HYPNOSIS AND STROKE REHABILITATION
Recent studies demonstrate that hypnosis is a valid support to rehabilitation programs that follow cerebrovascular accidents (Priftis et al., 2011, Cagiada et al., 2012). An increasing number of researches focus on the importance of considering emotional variables in rehabilitation. Recent studies (Ostir, Berges, Ottenbacher, Clow, & Ottenbacher, 2008) found that one of the most important factors in the prediction of final outcomes of rehabilitation are positive emotions. People who are able to fight negative emotions and anxiety are able to keep their motivation to treatment high and, consequently, their performance increases; they maintain and foster social relationships and more easily return to an active lifestyle.
The uncertain outcome of treatments, the stress that patients and their families experience, fatigue, suffering and frustration can lead to emotional reactions that can be very strong: crying spells, depression, anger, anxiety (Hibbard et al., 1998, Parr, Byng, Gilpin, Ireland, 1998). Of such emotional reactions the most deeply investigated one is depression. Depression is a very common response to strokes (around one third of patients) (Tuner-Stokes et al., 2005), and often persists even in the chronic phases of the disease causing a reduction of social interactions, self-esteem and motivation (Code & Herrmann, 2003). It is a condition characterized by a complex constellation of symptoms: long lasting bad mood, significant weight loss (or gain), loss or reduction of personal interests, sleep disturbances, decreased appetite, fatigue, feelings of guilt or worthlessness, attention problems, recurrent suicidal thoughts.
However, the true cause of depression after brain damage is still highly controversial. Depression can be directly caused by the type of cerebral lesion, its location and extension. The lesion, in fact, can modify, destroy or interfere with the delicate neuro-biochemical balance that underlies emotional experiences (Code & Hermann, 2003). However this doesn't rule out the possibility that depression can be a natural response to physical deficits and to communicative and cognitive impairments caused by the stroke (Code & Hermann, 2003). Code and Herrmann (2003) presented a model to analyze the causes of depression in patients who suffered from strokes. This model focuses on the timing of onset of depression. The authors, however, emphasized that reactions to strokes are unique and individual and are influenced by personal characteristics. Depression, according to their model, during acute phases of the stroke (0-3 months after the stroke) seems more related to the location of the lesion than the severity of cognitive impairments or the quality or quantity of social interactions. In this case depression is labeled as “primary”.
In the 6 months following the accident, the correlation between depression and severity of cognitive and motor impairments grows greatly; this evidence lead the authors to label it “reactive or secondary”. According to Herrmann and Wallesh (1993) there are two kinds of people who are particularly exposed to develop reactive depression: the first kind comprises those who initially deny the consequences of the stroke and subsequently have to face the whole range of their social, cognitive and functional disabilities. The second kind comprises those patients who expect a quick recovery and then realize that they will have to live with their deficits for long periods of time, if not forever.
The most interesting part of the model describes another type of depression, the tertiary one, which often appears when patients return home after hospitalization. This transition often means that the recovery phase has begun and thus patients experience it with a sense of relief. Right when they start trying to readjust to everyday reality in the social structure that characterized their lives before the stroke, they find themselves forced, maybe for the first time, to face the true impact of the communicative impairment.
Bibliografia
Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13(1-2), 109-132.
Herrmann M., Wallesch C.W., “Depressive changes in stroke patients“ in Disability and Rehabilitation, 15, pp 55-66, 1993
Hibbard, M. R., Uysal, S., Keple, K., Bogdany, J., & Silver, J. (1998). Axis I psychopathology in
individuals with traumatic brain injury, Journal of Head Trauma Rehabilitation, 13, 24-49
Parr, S., Byng, S., Gilpin, S., & Ireland, C. (1997). Talking about aphasia: Living with loss of language after stroke. McGraw-Hill International.
Seale, G. S., Berges, I. M., Ottenbacher, K. J., & Ostir, G. V. (2010). Change in Positive Emotion and Recovery of Functional Status Following Stroke. Rehabil Psychol, 55(1), 33-39.
Tuner-Stokes L., Kalmus M., Hirani D., Clegg F., The Depression Intensity Scale Circles (DISCs): a first evaluation of a simple assessment tool for depression in the context of brain injury” in J. Neurol. Neurosurg. Psychiatry, ,76;pp 1273-1278, 2005
The uncertain outcome of treatments, the stress that patients and their families experience, fatigue, suffering and frustration can lead to emotional reactions that can be very strong: crying spells, depression, anger, anxiety (Hibbard et al., 1998, Parr, Byng, Gilpin, Ireland, 1998). Of such emotional reactions the most deeply investigated one is depression. Depression is a very common response to strokes (around one third of patients) (Tuner-Stokes et al., 2005), and often persists even in the chronic phases of the disease causing a reduction of social interactions, self-esteem and motivation (Code & Herrmann, 2003). It is a condition characterized by a complex constellation of symptoms: long lasting bad mood, significant weight loss (or gain), loss or reduction of personal interests, sleep disturbances, decreased appetite, fatigue, feelings of guilt or worthlessness, attention problems, recurrent suicidal thoughts.
However, the true cause of depression after brain damage is still highly controversial. Depression can be directly caused by the type of cerebral lesion, its location and extension. The lesion, in fact, can modify, destroy or interfere with the delicate neuro-biochemical balance that underlies emotional experiences (Code & Hermann, 2003). However this doesn't rule out the possibility that depression can be a natural response to physical deficits and to communicative and cognitive impairments caused by the stroke (Code & Hermann, 2003). Code and Herrmann (2003) presented a model to analyze the causes of depression in patients who suffered from strokes. This model focuses on the timing of onset of depression. The authors, however, emphasized that reactions to strokes are unique and individual and are influenced by personal characteristics. Depression, according to their model, during acute phases of the stroke (0-3 months after the stroke) seems more related to the location of the lesion than the severity of cognitive impairments or the quality or quantity of social interactions. In this case depression is labeled as “primary”.
In the 6 months following the accident, the correlation between depression and severity of cognitive and motor impairments grows greatly; this evidence lead the authors to label it “reactive or secondary”. According to Herrmann and Wallesh (1993) there are two kinds of people who are particularly exposed to develop reactive depression: the first kind comprises those who initially deny the consequences of the stroke and subsequently have to face the whole range of their social, cognitive and functional disabilities. The second kind comprises those patients who expect a quick recovery and then realize that they will have to live with their deficits for long periods of time, if not forever.
The most interesting part of the model describes another type of depression, the tertiary one, which often appears when patients return home after hospitalization. This transition often means that the recovery phase has begun and thus patients experience it with a sense of relief. Right when they start trying to readjust to everyday reality in the social structure that characterized their lives before the stroke, they find themselves forced, maybe for the first time, to face the true impact of the communicative impairment.
Bibliografia
Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13(1-2), 109-132.
Herrmann M., Wallesch C.W., “Depressive changes in stroke patients“ in Disability and Rehabilitation, 15, pp 55-66, 1993
Hibbard, M. R., Uysal, S., Keple, K., Bogdany, J., & Silver, J. (1998). Axis I psychopathology in
individuals with traumatic brain injury, Journal of Head Trauma Rehabilitation, 13, 24-49
Parr, S., Byng, S., Gilpin, S., & Ireland, C. (1997). Talking about aphasia: Living with loss of language after stroke. McGraw-Hill International.
Seale, G. S., Berges, I. M., Ottenbacher, K. J., & Ostir, G. V. (2010). Change in Positive Emotion and Recovery of Functional Status Following Stroke. Rehabil Psychol, 55(1), 33-39.
Tuner-Stokes L., Kalmus M., Hirani D., Clegg F., The Depression Intensity Scale Circles (DISCs): a first evaluation of a simple assessment tool for depression in the context of brain injury” in J. Neurol. Neurosurg. Psychiatry, ,76;pp 1273-1278, 2005
