia: It is the failure to make precise movements with an arm, finger, or leg. For example, a person may have trouble tying their shoes, waving hello, or typing on a computer.
Pathophysiology
Ideational apraxia patients may be diminished in sequencing a sequence of acts, or make contented errors, also stated to as `conceptual apraxia' by some investigators[9]</ref>. Patients with ideomotor apraxia (IMA) make temporal and spatial errors discrete to the primary motor deficit, whereas patients with limb-kinetic apraxia present with elemental motor deficits such as loss of independent finger movements and slow-stiff movements in the absence of weakness.
Ideomotor apraxia causes the damage of either the corticocortical connecting pathways or the dominant cerebral cortex. The studies hypothesize that cortical lesions in the perirolandic or suprasylvian region of the left dominant hemisphere. However, to detect one specific cortical locus, when this pathology induces IMA, it recommends that a distributed modular system intermediates praxis[10]</ref>. Major strokes involving the middle cerebral artery not only extend outside specific cortical areas but often extend subcortically to periventricular white matter and basal ganglia structures. Due to infarction, there can be areas of decreased blood flow which are inadequate to cause cystic infarction but are enough to cause ischaemic neuronal damage. Infarctions restricted to the basal ganglia are not common, and other structures such as the insula, thalamus, and surrounding white matter are often involved.
Causes
Common causes of Apraxia may include:
- It could be due to a defect in the brain pathways that comprise memory of learned forms of movement. Any disease that is related to these areas can lead to apraxia, stroke, dementia are the leading causes, but there are many other causes as well.
- The lesion cause could be because of certain metabolic, neurological, or other disorders that influence the brain, predominantly the frontal lobe, inferior parietal lobule of the left hemisphere of the brain. In this area, complex, 3-dimensional depictions of formerly learned patterns and movements are stored[11]</ref>.
- Patients with apraxia cannot regain these representations of stored, skilled actions.Therefore, patients with apraxia are unable to perform daily living activities well.
Differentiating Xyz from Other Diseases
Epidemiology and Demographics
Incidence
Apraxia is the common complication of left-brain damage that leads to a deficiency in performing motions to verbal imitation or command. Patients suffering from Limb apraxia are mainly impaired when asked to validate how to use an object or perform actions involving. Epidemiology studies account that Ideomotor Apraxia is present 13% of right-brain–and in 28% of left-brain damaged patients, during the acute stage of stroke.Ideomotor apraxia incidence is 34% of right-brain and 57% of left- brain-damaged patients.Basso and coworkers stated that ideomotor apraxia persisted to some degree in 45% of patients one year after stroke onset[12].
Prevalance
Prevalence rates of apraxia range among 0 and 34% for patients with Right hemisphere stroke and 28–57% for patients with Left hemisphere stroke[13].Real tool-use loss prevalence rates were stated with 25–54% impaired level of patients
Age
Apraxia commonly affects individuals older than 50 years of age.
Gender
Apraxia affects men and women equally.
Region
Apraxia is a rare disease that tends to affect patient population at high risk of having storke and Alzhiemer disease.
Risk Factors
Apraxia may be due to stroke. Stroke is the major cause of stroke and it is more common in older people[14].
Factors that may escalate risk of stroke comprise of:
- High blood pressure
- High cholesterol
- Diabetes
- Smoking
- Prior stroke or cardiovascular disease
- Prior transient ischemic attack (TIA)
- Dialysis treatment
Screening
There is insufficient evidence to recommend routine screening for Apraxia.
Natural History, Complications, and Prognosis
The symptoms of apraxia typically develop during early or later years depending on the cause and the location affected.
Often, patients with apraxia are not aware of their shortfalls. Therefore, the history of a patient's capability to accomplish skilled movements should be obtained from the patient's caregiver or the patient himself[15]. Caregivers should be asked about the capability of patients to perform activities of daily living and perform tasks involving household tools such as using a toothbrush, knife, and fork appropriately, using kitchen utensils correctly and safely to prepare a meal; using tools such as scissors or hammer correctly.
Caregivers should also be asked about the whole activity level of the patient and whether decreases in his or her total actions have happened. The patient may sit on the couch and watch television without showing interest in essential activities he or she use to do in the past. This indifference can be related to many kinds of brain dysfunction, but it sporadically occurs because the patient is incapable of performing his or her usual activities[16].
Common complications of Apraxia include:
- Broca's Aphasia
- Acalculi
- Right-left Confusion
- Alexia with agraphia
- Wernicke's Aphasia.
Depending on the extent of the Apraxia progression at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.Therefore prognosis of apraxia differs and depends partially on the original cause. Some people improve while others may display minimal improvement.
Over-all, patients with apraxia become to rely on others for their daily activities and need at least some notch of command; skilled nursing care may be obligatory. Patients with the tumor or degenerative diseases usually develop into amplified levels of dependence.
Patients with stroke may have a steady progression and may even recover somewhat. Persistence of apraxia of speech after 12 months is related to a larger volume of the left hemispheric stroke connecting Broca's area.
Diagnostic Study of Choice
- There is no single diagnostic study of choice for Apraxia's diagnosis, but Apraxia can be diagnosed based on neuroimaging and activity of daily living. When diagnosing Apraxia, specialists may look for the manifestation of other symptoms. For example, they may look for difficulties or weaknesses with verbal comprehension. Both of these are suggestive of other conditions, and their occurrence would support rule out Apraxia.
- For people with potential acquired Apraxia, they should go through neuroimaging—magnetic resonance imaging (MRI) or computed tomography (CT) scanning MRI which may be beneficial to determine the location and extent of any brain damage. It will also help evaluate possible atrophy expressive of a degenerative condition and exclude a mass lesion.
- Whitwell et al. in a study to determine the metabolic and neuroanatomical relate to aphasia and progressive Apraxia of speech (AOS), associations between the Token Test to assess Aphasia, Western Aphasia Battery and AOS rating scale (ASRS), 18-F fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging and 3-Tesla MRI, were assessed. The only region that interconnected to ASRS was left-superior promotor volume[1].
- A broad assessment of Apraxia should consist of observation of daily routines, formal testing, self-report questionnaires, standardized measurements of ADLs, and targeted interviews with the patients and their relatives[2]. Apraxia should not be mixed up with aphasia (the inability to understand language); though, they often occur together.
- History and Symptoms
Physical Examination
Physical examination of patients with Apraxia is usually dependent on what type of Apraxia they have for example Ideomotor apraxia, Buccofacial apraxia, and Constructional apraxia.
Ideomotor apraxia:
Patients with ideomotor apraxia are tested based on the physical examination performed at the bedside with simple tests for the capability to use tools. The examiner requests patients to achieve three types of activities. For example, the patient is asked to hammer a nail into the (unreal) wall in front of them; patients are given a pair of scissors to cut a piece of paper. [8]
However, different pantomimes could be made, including cutting with a saw, brushing teeth, peeling a potato or whipping eggs with an eggbeater. Any error in carrying out the above activities indicates a loss of familiarity about the movement to be completed. The response is recorded as an error[17].
Buccofacial apraxia:
Buccofacial apraxia indicates an entirely different lesion and process; it is tested separately. Buccofacial apraxia (also named oral apraxia), patients cannot do skilled actions, including the lips, tongue, and mouth, regardless of the absence of paresis. Buccofacial apraxia is evaluated by asking the patient to perform tasks with his or her mouth, such as kissing, blowing out a match, or brushing her or his teeth.
Constructional apraxia:
Constructional apraxia patients are tested by absolute examination failure to copy or draw quality images, such as the Rey-Osterreith figure, interlocking pentagons, or complex figures. Constructional apraxia can localize damage to several brain regions, including the frontal or left or right parietal area[18].
Laboratory Findings
Electrocardiogram
There are no ECG findings associated with Apraxia.
X-ray
There are no x-ray findings associated with Apraxia.
Echocardiography and Ultrasound
There are no echocardiography/ultrasound findings associated with Apraxia.
CT scan
Brain CT scan may be helpful in the diagnosis of Apraxia. Findings on CT scan suggestive of/diagnostic of Apraxia include
- To look for a mass lesion and
- To evaluate for possible atrophy expressive of a degenerative condition.
MRI
Brain MRI may be helpful in the diagnosis of Apraxia. Findings on MRI suggestive of/diagnostic of Apraxia include atrophy, ischemic changes, and mass lesion.
Other Imaging Findings
There are no other imaging findings associated with Apraxia.
Other Diagnostic Studies
Diagnostic study PET may be helpful in the diagnosis of Apraxia. Findings suggestive of/diagnostic of Apraxia include Relative cerebral glucose metabolism.
Treatment
Medical Therapy
The mainstay of treatment for Apraxia is various therapy.
Interventions
There are no specific recommended therapeutic interventions for the management of Apraxia.
Apraxia is believed to have an adverse impact on the Activity of Daily Living independence[19]</ref> . There are limited information and research available regarding various treatments[20]</ref>. Various interventions include:
- Daily living doings training: this method explains internal and external compensatory approaches that permit a functional mission to be accomplished[21]</ref>.
- Sensory Stimulation: Including deep pressure stimulation, soft and sharp touch are useful to the patients' limbs[22]</ref>.
- Chaining (forward or backward): This method is fragmented down into its sections. The task is done with assistance from the therapist separately from the final element through backward chaining, which the patient performs out unassisted. If positive next time, additional steps are presented. Forward chaining is the opposite of backward chaining;
- Proprioceptive stimulation: The patient props on and puts his weight through their upper and lower extremities;
- Cueing, physical or verbal stimuli: This technique enables each phase of the task to be completed;
Surgery
Surgical intervention is not recommended for the management of Apraxia.
Primary Prevention
There are no established measures for the primary prevention of Apraxia. It is difficult to prevent this acquired condition which is mostly linked to stroke. Following measures to prevent a stroke may help[23]</ref>. Some steps include:
- Exercise regularly.
- Eat a healthy diet.
- Limit how much alcohol you drink.
- Quit smoking
- Check your blood pressure often.
Secondary Prevention
Secondary prevention of stroke is the mainstay of preventing Apraxia as it is the leading cause of the various type of Apraxia[24]</ref>. Effective measures for the secondary prevention of Apraxia include:
- Aspirin, clopidogrel, extended-release dipyridamole, ticlopidine
- Anticoagulants (apixaban, dabigatran, edoxaban, rivaroxaban, warfarin)
- Blood pressure-lowering medications.
- Diabetes Control
- Low-fat diet
- Cholesterol-lowering medications, Cessation of cigarette smoking, carotid revascularization
- Weight loss and Exercise
References
- ↑ <ref name="pmid1115438">Geschwind N (1975). "The apraxias: neural mechanisms of disorders of learned movement". Am Sci. 63 (2): 188–95. PMID 1115438.
- ↑ Schnider A, Hanlon RE, Alexander DN, Benson DF. Ideomotor apraxia: behavioral dimensions and neuroanatomical basis. Brain Lang. 1997;58(1):125-136. doi:10.1006/brln.1997.1770
- ↑ <ref name="pmid8292325">Rapcsak SZ, Ochipa C, Beeson PM, Rubens AB (1993). "Praxis and the right hemisphere". Brain Cogn. 23 (2): 181–202. doi:10.1006/brcg.1993.1054. PMID 8292325.
- ↑ <ref name="pmid82923253">Rapcsak SZ, Ochipa C, Beeson PM, Rubens AB (1993). "Praxis and the right hemisphere". Brain Cogn. 23 (2): 181–202. doi:10.1006/brcg.1993.1054. PMID 8292325.
- ↑ <ref name="pmid8174333">Yanagisawa N, Ueno E, Hayashi R, Tokuda T, Takou K (1993). "[Apraxia of gait and disorders in posture and locomotion]". Rinsho Shinkeigaku. 33 (12): 1310–2. PMID 8174333.
- ↑ <ref name="pmidhttps://doi.org/10.1016/S0010-9452(64)80020-4">Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1016/S0010-9452(64)80020-4 Check
|pmid=
value (help). - ↑ <ref name="pmid30311153">Khalili M, Wong RJ (2018). "Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net". Dig Dis Sci. 63 (12): 3250–3252. doi:10.1007/s10620-018-5316-9. PMC 6436636. PMID 30311153.
- ↑ <ref name="pmid8174333">Yanagisawa N, Ueno E, Hayashi R, Tokuda T, Takou K (1993). "[Apraxia of gait and disorders in posture and locomotion]". Rinsho Shinkeigaku. 33 (12): 1310–2. PMID 8174333.
- ↑ <ref name="pmid3179688">De Renzi E, Lucchelli F (1988). "Ideational apraxia". Brain. 111 ( Pt 5): 1173–85. doi:10.1093/brain/111.5.1173. PMID 3179688.
- ↑ <ref name="pmid17507030">Wheaton LA, Hallett M (2007). "Ideomotor apraxia: a review". J Neurol Sci. 260 (1–2): 1–10. doi:10.1016/j.jns.2007.04.014. PMID 17507030.
- ↑ <ref name="pmid15509449">McClain M, Foundas A (2004). "Apraxia". Curr Neurol Neurosci Rep. 4 (6): 471–6. doi:10.1007/s11910-004-0071-z. PMID 15509449.
- ↑ <ref name="pmid10768524">Smania N, Girardi F, Domenicali C, Lora E, Aglioti S (2000). "The rehabilitation of limb apraxia: a study in left-brain-damaged patients". Arch Phys Med Rehabil. 81 (4): 379–88. doi:10.1053/mr.2000.6921. PMID 10768524.
- ↑ <ref name="pmid31002018">Buchmann I, Dangel M, Finkel L, Jung R, Makhkamova I, Binder A; et al. (2020). "[Formula: see text] Limb apraxia profiles in different clinical samples". Clin Neuropsychol. 34 (1): 217–242. doi:10.1080/13854046.2019.1585575. PMID 31002018.
- ↑ <ref name="pmid18957186">Gross RG, Grossman M (2008). "Update on apraxia". Curr Neurol Neurosci Rep. 8 (6): 490–6. doi:10.1007/s11910-008-0078-y. PMC 2696397. PMID 18957186.
- ↑ https://pubmed.ncbi.nlm.nih.gov/24795685/
- ↑ https://emedicine.medscape.com/article/1136037-overview#a12
- ↑ https://reference.medscape.com/medline/abstract/17339607
- ↑ Lezak MD. Neuropsychological Assessment. 3rd ed. NY: Oxford Univ Press; 1995.
- ↑ <ref name="Hagmann1998">Hagmann, Georg Goldenberg Sonja (1998). "Therapy of Activities of Daily Living in Patients with Apraxia". Neuropsychological Rehabilitation. 8 (2): 123–141. doi:10.1080/713755559. ISSN 0960-2011.
- ↑ <ref name="pmid18254038">West C, Bowen A, Hesketh A, Vail A (2008). "Interventions for motor apraxia following stroke". Cochrane Database Syst Rev (1): CD004132. doi:10.1002/14651858.CD004132.pub2. PMC 6464830. PMID 18254038.
- ↑ <ref name="van HeugtenDekker2016">van Heugten, C M; Dekker, J; Deelman, B G; van Dijk, A J; Stehmann-Saris, J C (2016). "Outcome of strategy training in stroke patients with apraxia: a phase II study". Clinical Rehabilitation. 12 (4): 294–303. doi:10.1191/026921598674468328. ISSN 0269-2155.
- ↑ <ref name="Butler2016">Butler, Jenny (2016). "Intervention Effectiveness: Evidence from a Case Study of Ideomotor and Ideational Apraxia". British Journal of Occupational Therapy. 60 (11): 491–497. doi:10.1177/030802269706001109. ISSN 0308-0226.
- ↑ <ref name="pmid2799873">"Stroke--1989. Recommendations on stroke prevention, diagnosis, and therapy. Report of the WHO Task Force on Stroke and other Cerebrovascular Disorders". Stroke. 20 (10): 1407–31. 1989. doi:10.1161/01.str.20.10.1407. PMID 2799873.
- ↑ <ref name="pmid26300647">Esenwa C, Gutierrez J (2015). "Secondary stroke prevention: challenges and solutions". Vasc Health Risk Manag. 11: 437–50. doi:10.2147/VHRM.S63791. PMC 4536764. PMID 26300647.