Although many cases have been reported on impairment of tool use and behavioral disturbance due to brain damage, the precise brain mechanisms regulating human behavior are still unknown.
In this report, an outline of behavioral abnormalities caused by brain damage, including utilization behavior (UB), imitation behavior (IB), and apraxia are presented. Next, a case of UB and IB elicited only by a key person is reported, and interpretation of his symptoms is discussed. Lastly, the general structure of information processing in the human brain for tool use and behavior are discussed. I speculate that there are two distinct systems in the human brain, that is, a control system and a substantial information processing system. The former corresponds to attention and emotion. This distinction should have importance when considering tool use and behavior in human beings.
A right-handed, 70 year-old man suffered bilateral anterior cerebral artery occlusion that resulted in bilateral frontal lobe infarction. He was inert, and his attention was impaired. He showed typical UB and IB which were elicited only by his chief physician and only in examination situations. Both UB and IB were lacking in his daily life and were never elicited by his family members or other medical personnel. Another report also gives evidence of cases in which a key person is required for UB and/or IB to be elicited.
Generally, an object could be considered to always show its meaning as a tool, which implies that its affordace emerges from the object itself. The behavior presented by the key person also can be regarded as a releaser for the patient to imitate behavior. Thus his essential impairment can be attributed to failure to grasp the correct relation of the meaning of objects or of behaviors and situations. This should be called a type of semantic impairments.
On the other hand, the patient's inertia and impaired attention is indicative of emotional disturbance. In fact, his cerebral lesions involve some parts of the limbic system. This suggests that he lost active perception which resulted in his being very easily captured by external stimuli. His unique symptoms should not be attributed to the traditional explanation in which UB and/or IB emerge from simple disinhibition of the parietal lobe function from the frontal lobe function.
