Different Forms of Apraxia - Coursework Example

Different forms of Apraxia Student’s Name Institution Affiliation Course Date Introduction Apraxia is a term used to refer to a neurological disorder that is characterized by the loss of the capacity to effect coordinated movements and gesticulations despite the need and physical ability to execute them. This disorder is caused by the dysfunction of the rational part of the brain and in particular, the parietal lobe that results to too many maladies or injury to the brain (National Institute of Health, 2015, p. N.p). In normal circumstances, these brain regions operate together to help process an action. Thus, the web of structures that underlie praxis is prospected to consist the basal ganglia, anterior and parietal cortex, and projections contained between the tracts of white matter (Gross & Grossman, 2008). There exists various different forms of apraxia and may occur individually or combined. However, the most common type of apraxia is buccofacial that is also known as orofacial. It is characterized by the inability to execute facial actions such as whistling, winking, licking of lips, or coughing (National Institute of Health, 2015, p. N.p). Other kinds of apraxia are limb-kinetic apraxia, ideomotor apraxia, ideational apraxia, verbal apraxia, and oculomotor apraxia. Therefore, it is important to distinguish the various kinds of apraxia and indicate how best they may explained. Buccofacial Apraxia (BFA) Also known as, orofacial apraxia, buccofacial apraxia (BFA) is the inability to execute facial actions such as whistling, winking, licking of lips, or coughing (National Institute of Health, 2015, p. N.p). In most cases, BFA is commonly confused with automato-voluntary dissociation (AVD) that also affects the face (Woolley, 2003, p. 395). In AVD, a facial corticospinal innervation is normally impaired thus resulting to the loss of deliberate mechanism of the face. On the other hand, involuntary emotional responses like crying and smiling, which are seemingly sub-served by subcortical passageways, remain undamaged. Moreover, BFA is also often said to be a subcategory of ideomotor apraxia especially when diagnosis is based on observations (Gross & Grossman, 2008). On the other hand, for one to be diagnosed with BFA, the patient should have deficits that are specific to imitating actions with their face. Additionally, the patient should not be paralyzed of voluntary movements (Woolley, 2003, p. 396). Thus, a mere observation that a patient cannot execute facial movements to imitation and does not indicate any signs of complete facial paralysis should be used to diagnose BFA because casual observation is insufficient to separate voluntary movements from those that are involuntary. Hence, when diagnosing patients of BFA, health practitioners should ask their patients to execute buccofacial tasks using real objects like sucking on a straw to help rule out AVD formally (Woolley, 2003, p. 396). According to a wide array of studies, BFA is associated with the left anterior operculum and the surrounding tissues because they comprise the premotor cortex for the face that is known to be of importance in preparing considered facial movement (Woolley, 2003, p. 400). Additionally, the available evidence also suggests that at least three unique neural circuits innervate the face. One of the neural circuit is the subcortical circuit that sub serves impulsive emotional expression. The other one is a presumably multiple represented circuit that sub serves voluntary emotional expression while the last one is a circuit containing the left anterior cortical lobe which sub serves complex as well as learned movements that get disordered in BFA (Woolley, 2003, p. 400). To assess BFA, health practitioners should ask their patients to perform simple single movements to decipher whether they preserve automatic reflexes of the same muscles. Limb-Kinetic Apraxia Limb-kinetic apraxia is the inability to perform fine and precise movements using the arms or the legs (National Institute of Health, 2015, p. N.p). It is also defined as the loss of dexterity for both the hands and fingers because of an individual’s inability to coordinate his or movements (Zadikoff & Lang, 2005, p. 1482). Limb-kinetic apraxia includes a vast array of higher-order motor maladies that are as a result of acquired brain disease that affect the performance of both skilled and learned movements using the anterior appendages with or without maintenance of the capacity to execute the identical movement away from the clinical context in the proper environment (Leiguarda & Marsden, 2000, p. 860). Over the last 40 years, approximately more than 20 assessments for limb apraxia have been published. One of the reason for this high number of varying assessments is due to the heterogeneity nature of apraxia syndrome where by a large number of the assessments seize merely single features of the disorder which are either use of object or imitation of gestures. In evaluating limb apraxia, a critical order is followed to help identify its presence and classify it correctly based on the nature of the praxis deficit that are evident according to the errors made by the patient. Moreover, the critical order is also followed to help gain insight into the mechanisms lying beneath a patient’s uncoordinated motor behavior that can be further defined using kinematic analysis (Leiguarda & Marsden, 2000, p. 862). Therefore, various kinds of transitive movements are thus used to evaluate limb praxis where it is common to find that limb apraxic patients execute some but not every movement in a specifically disordered manner and that individual differences may be evident in some but not in every component of a particular movement (Leiguarda & Marsden, 2000, p. 862). In clinical testing for limb apraxia, all the movements are considered to be affected both symbolic and the non-symbolic, transitive, which includes the use of tools and instruments such as hammers or hairbrush, and intransitive, that affects communicative gestures such as waving goodbyes. In most cases, it is distal in hand and finger. The movements are commonly uneven and mutilated with no deliberate automatic dissociation (Zadikoff & Lang, 2005, p. 1482). In terms of location, all limb apraxia cases that have been pathologically confirmed indicate that a degenerative process that involves the parietal and anterior cortices or chief motor cortex are the causes (Zadikoff & Lang, 2005, p. 1482). Ideomotor Apraxia Ideomotor apraxia is defined as the incapacity to make the appropriate response to an oral command (National Institute of Health, 2015, p. N.p). Moreover, it is also known as a disorder of goal-oriented movement. Patients with ideomotor apraxia are characterized with the knowledge of what to do but do not know how to do it. Therefore, the patients experience a disorder of spatial organization, amplitude, timing, configuration, and sequencing of gestural movements (Zadikoff & Lang, 2005, p. 1482). As a result, the often use their limbs as objects instead of demonstrating how the object should be used. Nonetheless, patients are able to engage in same activities without difficulty throughout their lives. However, from recent studies with patients that suffer from left hemisphere stroke have indicated that the severity of ideomotor apraxia is linked to patients’ dependence on their caregivers performing various physical activities in daily life (Gross & Grossman, 2008). Patients diagnosed with ideomotor apraxia are seen to exhibit various levels of impairment based on testing conditions. For example, patients generally have a hard time performing actions prompted by oral command. However, they tend to have less hardship acting to respond to objects that have been presented visually or imitating gestures (Gross & Grossman, 2008). Other symptoms are abnormal amplitude, use of body parts as substitutes for objects, and abnormal orientation of parts of the body when performing an action. When a patient uses their own finger as a representation of a toothbrush when they are asked to brush their teeth is an example of use of body parts as substitutes for objects (Zadikoff & Lang, 2005, p. 1482). Additionally, transitive actions are more effected compared to the intransitive. There is also the presence of voluntary automatic dissociation such that deficit becomes more evident in a clinical context compared to that of an everyday life. The locality associated with ideomotor apraxia is the anatomically varied lesions particularly in the left hemisphere of the brain. Generally, it involves parietal linking areas as well as white matter bundles that connect parietal and anterior association areas (Zadikoff & Lang, 2005, p. 1482). Additionally, sometimes the supplementary motor cortex and the premotor may be involved including the thalamus and basal ganglia. Moreover, unilateral lesions located in the left hemisphere of the brain in patients that are right-handed produce mutual deficits that are normally more severe in the right limb than the left limb (Zadikoff & Lang, 2005, p. 1482). Ideational Apraxia Ideational apraxia, which is also referred to as conceptual apraxia, is defined as the incapacity to coordinate actions such as bathing, dressing, and eating using multiple sequential movements (National Institute of Health, 2015, p. N.p). Ideational apraxia is characterized by patients’ lack of knowledge on what to do and presence of content errors (Zadikoff & Lang, 2005, p. 1482). Among the content errors include impairment in executing sequences of activities that require the use of varying objects in the right order to help accomplish the intended purpose and the loss of knowledge concerning tool action. The movements of patients appear to be confused because they cannot decipher a plan on the manner in which to sequence the movements (Molyneux, n.d., p. 6). For a patient with ideational apraxia disorder, some of the clinical testing that are evaluated are the client’s ability to execute a task that has multiple steps outstanding to miscalculations such as preservation. An example of such a task is preparing a letter to be mailed (Zadikoff & Lang, 2005, p. 1482). Additionally, the disturbance of a single tool use should be assessed. A patient is diagnosed with ideational apraxia if they cannot link an object or tool with the corresponding action. For example, the patient is unable to select a hammer as the tool that should be used to drive in a nail or they appropriately pantomime an action that is very different from that which was expected of them (Zadikoff & Lang, 2005, p. 1482). Where a patient has no tool knowledge such as toothpaste or toothbrush and thus incorrectly uses the objects at hand by smearing the toothpaste on the face is another clinical example of a patient with ideational apraxia disorder (Molyneux, n.d., p. 7). In terms of locality, there has not been a single anatomical region that has been pointed out to be the cause of ideational apraxia. However, in focal hemispheric lesions, a large number of them cause injury to the left hemisphere (Zadikoff & Lang, 2005, p. 1482). Normally, the damage has been typically thought to affect the left paretotemporal and parieto-occipital regions. Consequently, the damage affects the areas that plan and process IDEA and thus leads the patients to lose the thought or knowledge of what tools and objects represent (Molyneux, n.d., p. 6). Verbal Apraxia Verbal apraxia also known as apraxia of speech or dyspraxia is defined as the difficulty of coordinating speech and mouth movements (National Institute of Health, 2015, p. N.p). Verbal apraxia is characterized by the inability of a person to communicate what they want or to communicate correctly and in a consistent manner (NIH, 2010). There are two major kinds of verbal apraxia, which are developmental verbal apraxia and acquired speech apraxia. Acquired apraxia occurs mostly in adults and at any age. Developmental apraxia on the other hand occurs in children and is always present from birth. Verbal apraxia occurs as a result of damage caused to those parts of the brain involved in speaking and thus leads to impairment of already existing speech abilities (NIH, 2010). The common symptoms of people with verbal apraxia are varying kinds of speech characteristics such as putting syllables and sounds in the right order to create words. Commonly, patients with apraxia of speech, longer words and those that are more complex are normally harder to communicate compared to shorter and simpler words (NIH, 2010). Additionally, people who have verbal apraxia tend to have inconsistent mistakes in their communications. For example, a person with apraxia of speech may say a hard word properly but then experience difficulty repeating it. In other cases, the people may say a given sound one time and then have difficulties with the same sound at other times (NIH, 2010). People who have speech dyspraxia often times appear to be fumbling for the appropriate word or sound and may attempt to say the word severally before it comes out clearly. The other common symptom of verbal apraxia is the wrong utilization of prosody, which is the varying patterns, stresses, and modulations of speech that help bring out meanings (NIH, 2010). To treat speech apraxia, some people that have the acquired dyspraxia may recover some or every bit of their communication aptitudes on their own. This recovery is referred to as spontaneous recovery. On the other hand, children that have developmental dyspraxia do not outgrow the disorder on their own and thus speech language therapy becomes a helpful tool for them and those individuals who do not recover from the problem on their own (NIH, 2010). Oculomotor Apraxia Oculomotor apraxia refers to the difficulty experienced in “moving the eyes on command” (National Institute of Health, 2015). People with oculomotor apraxia have difficulties moving their eyes from side to side and hence, to see things that are within their peripheral vision, they are forced to turn their heads. Therefore, people with this disorder constantly jerk their heads because of the failure of instigation of straight saccades especially in children (Orssaud, et al., 2009, p. 372). There are two types of oculomotor apraxia, which are types 1 and 2 caused because of mutations occurring in different genes. The clinical appearance of oculomotor has been evidenced to improve with age. On the other hand, the residual manifestations which is easily compensated tend to persist in adults and becomes more apparent when they under stress. In this case, the oculomotor apraxia symptoms are blinks or both eye and head jerk movements. The control of saccadic movement of the eye is typically abnormal in adults despite the movements being quite normal from a clinical perspective (Orssaud, et al., 2009, p. 372). According to Orssaud, et al. (2009, p. 372), the pysio-pathogenic mechanisms associated with oculomotor apraxia are not clear. Nonetheless, cerebellar vermis hypoplasia are linked to the disorder. Thus, disorders of the cerebellar structures together with lesions of the outcrops from the “rostral interstitial nucleus and the larger colliculus to the brainstem” (Orssaud, et al., 2009, p. 372) are assumed to be possible causes of oculomotor. Conclusion There are different forms of apraxia that have a clear distinction between them. These are; Buccofacial Apraxia, limb-kinetic apraxia, ideomotor apraxia, ideational apraxia, verbal apraxia, and oculomotor apraxia. All these disorders are associated with damage of the left hemisphere of the brain. They are associated with lack of coordination in various forms of activities but distinct to each kind of disorder. References Gross, R. G. & Grossman, M., 2008. Update on apraxia. Current neurology and neuroscience reports, 8(6), pp. 490-496. Leiguarda, R. C. & Marsden, C. D., 2000. Limb apraxias. Brain, 123(5), pp. 860-879. Molyneux, M., n.d. Apraxia: An intervention guide for occupational therapists, Gainesville, Florida: MOT OTR/L Shands Rehab Hospital . National Institute of Health, 2015. National Institute of Neurological Disorders and Stroke: NINDS Apraxia Information Page. [Online] Available at: http://www.ninds.nih.gov/disorders/apraxia/apraxia.htm [Accessed 20 October 2016]. NIH, 2010. National Institute of Deafness and other Communication Disorders. [Online] Available at: https://www.nidcd.nih.gov/health/apraxia-speech [Accessed 6 October 2016]. Orssaud, C. et al., 2009. Familial congenital oculomotor apraxia: Clinical and electro-oculographic features. european journal of paediatric neurology, 13(4), pp. 370-372. Woolley, J. D., 2003. Buccofacial apraxia and the expression of emotion. Annals of the New York Academy of Sciences, 1000(1), pp. 395-401. Zadikoff, C. & Lang, A. E., 2005. Apraxia in movement disorders. Brain , 128(7), pp. 1480-1497. Read More

Hence, when diagnosing patients of BFA, health practitioners should ask their patients to execute buccofacial tasks using real objects like sucking on a straw to help rule out AVD formally (Woolley, 2003, p. 396). According to a wide array of studies, BFA is associated with the left anterior operculum and the surrounding tissues because they comprise the premotor cortex for the face that is known to be of importance in preparing considered facial movement (Woolley, 2003, p. 400). Additionally, the available evidence also suggests that at least three unique neural circuits innervate the face.

One of the neural circuit is the subcortical circuit that sub serves impulsive emotional expression. The other one is a presumably multiple represented circuit that sub serves voluntary emotional expression while the last one is a circuit containing the left anterior cortical lobe which sub serves complex as well as learned movements that get disordered in BFA (Woolley, 2003, p. 400). To assess BFA, health practitioners should ask their patients to perform simple single movements to decipher whether they preserve automatic reflexes of the same muscles.

Limb-Kinetic Apraxia Limb-kinetic apraxia is the inability to perform fine and precise movements using the arms or the legs (National Institute of Health, 2015, p. N.p). It is also defined as the loss of dexterity for both the hands and fingers because of an individual’s inability to coordinate his or movements (Zadikoff & Lang, 2005, p. 1482). Limb-kinetic apraxia includes a vast array of higher-order motor maladies that are as a result of acquired brain disease that affect the performance of both skilled and learned movements using the anterior appendages with or without maintenance of the capacity to execute the identical movement away from the clinical context in the proper environment (Leiguarda & Marsden, 2000, p. 860). Over the last 40 years, approximately more than 20 assessments for limb apraxia have been published.

One of the reason for this high number of varying assessments is due to the heterogeneity nature of apraxia syndrome where by a large number of the assessments seize merely single features of the disorder which are either use of object or imitation of gestures. In evaluating limb apraxia, a critical order is followed to help identify its presence and classify it correctly based on the nature of the praxis deficit that are evident according to the errors made by the patient. Moreover, the critical order is also followed to help gain insight into the mechanisms lying beneath a patient’s uncoordinated motor behavior that can be further defined using kinematic analysis (Leiguarda & Marsden, 2000, p. 862). Therefore, various kinds of transitive movements are thus used to evaluate limb praxis where it is common to find that limb apraxic patients execute some but not every movement in a specifically disordered manner and that individual differences may be evident in some but not in every component of a particular movement (Leiguarda & Marsden, 2000, p. 862). In clinical testing for limb apraxia, all the movements are considered to be affected both symbolic and the non-symbolic, transitive, which includes the use of tools and instruments such as hammers or hairbrush, and intransitive, that affects communicative gestures such as waving goodbyes.

In most cases, it is distal in hand and finger. The movements are commonly uneven and mutilated with no deliberate automatic dissociation (Zadikoff & Lang, 2005, p. 1482). In terms of location, all limb apraxia cases that have been pathologically confirmed indicate that a degenerative process that involves the parietal and anterior cortices or chief motor cortex are the causes (Zadikoff & Lang, 2005, p. 1482). Ideomotor Apraxia Ideomotor apraxia is defined as the incapacity to make the appropriate response to an oral command (National Institute of Health, 2015, p. N.p).

Moreover, it is also known as a disorder of goal-oriented movement.

Read More