Apraxia and optic ataxia are conditions that both derive from damage to different parts of the brain. The former can develop from damage to various parts of the brain, whereas optic ataxia derives from damage to a specific area of the brain. Both are associated with the inability to complete certain gestures and actions. Apraxia is the inability of the patient to execute a learned and skilled movement, whereas optic ataxia is concerned with the accuracy of conducting a movement. However, both have similarities in terms of anatomy and behaviour, as well as differences which will be discussed in this essay.
Apraxia is a disorder that affects the ability of a human being to perform a learned purposeful movement due to brain damage. This is associated with damage to the left hemisphere, in particular the prefrontal, parietal, and supramarginal areas of the brain. This particular hemisphere is used to control hand movements and hand gestures, therefore damage to it and the parietal lobes in particular will result in apraxia bilaterally (Kimura, 1982 as cited in Zaidel, D. W.,1994). It causes disruption to the shape and sequence of movements that create gestures. Ajuriaguerra, Hecaen and Angelergues (1960) as cited in Walsh, K. (1994) conducted a study and found that different forms of motor apraxia are produced in the left lesions of the brain, and none occurred in their 151 right-sided cases. This provides evidence that the left hemisphere is strongly related to apraxia. However, a number of studies have questioned the sole importance of the left hemisphere in apraxia. Researchers have found an importance for the role of the right hemisphere, especially the prefrontal area (Kolb & Milner, 1981 as cited in Zaidel, D. W., 1994). Others have proposed that the left and right hemisphere both have their own action system, and damage to either one will cause apraxia in the contrasting hand.
Apraxia can be classified into different subtypes, such as ideational, ideomotor, buccofacial, disconnection, conceptual, constructional, and dressing. The different subtypes arise from lesions with different parts of the brain. One common type is ‘motor apraxia’. This refers to the loss of kinaesthetic memory patterns needed for skilled movement (Liepmann, 1980 as cited in Walsh, K., 1994). Apraxia in this form is responsible for the finer movements carried out by humans, such as opening a safety pin and tying shoelaces.
Leipmann (1907) was the first to make a distinction between the two most common types of apraxia; ideational and ideomotor apraxia. Ideational apraxia refers to the inability to select the appropriate action, whereas ideomotor apraxia is the inability to carry out the motor action.
Ideomotor apraxia (IMA) is the most common type of motor apraxia and occurs as a result from damage to the inferior parietal lobe of the left hemisphere. It is a condition where patients have difficulty in implementing the mental representation of carrying out an action on verbal command. They fail to do this with either hand, but can do so automatically. Generally, patients suffering from ideomotor apraxia are incapable of imitating gestures and actions that are shown to them. The energy needed for the movement is restricted to the patients voluntary recall, therefore are unable to conduct the action. Suffering patients are weak at the execution of learned actions. Although they can select the appropriate act, they find difficulty in executing the action, contrasting to ideational apraxia. For example, when slicing bread, the patient may exaggerate the action or make it unnatural. However, ideomotor apraxics may still be able to perform some actions correctly but fail to do so with others. These individuals also tend to be poor at imitating pantomime or when engaged in meaningful imitation, and the use of actual objects (Goodlass & Kaplan, 1972). This may be due to the destruction of the engrams needed in motor performance as the parietal lobes are needed to recognize actions, people will show apraxic deficiencies in the both hands. In addition to this, ideomotor apraxics often see cue-dependent gradient of performance. It has been found that performance is worst at pantomime, however it improves with a tool in the hand, and even more so with a tool and the object. For example, if a patient was instructed to perform the act of slicing bread in a ‘pure’ pantomime condition (no bread or knife), the patient would be incapable of doing this. However, performance can be improved if they are given either the bread or knife. To perfect this performance, the patient could be given the knife and the bread, although the apraxic will never be able to perform this as a fully functioning being would be able to do so.
The second most common form of apraxia as mentioned above is ideational apraxia. This is a behavioral disturbance found in patients with a lesion to the posterior parts of the hemisphere dominant for language (PMC damage). Suffering patients are unable to make sequences of movements or selecting the correct movement. Although the movement is performed correctly, the wrong movement is selected. This phenomenon was demonstrated by Kimura’s (1982) box test study. Patients were presented with apparatus that had three ‘action stations’. They were instructed to perform a sequence of three actions in the correct order (e.g. push button, pull handle, and turn key). It was found that ideational apraxics failed at this test, but could conduct each action individually, as opposed to in the correct sequence. This shows that they can conduct the movement, but fail to select the appropriate action. In addition to this, they are poor at responding to commands. For example, when asked to make several gestures such as wave goodbye or how to say ‘shhh’. Ideational apraxics are often impaired in carrying out everyday tasks as they cannot properly sequence movements together, and may make action errors in doing so, e.g. combing their hair with their toothbrush.
Where apraxia is concerned with inability of a person to perform a learned action, optic ataxia refers to the inaccuracies in body movements under visual control. Both apraxia and ataxia are the result of damage to the brain. However, apraxia can occur after lesions to different parts of the brain, whereas optic ataxia is associated with lesions to specific parts, in particular the superior parietal lobule (SPL) and the intraparietal sulcus (IPS). Given this, the symptoms associated with optic apraxia are less varied than that of apraxia. Optic ataxia is the inability to grasp visually presented stimuli and consists of errors in accuracy of goal-directed movements. In contrast to apraxia, optic ataxia is not related to motor, visual acuity, somatosensory or visual field deficits and cannot be divided into subtypes. Balint (1909) was the first to describe the term ‘optic ataxia’. He demonstrated that the visuomotor basis for optic ataxia was evident and present in the hand effect of his patient. When reaching for something under visual guidance, the patient only showed error in pointing with the impaired hand in one visual field. This showed that the deficit is not due to either strictly visual or motor, whereas apraxia is concerned with both.
Optic apraxics can develop impairments such as pointing in the peripheral visual field, ‘posting’ their hand through a slot, manual tracking of a moving object and grasping an object. However, performance on these actions can be improved and rectified by pointing in central vision, grasping familiar objects, with practice, and with fixation of the target.
The pattern of spared and impaired actions in optic ataxia has caused disputes, in so that it represents a deficit in on-line control, and not deficit in action. Pisella et al (2000) argued this in their study; that optic ataxia may signify a deficit in on-line control and not action. They had optic apraxics and healthy patients point to a target that could suddenly change when movement was detected. The healthy participants and the optic ataxic IG pointed correctly to the targets when they were still. However, when the target changed position, the healthy participants were able to adjust to it easily whereas IG failed to do so. This was supported by Grea et al. (2002) who also found that IG could not adapt in grasping a target that suddenly changed position.
In conclusion, patients of apraxia and ataxia understand what they are being asked to do, or know what they are trying to do, however fail in doing so. Both of the disorders present a difficulty in either converting visual information into the appropriate action, or in the case of apraxia, have difficulty in converting heard commands into the correct movement. The main similarity of both disorders is that both disorders cannot be explained by deficits in vision, movement, somatosensation, and attention or language comprehension. The main difference in anatomy is that apraxia consists of subtypes which occur from damage to different parts of the brain, whereas optic ataxia is a single disorder which occurs from damage to a specific part of the brain. However, individual differences do occur in both and the symptoms may vary between individuals.