Discuss the probable alterations in behaviour after frontal lobe damage

Discuss the probable alterations in behaviour after frontal lobe damage. Critically discuss how might you assess this damage?

Over the past fifty years neuropsychologists, thanks in part to the rapid development of imaging technologies, have identified many of the cognitive and behavioural correlates of organic brain impairments. Over the same period, a range of new psychological tools have proven effective as diagnostic indicators of lesions or other malfunctions. The present analysis focuses specifically on the frontal lobe regions, the types of damage that might occur, the associated behavioural problems, and measures that have been formulated to assess the nature and extent of that damage.

The idea of cerebral localisation of psychological functions has existed in various forms since Gall (1935), but only recently have researchers been able to locate specific psychological processes to particular brain structures with any confidence; and studies of malfunction have been found to hold critical value here in identifying normal functioning. Kolb and Whishaw (2003) offer five discrete categories of psychological abnormality associated with frontal lobe lesions: (1) disturbances of motor functions; (2) loss of divergent thinking; (3) impaired response inhibition and inflexible behaviour; (4) poor temporal memory, and (5) impaired social and sexual behaviour imaging. Evidence, however, suggests a degree of overlap and interaction between categories. For the present analysis, the ‘cognitive’ categories, (2) and (4), will be discussed together, as will the categories relating to social behaviour and inhibition: (3) and (5).

Lesions in the motor cortex may lead to impaired motor functions, but there is evidence that damage to the prefrontal cortex also results in certain motor-control problems. For example, Fuster (1997) notes that inactivity through hypokinesia is associated with an impaired reactivity to stimuli involved with attention; impaired reactivity may also affect normal language processing functions resulting in mutism.

Damage to the motor cortex itself can lead to a reduced capacity to make fine, independent finger movements, though speed and strength of hand movements may be limited through damage to either the motor cortex or the dorsolateral area of the prefrontal cortex. Kolb and Milner (1981) carried out an experiment in which subjects who had undergone unilateral frontal lobectomies (a surgical intervention not affecting the prefrontal cortex) showed an impaired ability to copy facial and arm movement, a second group suffering left parietal lobe lesions made significantly more copying errors, while a third group suffering both left- and right frontal lobe lesions were very poor indeed at copying tasks. These findings suggest that impaired motor activities may involve a reduced capacity for the organisation and temporal programming of physical activities. (Problems of organisational disruption may relate to difficulties with temporal memory, to be discussed presently.)

Evidence suggests that Kolb and Whishaw’s (2003) category of impaired social and sexual behaviour imaging may share some common physical causal factors with that of impaired response inhibition and inflexible behaviour: specifically the inability of patients with frontal lobe lesions to demonstrate normal inhibitory responses in a range of social, emotional and decision-making contexts.

For example, Berlin et al. (2004) report that sufferers of frontal lobe lesions show inappropriate behaviour and difficulty with using normal social cues and information to monitor and control their own behaviour. Also, impaired inhibition may lead to a person to persist in a task that is obviously failing. Risk-taking, rule-breaking and reckless gambling behaviour may also be evident, as well as inappropriate sexual behaviour. Goel et al. (2004) have found evidence that failures in social reasoning may be specifically associated with left-lobe damage, rather than the right.

However, hemispheric asymmetry may play a different role in patterns of inflexible behaviour shown in age-related physical deterioration, such as is demonstrated by dementia sufferers. Goldberg (2001) argues that the right cerebral hemisphere is normally specialised for dealing with novelty and new procedural information, while the left is more specialised for routine and familiar tasks. (The left hemisphere is believed to be generally more resilient to deterioration through ageing.)

Early onset of frontal lesions tends to show far greater behavioural disruption than adult-onset lesions. Anderson et al. (1999), have noted that antisocial behaviours such as stealing and violence are more prevalent in child-onset cases, through an impulsive tendency to act on immediate cues and an inability to suppress inappropriate behaviours. Eslinger et al. (2004) cite the case of a girl who experienced a frontal lesion at the age of seven. Throughout her subsequent life she was to show consistent patterns of disruptive, antisocial and uncooperative behaviours: typically erratic, impulsive and failing to understand or empathise with others. Her failure to recognise normal societal boundaries led to serious social problems.

It was noted earlier that specific aspects of brain architecture and function have been associated with particular psychological behaviours since the nineteenth century. However, as Thimble (1990) notes,

‘It is remarkable how frontal lobe pathologic conditions often go unnoticed clinically, and indeed how the relevance of frontal lobe syndromes in man to an understanding of brain-behavior relationships has been neglected.’ (p.1)

In cases such as those cited where disinheriting through frontal lesions results in dysfunctional behaviours, the behavioural ‘abnormality’ tends to be socially, rather than clinically defined. Hence it is understandable that many cases of brain lesion may go unnoticed and undiagnosed. However, it is perhaps in researching categories of psychological disturbance dealing with cognition and memory that psychologists have been most successful in rectifying that earlier neglect of frontal-lobe symptom logy, as this area is most readily-suited to structured, task-based investigations.

The cognitive processes associated with the frontal lobes are those typically associated with ‘working memory’. Baddeley and Hitch’s (1974) model of short-term processing that stresses the role of specialised immediate storage modules under the control of a ‘central executive’. Bechara (1998) suggests that the prefrontal cortex provides the physical mechanism for this behavioural organiser. Anderson et al. (1999) found that certain types of lesion can result in castrophic interference with short-term memory-processing, whilst leaving other cognitive measures of IQ and long-term memory unaffected. Dimitrov et al. (1999) have found that short-term memory malfunction is especially marked in free-recall, rather than cued-recall tasks. ‘Divergent’ (or creative) thinking is also very limited in frontal lesion sufferers. ‘Convergent thinking’ (where a specific right-or-wrong answer is given to a specific question) is less affected. Again, this would appear to lend support to Goldberg’s hemispheric-asymmetry hypothesis, in that novel or original thinking is more severely affected than is the processing of familiar information. New learning is also typically impaired by frontal-lobe damage.

Many problems arise through poor ‘temporal’ memory, or an inability on the part of a lesion sufferer to organise information in an appropriate temporal sequence. Shimamura et al. (1990) found that subjects with frontal lesions, whilst showing a basic level of recall that matched that of controls, were significantly less to place lists of words into their temporal, presentation sequence, or to organise the sequence of chronological facts into their correct narrative order.

A whole battery of ‘frontal lobe tasks’ have been developed by psychologists (eg., see Thimble, 1990) which may serve as indicators of organic lesions. These include maze tests, rhythm-copying tasks, the Wisconsin card-sorting task and the Towers of London task. All tend to show impaired performance on the part of frontal-lesion subjects compared to controls, although variations in response patterns have been linked to laterality and other factors. For example, subjects with right-side lesions are more prone to risk-taking when carrying out the Iowa Gambling task, when compared to left-side lesion subjects and controls (Clark et al., 2003).

In conclusion, when evaluating any psychological research methodology, useful as these may be, it should perhaps be stressed that one may never infer causation from correlation, although, in many areas of clinical psychology, behaviours that start out as correlates may quickly become ‘indicators’ of a given condition. An indicator, however useful, can only be suggestive of brain malfunction, rather than conclusive evidence. A poor performance on a cognitive or other psychological task may arise for a range of reasons, and the same may be said of observed socially-dysfunctional behaviours; similarly a ‘normal’ performance is not ‘evidence of absence’. Ultimately, physical damage can only be confirmed by physical diagnostic methods. Although limited in this respect, perhaps the chief value of the kind of psychological studies cited here is, through working alongside neurology, to point clinicians in the right direction.

REFERENCES:

Anderson, Stephen W., Antoine B., Damasio H., Tranel D., Damasio Antonio R. (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience,2(11),1032-1036.

Baddeley, A.D, Hitch, G.J. (1974) Working Memory, In G.A. Bower (Ed.), Recent advances in learning and motivation (Vol. 8, pp. 47-90). New York: Academic Press.

Bechara et al. (1998), Dissociation of working memory from decision making within the human prefrontal cortex. Journal of Neuroscience 18, 428-37.

Berlin,H., Rolls, ET, and Kischka,U. (2004). Impulsivity, time perception, emotion,. and reinforcement sensitivity in patients with orbitofrontal cortex lesions. Brain, 127, 1108-1126.

Clark, L., Manes, F., Antoun, N., Sahakian, B.J., Robbins, T.W. (2003). The contributions of lesion laterality and lesion volume to decision-making impairment following frontal lobe damage. Neuropsychologia, 41: 1474-1483.

Dimitrov, M., Granetz, J., Peterson, M., Hollnagel, C., Alexander, G. & Grafman, J. (1999). Associative learning impairments in patients with frontal lobe damage. Brain and Cognition 41: 213-230.

Eslinger, P.J., Flaherty-Craig, C.V., Benton, A.L., (2004). Developmental outcomes after early prefrontal cortex damage. Brain and Cognition 55: 84-103.

Fuster, Joaquin, M.(1997). The Prefrontal Cortex Anatomy, Physiology, and Neuropsychology of the Frontal Lobe. In Human Neuropsychology.(3rd Ed. pp.150-184) Philadelphia, NY: Lippincott-Raven.

Gall, F.J. (1835) On the Functions of the Brain and of Each of its Parts. Lewis, W. Jr., Ray, I, translators. 6 vols. Boston: Marsh, Capen & Lyon.

Goel, V., Shuren, J., Sheesley, L. and Grafman, J. (2004). Asymmetrical Involvement of Frontal Lobes in Social Reasoning. Brain. Vol. 127, 783-790.

Goldberg, E. (2001) The Executive Brain: Frontal lobes and the civilised mind. Oxford University Press.

Kolb, B. & Milner, B. (1981), `Performance of Complex Arm and Facial Movements After Focal Brain Lesions’. Neuropsychologia, 19, 491- 504.

Kolb, B. & Whishaw, I.Q. (2003) Fundamentals of Human Neuropsychology. New York: Worth Publishers.

Shimamura A.P. et al (1990). Memory for the temporal order of events in patients with frontal lobe lesions and amnesic patients. Neuropsychologia 28: 803-813.

Thimble, M.H. (1990) Psychopathology of Frontal Lobe Syndromes. Seminars in Neurology Volume 10, No. 3, September 1990.