1) The purpose of this chapter is to describe the brain of the patient with dementia in relation to the doctor–patient relationship. The crucial point here is that the four steps that have been described throughout the book, i.e. ‘feeling sick’, ‘seeking relief’, ‘meeting the therapist’, and ‘receiving the therapy’ are all modified, or totally absent, in the demented patient. Whereas this is true in many medical conditions, like dementia, autism and vegetative state, and in some patients populations, like children, this chapter focuses on patients suffering from dementia as an example of the...
1) The purpose of this chapter is to describe the brain of the patient with dementia in relation to the doctor–patient relationship. The crucial point here is that the four steps that have been described throughout the book, i.e. ‘feeling sick’, ‘seeking relief’, ‘meeting the therapist’, and ‘receiving the therapy’ are all modified, or totally absent, in the demented patient. Whereas this is true in many medical conditions, like dementia, autism and vegetative state, and in some patients populations, like children, this chapter focuses on patients suffering from dementia as an example of the effects of impaired doctor–patient communication. 2) In relation to ‘how the demented patient feels sick’, different types of dementia may lead to changes in the perception of some symptoms. Most research has been performed in the field of pain. For example, patients with Alzheimer's disease can discriminate between a tactile and a painful stimulus, though their tolerance to pain is increased in some circumstances. Despite Alzheimer patients can recognize a painful stimulus, their autonomic responses to pain, such as heart rate and blood pressure, are blunted, thereby indicating that autonomic assessment is not reliable to understand whether a demented patient feels pain or not. 3) Patients with vascular dementia may experience pain in a completely different way. In fact, subcortical ischemic vascular dementia with white matter lesions may lead to hyperalgesia, which is attributable to deafferentation of the cortex, because of the interruption of thalamocortical pathways. 4) Frontotemporal dementia with hypoperfusion of frontal and temporal lobes leads to reduced pain perception. This is mainly due to the heavy neuronal degeneration and malfunctioning of the frontal lobes which play a critical role in the awareness of pain and in the global experience of pain. 5) As to ‘seeking relief’, the demented patient does not have a purposive behavioural repertoire that is aimed at seeking a doctor for relieving his own symptoms. Dementia has a powerful impact on cognitive functions, thus the demented patient does not have expectations of future rewards, for example, of future positive therapeutic outcomes, as we have seen in Chapter 4. 6) Similarly, in ‘meeting the therapist’ the cognitively impaired patient cannot interact with health professionals. All the complex functions that have been analysed in Chapter 5, such as trust and hope, are not present in dementia, thus they do not take part in the doctor–patient relationship. As in any condition whereby communication is not present, the central point of the interaction is based on the doctor's inference of the symptoms through observation. This is done through the use of observation scales that are aimed at understanding the suffering and the needs of the demented non-communicative patient. 7) As far as ‘receiving the therapy’ is concerned, there is compelling evidence that demented patients are undertreated in the presence of painful conditions. This is attributable to several factors, including impaired communication. In other words, although the demented patient may suffer from a painful condition, he is not able to communicate his own suffering. 8) When undergoing a therapeutic intervention, placebo and expectation effects are reduced, or even absent, in Alzheimer patients. This is due to the disruption of prefrontal executive functions and to the functional disconnection of the prefrontal lobes from the rest of the brain. The disruption of placebo and expectation mechanisms underscores the need of considering a possible revision of some therapies in Alzheimer patients in order to compensate for this disruption. 9) As the prefrontal cortex can be severely affected in other neurodegen-erative conditions, the neuroanatomical localization of placebo- and expectation-related mechanisms in prefrontal regions should alert us to the potential disruption of placebo and expectation mechanisms in all those conditions whereby the prefrontal lobes are involved. 10) In relation to the disruption of placebo responses in a clinical condition such as Alzheimer's disease, there is today compelling evidence that the experimental inactivation of prefrontal functioning in the laboratory setting in healthy subjects disrupts the placebo response. In fact, blockade of opioid neurotransmission in the prefrontal cortex or its inactivation by means of transcranial magnetic stimulation abolish placebo responsiveness. Therefore, if there is no prefrontal control, there is no placebo response.
Chapter. 9421 words. Illustrated.
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