Which frequency improves the functional intelligence of the brain

A clinical study on the use of the sound bed in patients with stroke or traumatic brain injury. Thesis

Transcript

1 Music in neurological rehabilitation taking into account cognitive performance, conviction of control and physical functional level A clinical study on the use of the sound bed in patients with stroke or traumatic brain injury. Diploma thesis for obtaining the master's degree submitted to the Natural Science Faculty of the Paris-Lodron University in Salzburg by Andrea Krug-Wieder Salzburg, June 2006

2 Acknowledgments Without the support, encouragement and active help of many companions, it would never have been possible to carry out this project. Therefore I would like to thank everyone who contributed to the completion of this diploma thesis: At Prim. Univ.-Prof. Dr. Gunther Ladurner, as supervisor of this thesis at Univ.-Prof. Dr. Ursula Wranek, who was at our side with help and advice. Mrs. Gabi Wallner, who always helped us with organizational and practical questions regarding the sound bed. With the ward nurses Ada (neurorehabilitation), Emma (day clinic), Isabella (stroke ward) and Elsbeth (1st class men), as well as the nursing staff of the neurorehabilitation, who took over the transfer of the patients for us. With Mag. Stefan Hawelka, for the statistical evaluation and especially with all patients and test persons for the willingness despite their difficult situation in this study Many thanks also to our parents and friends, who always believed in our potential, promoted our abilities and motivated us again and again to overcome our fixed limits. Thank you for your love and support. Special thanks go to my colleague, friend and colleague Andrea Walter, who set this project up with me. Thank you for holding out with me to the end and fighting bravely against all odds.

3 Table of contents 0. Introduction 5 A THEORETICAL PART 7 1. Rehabilitation Definition tasks of rehabilitation Therapeutic measures in rehabilitation Neuropsychological rehabilitation (NPR) Further therapeutic measures in rehabilitation Influencing variables on the rehabilitation of neurological patients General influencing variables Psychological factors Cognitive performance Introduction Procedure for measuring the Cognitive performance Cognitive performance after a stroke or 16 traumatic brain injury Control belief Introduction Control belief in illness and health The importance of control belief in the development 21 of mental disorders Methods for measuring control belief in control after a stroke or 22 traumatic brain injury 2. Traumatic brain trauma Definition epidemiology Classification Head trauma Skull contusion Skull fracture Brain trauma Open brain injuries Covered brain injuries 2 9

4 Brain contusion Brain contusion Traumatic decerebration Secondary damage Late complications and long-term consequences Post-traumatic late epilepsy Chronic cognitive deficits Diagnosis Therapy Stroke Definition Epidemiology Neurophysiological basis of cerebral blood flow Cerebral metabolism Regulatory mechanisms Pathophysiology of the stroke Classification Classification according to pathogenetic aspect Hemorrhages Classification according to pathogenetic aspect Haemorrhagic disease Classification according to pathogenetic aspect Thrombosis Classifications Thrombosis Disease and hemorrhage Aetiology Aetiological aspects Haemorrhoidalemia Classification, Disease, Hemorrhages, Etiology, Etiology, Aetiology, Haemorrhage, Classification, Classification, Disease, Hemorrhages, Etiology, Hemorrhages, Classification, Classification, Disease, Hemorrhages, Hemorrhages, Classifications, Diseases, Hemorrhages, Hemorrhages, Diseases, Hemorrhages Symptoms Neurological symptoms Neuropsychological symptoms Risk factors Diagnostics Medical apparatus-based procedures Neuropsychological procedures Therapy 65

5 4. Music Introduction Neuroanatomical and physiological fundamentals of auditory information processing Structure and function of the hearing system Central transmission Central nervous signal processing Man and music Historical development of music effects research Musical elements in music effects research The influence of music on physiological parameters The influence of music on psychological parameters Selected Areas of application of music Music in medicine Music in rehabilitation Music as psychotherapy 79 EMPRICAL SECTION Introduction Questions Method Description of the sample Inclusion criteria Exclusion criteria Examination procedure Test procedures used Mini-Mental-Status-Test (MMST) Questionnaire to ascertain control belief 91 about illness and health Barthel -Index Description of the sound bed Music used Planned statistical analysis 96

6 7. Presentation of the results Cognitive performance control conviction, physical functional level Interpretation of the results Introduction Cognitive performance, control conviction, physical functional level Discussion 111 C LITERATURE LIST 113 D APPENDIX 122

7 0. Introduction Stroke is a widespread disease and is the third most common cause of death in industrialized nations after heart disease and malignant tumors (Diener & Forsting, 2002; Mumenthaler & Mattle, 1997; Soyka, 1988). The damage to the brain caused by trauma is also an increasingly common challenge for the medical system (Berlit, 1992). This creates an enormous effort for the public health system. In many discussions about this topic, however, the real problem, the individual suffering of the individual, is not taken into account. Aldridge (2001) emphasizes the loss of physical integrity, the deterioration of cognitive competence, the flattening of emotional coherence, and the danger of social isolation. In addition, there is also the fear of failing in a consumption- and performance-oriented society. However, these facts not only have an impact on the person directly affected, but also on the family and the social environment (Aldridge, 1998; quoted in Aldridge, 2001). It is the task of society to respond appropriately to the suffering of our fellow human beings. Any procedure that can bring even the slightest relief to those affected is of immense importance in the treatment and procedures of modern neurological rehabilitation. Tomaino (2002) advocates the use of music in the treatment of neurological disorders, as elements such as rhythm, melody and harmony can induce neurological reactions in patients. Music is a diverse medium whose area of ​​application has expanded significantly, especially recently. Spintge (2002, p. 83) describes music as the most effective emotional and aesthetic means of communication in human culture. In medicine, too, music has increasingly established itself as an alternative form of therapy. Music is used as a form of therapy in many areas of health promotion.

8 The acceptance of alternative forms of therapy has risen continuously in recent years, but there is still a certain amount of skepticism. In order to increase the frequency of the use of alternative forms of therapy, it is necessary to show the entire staff of the rehabilitation centers the effectiveness and importance of the treatment for the psychological and physical situation of the patients. This can be achieved through a systematic investigation of alternative forms of therapy. The present study is part of a research assignment given by Prim. Univ.- Prof. Dr. Gunther Ladurner and tries to evaluate the effects of music in the neurological rehabilitation of the Christian-Doppler-Klinik Salzburg. Thanks to a special construction, the sound bed, the music is not only made audible, but also made tangible. This should enable a targeted effect of the music on physical and psychological functions. Using standardized measurement methods, the attempt is made to obtain an objective picture of depression, cognitive performance, control beliefs about illness and health, physical function level and the quality of life of the test subjects. The present study deals with the areas of cognitive performance, beliefs in control of illness and health, and the level of physical functioning

9 A Theoretical part

10 1. Rehabilitation 1.1. Definition The term rehabilitation comes from the Latin word habilitas, which means skillful facility. Rehabilitation describes the restoration of a skillful, useful system (Wiedemann, 1977). The Federal Community for Rehabilitation (1994, p. 26) understands rehabilitation as efforts not to let a functional disorder become a permanent restriction / impairment of the social and professional living conditions or at least to reduce the effects on the mentioned areas of life to a minimum. Zuber, Weis and Koch (1998) also emphasize these aspects of rehabilitation in their definition. Rehabilitation is understood to mean efforts to prevent an illness or disability from becoming a permanent impairment of personal, social and professional living conditions and, in the event that complete rehabilitation cannot be achieved, these effects on the mentioned areas of life to a minimum to reduce. (Zuber, Weis & Koch, 1998, p. 486). Rehabilitation is not only about improving the state of health, but also about preventing the disease process from progressing. Sufferers should learn to cope in their everyday life despite their illness. (Weber-Falkensammer & Vogel, 1997)

11 1.2. Tasks of rehabilitation The task of rehabilitation is seen by Zuber, Weis & Koch (1991) in preventing a disability into a permanent impairment. However, if complete rehabilitation is unattainable, the effects on social, personal and professional living conditions should be kept as low as possible. Cvetkova (1996, S) emphasizes the following tasks of rehabilitation therapy: Not the restoration of individual, isolated abilities and skills, but restitution of the disturbed functions as psychological activity Complete or partial restitution of functions, not adapting the patient to his damage, returning the patient to the normal social milieu , not in the simplified above all restoration of the communication skills of the language, not of its individual sides (relationships, repetitions, etc.) restoration of the various forms of communication skills (verbal and non-verbal) The Association of German Pension Insurance Institutions (1991, S) differentiates between the following tasks of rehabilitation: 1. Diagnosis of the disease itself and the damage to health (if not done sufficiently or if the available findings are no longer up-to-date), functional diagnosis (physical, mental and psychological performance possibilities and limits) un d psychosocial diagnostics 2. Creation of a rehabilitation plan for the patient, which is based on the treatment concepts of the pre-treatment provider, on the results of the (progress) diagnostics in the rehabilitation facility and takes into account the individual requirements and possibilities of the patient as well as the special demands on him in work and everyday life

12 3. Informing the patient about the illness and its consequences 4. Optimizing medical therapy and carrying out physical, psychological and other therapeutic measures 5. Promoting an appropriate attitude towards the illness: acceptance of the disability, motivation to actively cope with the illness (change from being treated to acting ) and development of self-responsible health awareness 6. Modification of behavior with the aim of developing nutritional, physical activity and leisure behavior appropriate to the disease and reducing health-damaging and health-promoting behavior 7. Training of residual functions and training of new skills to compensate for functional limitations 8. Instruction / Training in the possibilities of self-control and self-treatment of the disease 9. Advice to caregivers on how to adequately deal with the rehabilitation patient and his or her illness / disability 10. Social med ical assessment of the rehabilitation candidate's performance 11. Advice to the patient with regard to professional activity and everyday life on the basis of the performance capacity achieved 12. Planning and suggestion of further measures (follow-up care, professional development) and preparation of the patient accordingly

13 1.3. Therapeutic measures in rehabilitation The therapeutic measures should be included in the rehabilitation plan as soon as the general condition of the patient allows. This can accelerate the natural healing process (Nau & Jochheim, 1988). In medical rehabilitation, methods from the fields of psychotherapy, occupational therapy, disabled sports, technical aids, etc. are often combined. The aim of these measures is to restore physical, psychological and social adaptation to the defect, as well as to prepare for reintegration into society (Nau & Jochheim, 1988) Neuropsychological Rehabilitation (NPR) Adams defines neuropsychology as the study of brain-behavior relationship. Clinical neuropsychology as a practice is the application of these brain-behavior relationship principles to the individual patient for assessment, treatment, and rehabilitative purpose. (Adams, 2002, p.1). Neuropsychological and cognitive rehabilitation has undergone strong development over the past 20 years. This happened, among other things, as a reaction to the increased emphasis on neurorehabilitation after traumatic brain injury, stroke and other neurological disorders. Further developments in medical technology and emergency care have allowed more patients with severe cognitive and behavioral impairments to survive and now require more intensive and lengthy cognitive rehabilitation (Hanlon, 1994). Neuropsychological rehabilitation has its own rehabilitation methods, which can be divided into at least two groups. The first group includes methods aimed at regaining impaired cortical functions. The second group aims to restore the person's social and personal status. Both groups cannot be seen in isolation; they are closely interrelated.

14 However, at each stage of rehabilitation, one or the other group of methods will lead the way (Cvetkova, 1996). Rehabilitation therapy is one of the most important and effective methods for restoring impaired functions. The theoretical basis of rehabilitation therapy is the modern psychology conception of cortical functions as a functional system, the conception of their systematic and dynamic localization, their formations during lifetime, their socio-historical origin and the mediated structure. (Cvetkova, 1996, p. 110). The effectiveness of the neuropsychological function training to improve performance could be proven. Neuropsychological therapy is all the more effective the earlier it begins after the point in time of the lesion, the milder the impairment, and the younger the person concerned is. Furthermore, the intensity and duration of the treatment, as well as motivation, mood and premorbid personality have an influence on the improvement in performance (Grimm, 1983; quoted in Schlösser, 1988) Further therapeutic measures in rehabilitation The tasks of speech therapy consist of activation, motivation and relearning of Language content (Poeck & Hacke, 1998). The earlier it begins, the more effective speech therapy is (Berlit, 1992). Speech therapists often have a better understanding of the language understanding they have received and the resumption of language production than the treating physicians, because they deal with the language of those affected in their daily sessions (Poeck & Hacke, 1998). Linguistically oriented speech therapy must always be based on the speech or speech disorder present (Berlit, 1992). Physiotherapy is described as the treatment of illnesses with natural means such as water, warmth, light, air. (Duden, 1982, p. 593, keyword physiotherapy) The independence training, which aims to give the patient responsibility in daily life again, is of particular importance here (Nau & Jochheim, 1988).

15 Der Duden (1982, p. 225, keyword occupational therapy) defines occupational therapy as occupational therapy that has been expanded to include occupational therapy. According to Schlösser (1988), occupational therapy should help with disorders of manual fine motor skills. Dirschauer, Burfeind, Hohenhövel and Schütte (1995) see the goal of this therapy in eliminating functional disorders of the musculoskeletal system through meaningful occupation. In addition to mobilizing the joints and strengthening the muscles, the therapy should also include targeted exercises in daily life to regain independence. A special form of this is sports therapy, which, according to Nau and Jochheim (1988, p. 147), aims at two areas of indication: 1. Medical indication: stabilization of organic performance and improvement of motor function 2.Psychosocial indication: promoting personality development, increasing psychological resilience and improving social adaptability The connection of rehabilitative sport with other rehabilitation measures such as physiotherapy, psychotherapy, occupational therapy, etc. is also of particular importance (Nau & Jochheim, 1988). Clinical psychology and psychotherapy can help with emotional processing (Schlösser, 1988). Psychologists not only take on tasks such as building motivation, making diagnostics, and helping with depressive moods, but also coordinating psychotherapeutic measures (Nau & Jochheim, 1988).

16 1.4. Influencing variables on the rehabilitation of neurological patients General influencing variables Rehabilitation should follow acute treatment as quickly as possible and include various treatment methods (Schlösser, 1988) Poeck and Hacke (1998) also emphasize that rehabilitation of the patient begins on the day of illness. Acute therapy can only be carried out in the first few hours, perhaps the first 24 hours. Medical treatment for complications usually ends after the first week. During this time it is necessary to initiate the rehabilitation process with combined physiotherapy, speech therapy and medical treatment. (Poeck & Hacke, 1998, p. 230) In neurological early rehabilitation it has been shown that the medium to long-term rehabilitation result (outcome) depends on both biographical and medical variables. Heubrock and Petermann (1997) ascribe particular importance to age. The clinical outcome and thus the long-term reintegration chances are significantly better in younger patients. According to Zihl (1988, pp. 2-3), the following prerequisites are necessary in order to guarantee an effective treatment of the performance impairment: a diagnostic recording of the performance disorder oriented towards the treatment the availability of suitable treatment methods methods to prove the treatment effect the sufficient intactness of specific services (e.g. Speech comprehension and memory skills for the implementation of perceptual or motor training) a sufficient availability of so-called global services (attention, resilience) at least for short periods of time a minimum motivation on the part of the patent

17 Psychological influencing variables Psychological aspects such as cognitive performance or assessment of self-efficacy are of great importance in rehabilitation. On the one hand, these can help shape the success of the rehabilitation, on the other hand, they can also be influenced by the rehabilitation. Cognitive performance Introduction Learning and memory disorders are among the most common consequences of brain damage with around 60% of patients (Schuri, 1988). The learning and memory disorders of most patients are not very pronounced and rarely appear in isolation, but rather together with other brain disorders such as e.g. a reduced information processing speed (Schuri, 1988). Memory impairments can make neurological rehabilitation very difficult, as the effectiveness of rehabilitation measures can be reduced, e.g. because prescribed aids are not used (Bodenburg, 2001). Method for measuring cognitive performance. In the case of physical illnesses in which psychological functions such as perception, learning or memory are restricted by pathological changes, usually in the central nervous system, a precise diagnosis of of central importance. The main task of neuropsychological diagnostics is to determine the current functional limitations of the person concerned.

18 On this basis, indications for appropriate treatments or rehabilitation measures can be established and treatment effects can be assessed. A measuring instrument used in numerous studies to assess cognitive performance is the Mini-Menta-Status-Test (MMST) (Folstein, 1975). A detailed description of this test can be found in Chapter The use of this test in studies on cognitive performance after a stroke is often criticized because it is highly dependent on the verbal skills of the test subjects (Kauhanen et al, 1999) Cognitive performance after a stroke or cranial Brain trauma A stroke can cause cognitive impairment (Kauhanen et al., 1999). Areas particularly susceptible to this are memory, orientation, language and attention (Tatemichi et al., 1994, cited in Kauhanen et al., 1999). However, a stroke not only triggers focal neurological deficits, but is also associated with a higher risk of developing dementia. However, there are not too many studies on this yet (e.g. Babikian, Wolfe, Linn, Knoefel & Albert, 1990, quoted in Prencipe et al., 1997). A study (Tatemichi et al. 1992, cited in Prencipe et al., 1997) found a 9.4 times higher risk for stroke patients to develop dementia than in the normal population. In the study by Zhu et al. (1998) examined the impact of stroke on the cognitive and functional status of all residents over 75 years of age in a district of Stockholm. A third of the stroke patients were diagnosed with dementia, which corresponds to a 3 times higher risk for stroke patients than in healthy subjects. The result also shows a significant relationship between stroke and cognitive impairment (without dementia).

19 The study by Kauhanen et al. (1999) shows a relationship between the tendency to depression after a stroke and cognitive impairment. Memory, non-verbal problem solving, attention and psychomotor speed were particularly impaired in this context. The cognitive impairment was measured with the MMST. 30% of stroke patients were classified as demented. A number of studies (e.g. Fleminger, Oliver, Lovestone, Rabe-Hesketh & Giora, 2003; Mehta et al., 1999; Plassman et al., 2000; Salmon, Chatfield, Menon, Pickard & Sahakian 2005) deal with the long-term effects a brain injury caused by trauma to the cognitive system. Salmond et al. (2005) report that the patients with traumatic brain injuries exhibited a neuropsychological profile that resembles a chronic cholinergic deficit. The patients had significant deficits in attention span, association learning, and reaction time. Salmond et al. (2005) call for drug treatment of the cholinergic system in order to achieve a significant improvement in the subsequent sequelae of a traumatic brain injury. Fleminger et al. (2003) report the significant role of a dysfunction of the cholinergic system as a risk factor for Alzheimer's disease. The authors also mention the importance of acetylcholine for the long-term effects of cranial brain injuries. Plassman et al. (2000) were able to show in their study that a traumatic brain injury in early years is associated with a significantly increased risk of dementia and Alzheimer's disease. It was shown that this risk is significantly increased, especially in moderate to severe cranial brain injuries. In contrast, no significant result could be identified for mild head trauma (Plassman et al., 2000). Mehta et al. (1999) are also convinced that a minor traumatic brain injury is not an increased risk of developing a later Alzheimer's disease. According to Plassman et al. (2000), the number of alleles on the APOE 4 gene is particularly important in the development of dementia after a traumatic brain injury. Mehta et al. (1999) could not establish a significant connection with the APOE 4 gene.

20 As with a stroke, a connection can also be found between cognitive impairment and depression after a traumatic brain injury (Rapoport, McCullagh, Shammi, & Feinstein 2005). Treatment of depression can increase the patient's cognitive performance (Fann, Uomoto, & Katon, 2001). In particular, the areas of psychomotor speed, cognitive performance, flexible thinking and short-term remembering have been positively changed by drug treatment of patients with antidepressants. The individual assessment of progress in cognitive performance, as well as the assessment of the severity of the trauma, could be improved by treating depression.

21 Control Belief Introduction The concept of control belief was introduced into psychology by Julian Rotter (1966, quoted in Pinquart, 1998) as a relatively stable personality trait. According to Amann and Wipplinger (2001), Rotter sees human behavior not only as determined by the environment. Behavior develops from the interaction between a person and their environment and not solely on the basis of environmental conditions or variables that are in a person. How a person is adapted to his social environment depends largely on the extent to which he experiences himself as a self-determined, active and planning individual. Every person has a tendency to interpret events as either self-caused or as not influenceable (Lohaus & Schmitt, 1998). The concept of generalized control expectations refers to the experience of one's own possibilities for individual influence on the respective situation. According to the control belief concept, individuals differ in whether they experience events as being controllable by themselves (internal control) or whether they ascribe the controllability to other forces outside of their own person (external control) (Lohaus & Schmitt, 1998). Individuals with an internal belief in control are convinced that the consequences of their actions are determined by their own actions (Amann & Wipplinger, 2001). The attitude that consequences can be influenced suggests that there is also a corresponding willingness to act (Lohaus & Schmitt, 1998). People with an external belief in control tend to ascribe the consequences of their own actions to others, factors beyond their control (Amann &, Wipplinger, 2001). This means that there will be little effort to want to influence conditions on one's own initiative (Lohaus & Schmitt, 1998). A third dimension, the fatalistic externality, was also introduced. People with fatalistic control believe that events depend mainly on chance, luck, or fate. This means that there is hardly any chance of influencing one's own condition in a targeted manner (Lohaus & Schmitt, 1998).

22 Belief in control over illness and health Within the area of ​​health and illness, the belief in control can be different. Prior knowledge and experience of different forms of disease can give rise to different expectations about the controllability of the diseases. Especially in the case of illnesses that occurred several times or over a longer period of time, it is obvious that there are learning experiences about the controllability of these specific illnesses, which may differ from the learning experiences about other illnesses. (Lohaus & Schmitt, 1998, p. 3). So it is possible that in individual cases there are different control beliefs within the area of ​​health and illness, whereby the generalized control beliefs in this area reflect the general and predominant learning experiences. The generalized control beliefs are of particular importance when problems arise for which no previous experience has been made. The type and extent of generalized control beliefs play a role in how new problems are approached (Lohaus & Schmitt, 1998). Of particular importance to the control beliefs about illness and health is the relationship to behavior that can influence one's own well-being. According to (Lohaus & Schmitt, 1998, p. 4), two main areas should be mentioned here: a) Action to promote health in the event of illness Adherence to medical advice Implementation of additional health-promoting measures b) Action to prevent illness in the event of health Implementation of preventive measures Avoidance of behavior that is harmful to health

23 The Significance of the Conviction of Control for the Development of Mental Disorders In the following, some relationships between depression and the conviction of control will be reproduced, as cited in Perrez (1998): Nolen-Hoeksema, Girgus and Seligman (1992) examined in their longitudinal study whether the Attribution style and critical life events have an impact on the development of depressive disorders in students. The authors came to the conclusion that critical life events (e.g. separation of parents or death of a family member) in the early phase of observation have a good predictability for the occurrence of a depressive mood. In connection with this, there is also a change in the attribution style. In older children, both the negative attribution style in general and the attribution style coupled with critical life events have good predictability for depressive symptoms. Rose, Abrahamson, Halberstadt and Leff (1994) found in their study of adults with major depression that those with the most serious attribution style were people who had a personality disorder in addition to depression, were victims of sexual abuse in childhood, and were gross or overcontrolling Parents had experienced. Metalsky and Joiner (1992) came to the conclusion in their longitudinal study that a negative attribution style acts as a diathesis factor. The negative attribution style moderates the likelihood of a depressed mood when there is additional stress. Depressives differ from nondepressants in their more generalized external belief in control (Benassi, Sweeney, & Dufour, 1998). Depressed people are more convinced that the negative consequences of their behavior depend on external conditions.

Methods for Measuring Control Beliefs Initially, research focused on generalized control beliefs that arise as a result of control experiences that develop across different areas of life. Later, more attention was paid to the collection of area-specific control beliefs, since it must be assumed that people in different areas of life have different control options and control experiences (Lohaus & Schmitt, 1998). The methods commonly used today therefore partly cover generalized competence and contingency expectations (e.g. questionnaire on competence and control beliefs FKK; Krampen, 1991, quoted in Kruse, 1998), and partly more area-specific control beliefs (e.g. the Multidimensional Health Locus of Control Scales MHLC for Health-related control belief; Muthny & Tausch, 1994, quoted in Kruse, 1998) Control belief after a stroke or traumatic brain injury In their study, Johnston, Morrison, MacWalter and Partridge (1999) examined stroke patients with regard to their control beliefs and physical impairment. The data were collected shortly after the stroke and after 1 or 6 months after their discharge. The results show a significant association between the belief in control and the stroke after one month. After 6 months, however, no more significance could be determined.

25 2. Traumatic brain injury 2.1. Definition There is still no generally accepted definition of traumatic brain injury. The Pschyrembel (1990, p. 1539, keyword SHT) describes traumatic brain injury as a generic term for covered or open skull injuries (with perforation of the dura mater, e.g. after skull fracture) with brain involvement. Williamson, Scott and Adams (2002, p. 9) define traumatic brain injury as any injury to the brain that endengers a change in consciousness. A traumatic brain injury can lead to different consequences depending on the severity, the speed, the direction and the attack surface of the violence (Soyka, 1991) Lead the brain to a profound brain contraction. (Mumenthaler & Mattle, 1997, p. 154) 2.2. Epidemiology The frequency (incidence) of traumatic brain injuries is increasing nowadays, especially due to traffic accidents. In the industrialized countries of the western world it amounts to about 8000 cases per million inhabitants in one year (Mumenthaler & Mattle, 1997). Poeck and Hacke (1998) assume that around 300 brain traumas of all degrees of severity occur in Germany every year. The traumatic brain injury shows an age-dependent distribution. People between the ages of 15 and 24 and over 75 are particularly at risk of traumatic brain injury (CDC, 1997, quoted in Rosenthal & Ricker, 2000). Especially in children, traumatic brain injury after an accident is the most common cause of hospital admission (Brock, Festge & Kintzel, 1976). Furthermore, traumatic brain injury is one of the most common causes of death in children and in younger adults.(Soyka, 1991, p. 169).

26 Gender also plays a role in the incidence of traumatic brain injury. About 2 to 3 times as often head trauma affects men (Rosenthal & Ricker, 2000) Ca of total head trauma patients can be classified as severe brain injuries. About half of them have to be admitted to a hospital. Around 2.5-5% of the injured later also require rehabilitation due to the serious impairments (Mumenthaler & Mattle, 1997, p. 154). Here, too, there is an age-dependent distribution. The incidence of severe impairment and vegetative syndrome appears to be higher in childhood (16%) than in adulthood. In contrast, the likelihood of a good recovery in childhood is significantly higher (over 50% after one year) than in adulthood. (Herrmann, 1991, p.165) According to Berlit (2000), the presence of multiple craniocerebral injuries, additional extracerebral injuries, the age of the patient and the duration of unconsciousness are decisive for the prognosis of moderate and severe traumatic brain injury. The overall prognosis after severe craniocerebral trauma, ie a value of 8 or less on the Glasgow Outcome Scale and a minimum duration of the coma between 6 and 24 hours, is still unfavorable (Klaus et al., 1985, cited above. in Herrmann, 1991). The lethality of moderate and severe craniocerebral trauma is around 50% (Berlit, 2000). It increases with age. The total mortality in the group of children and adolescents is around 30%. The adults show a mortality of about 45%. A mortality rate of 37-38% is to be expected in adults under 40 years of age and 43% between 40 and 60 years of age (Herrmann, 1991).

27 2.3. Classification The classification of traumatic brain injury has not yet been solved satisfactorily. There is currently no classification that equally records the history, the neurological findings and the result of the examination with imaging methods and is so descriptive that it does not anticipate socio-medical aspects, such as the assessment (Poeck & Hacke, 1998). In the case of traumatic head injuries that only affect the bony skull and do not lead to substance damage to the brain, a distinction is made between bruised skull and skull fracture. This distinction can be found consistently in the literature (e.g. Berlit, 1992; Poeck & Hacke, 1998). It is less easy to classify brain traumas. The terms Commotio and Contusio cerebri (e.g. Berlit, 2000; Delank, 1991; Delank & Gehlen, 2004; Mumenthaler & Mattle, 1997; Soyka, 1991) and Compressio cerebri (e.g. Delank, 1991; Delank & Gehlen, 2004) are largely obsolete today, according to Berlit (1992). Poeck and Hacke (1998) also rate the old division of brain traumas into commotio cerebri and contusio cerebri as outdated because it includes assertions about the morphological findings that are not always supported by the imaging procedures. They suggest using the terms commotion and contusion in a purely functional way. Head traumas Skull contusion Skull contusion is the simplest form of skull injury (Berlit, 2000). It almost always occurs through blunt force (blow, push, etc.). The initial symptom of a bruised skull is a sudden local or diffuse headache that can last from minutes to hours (Poeck & Hacke, 1998). There is no deeper disturbance of consciousness, as is characteristic of the commotion syndrome.

28 Symptoms such as dizziness, nystagmus, nausea and vomiting, but also hearing impairments that set in immediately or with latency and that even progressive hearing disorders can be due to the fact that damage to the inner ear has occurred at the same time, which is also possible without a temporal bone fracture (Poeck & Hacke, 1998). A bruise of the skull can generally occur with or without a bruise mark and laceration (Berlit, 2000) Skull fracture A skull fracture is also possible without commotion syndrome with appropriate violence (Poeck & Hacke, 1998). Skull fractures occur when the elastic limits of the bone are exceeded. (Delank, 1991, p. 183). Depending on the pathomechanics and the resulting fracture shape, a distinction is made between linear fractures (or fissures), bending, bursting and piece fractures as well as impression fractures. (Delank, 1991; Delank & Gehlen, 2004). Berlit (2000) also mentions expression fractures that occur when broken bone parts burst. Skull fractures can be classified according to the location of the violence: Focal cerebral symptoms and traumatological (late) epilepsy as a consequence of impression fractures of the skull (Delank & Gehlen, 2004) often occur in the case of skull fractures. Base fractures of the skull often appear as burst fractures and often occur in combination with skull fractures (Delank & Gehlen, 2004). Fractures of the base of the skull can often only be inferred by clinical signs and are often not detectable radiologically (Poeck & Hacke, 1998). Frontobasal fractures are most frequently localized in the area of ​​the lamina cribrosa. Even the smallest cracks can lead to CSF ​​leakage and can no longer heal spontaneously (Berlit, 2000).

29 In the case of temporo-basal fractures (petrous bone fractures), otoliquorrhoea, retroauricular hematomas, step formation in the external auditory canal and facial nerve palsy can be observed. (Delank & Gehlen, 2004, p. 275). Facial skull fractures can affect the lower jaw, zygomatic bone, temporomandibular joint, upper jaw, nose, ethmoid bone and orbital walls (Delank & Gehlen, 2004).

30 Brain traumas If a bruised skull leads to a temporary impairment of consciousness, a brain trauma must be diagnosed (Berlit, 1992). The injuries to the brain occupy a special position among the consequences of trauma, because they can leave behind both physical and severe psychological permanent consequences. (Bundesarbeitsgemeinschaft für Rehabilitation, 1994, p. 64) A general distinction is made between open and covered brain trauma: Fig. 1. Forms of open and covered brain trauma (from Delank & Gehlen, 2004, p. 276)

31 Open brain injuries The decisive criterion for an open brain injury is not the opening of the skull, but the opening of the meninges (dura) (Poeck & Hacke, 1998). In open brain injuries, there is a connection between the subdural space and the outside world as a result of a dural injury. This can lead to serious infections and must be treated surgically under all circumstances (Poeck & Hacke, 1998) Covered brain injuries If the violence extends to the brain without a penetrating injury, then a covered head injury is to be diagnosed (Soyka, 1991). Depending on the mechanism of the accident and the severity of the violence, a distinction is made between different forms of cranial brain trauma (Delank & Gehlen, 2004). when the pressure wave spreads over the entire brain and leads to a momentary neuronal dysfunction without causing lasting substantial damage. A cerebral commotio is anatomically not accompanied by a gross organic lesion of the brain and accordingly does not produce any clinically detectable neurological deficits (Berlit, 2000; Delank, 1991; Mumenthaler & Mattle, 1997; Soyka, 1991). Clinically, the cerebral commotio is characterized by a possibly very brief loss of consciousness, brief retrograde amnesia, and vomiting (Mumenthaler & Mattle, 1997; Soyka, 1991). The duration of unconsciousness is an important criterion for assessing the severity of the trauma suffered and, for commotio cerebri in the literature, is by definition a few minutes to a maximum of an hour (e.g. Berlit, 2000; Delank & Gehlen, 2004; Soyka, 1991).

32 The unconsciousness is usually followed by more or less long stages of clouding of consciousness and a continuity syndrome (Mumenthaler & Mattle, 1997). The memory gap for the duration of unconsciousness and the subsequent clouding of consciousness is referred to as anterograde amnesia (Mumenthaler & Mattle, 1997). Several minutes after a head trauma, a memory disorder occurs that can last up to an hour backwards (Poeck & Hacke, 1998). The cause of retrograde amnesia is probably a dysfunction in the basal parts of the temporal lobe (Poeck & Hacke, 1998). Common complaints of commotio cerebri include memory disorders, headaches, dizziness, fatigue and irritability quickly, sensitivity to the sun, temporary brain weakness, difficulty concentrating, general poor performance, increased affective reactivity, alcohol intolerance and circulatory lability (Delank, 1991; Delank & Gehlen, 2004; Mumenthaler & Mattle, 1997; Poeck & Hacke, 1998; Soyka, 1991) Squeezing the brain In all other cases of covered brain damage in which substantial tissue lesions have arisen, the term contusio cerebri is used (Soyka, 1991). A brain contusion or contusio cerebri is a brain lesion that is associated with organic findings, especially micro-bleeding. (Rothenberg, 1995, p. 725). In the case of contusio cerebri, there is morphologically detectable damage to the brain substance (Mumenthaler & Mattle, 1997). Contusion foci are particularly often located at the base of the frontal lobe and the temporal pole, less often at the mantle edge, laterally on the brain stem and at the base of the cerebellum (Mumenthaler & Mattle, 1997). The clinical signs of brain trauma with contusion syndrome are a post-traumatic disturbance of consciousness (amnesia), mostly unconsciousness and a post-traumatic twilight state (Berlit, 2000; Delank, 1991; Mumenthaler & Mattle, 1997; Soyka, 1991), cerebral focus symptoms (Poeck & Hacke, 1998 ) and a traumatic psychosis (Poeck & Hacke, 1998; Soyka, 1991).

33 The severe brain injuries can lead to unconsciousness for several days or even several weeks; the anterograde and retrograde amnesia also include longer periods of time, which can last from several minutes to days (Soyka, 1991). A wide variety of post-traumatic complaints can come to light depending on the location and severity of the brain injury. These include neurological deficits such as spastic paralysis, sensitive deficits, aphasia (Poeck & Hacke, 1998; Soyka, 1991), visual disturbances and epileptic seizures (Mumenthaler & Mattle, 1997). The regression of the initial symptoms is usually delayed in the case of a contusio cerebri. The symptoms usually last longer and are much more severe than with a commotio (Poeck & Hacke, 1998) Traumatic decerebration In the case of extensive intracerebral hemorrhage as well as space-occupying cerebral edema, there is an acute increase in intracranial pressure up to entrapment at the tentorial slit with decerebration syndromes (Soyka, 1991). Decerebration is a neurological syndrome in which disease processes of various kinds lead to a functional separation of the cerebral mantle and the brain stem. (Poeck & Hacke, 1998, p. 557). This condition is also called functional decortication (Soyka, 1991, p. 173). Another name for this is the apallic syndrome (pallium = cerebral mantle). An apallic syndrome is a condition that occurs as a result of severe brain injuries in which the patient lies motionless in bed with his eyes open, without showing any signs of conscious communication with the outside world. (Soyka, 1991, p. 173) The apallic syndrome is usually based on multiple, secondary tissue damage in the basal ganglia, in the limbic system, on different levels of the brain stem and in the medullary bed of the hemispheres (Poeck & Hacke, 1998). Some of the patients die within the first few hours, others only a few days after the brain is removed. Others remain in the apallic syndrome for up to several months (Poeck & Hacke, 1998).

34 2.4. Secondary injuries A distinction is also made between primary and secondary brain injuries. While primary brain injuries arise at the moment of the impact of violence as immediate consequences, injuries in secondary ones only occur with a time lag, which are mainly circulation-related damage without an infection consequence (Delank & Gehlen, 2004). Compressio cerebri is the most feared complication after a brain injury (Delank & Gehlen, 2004). Delank (1991) understands cerebral compression to be the increase in intracranial pressure as a result of a traumatic brain injury. Headache and vomiting can be the first signs. Clouding of consciousness, secondary dilation of the pupil, and slowly increasing hemiparesis are other signs (Delank & Gehlen, 2004). According to Delank (1991), hematomas, cerebral edema and inflammatory complications lead to cerebral compression. Hematomas: An epidural hematoma is an immediately vital-threatening complication of craniocerebral injuries, which usually arises from the rupture of the middle meningeal artery in a fracture of the temporal scale. The resulting arterial bleeding leads within a few hours to the development of a large hematoma between the skull and dura and thus to brain compression (Delank, 1991; Mumenthaler & Mattle, 1997; Soyka, 1991). The resulting hematoma causes the patient, whose state of consciousness began to brighten again in the first few hours after the accident, to become unconscious again. With the increasing compression of the brain, Jackson seizures or motor failures can occur contralaterally (Soyka, 1991). Only an immediate intervention with evacuation of the hematoma saves the patient's life. (Soyka, 1991, p. 176) Subdural hematomas are located between the dura and the soft meninges and are the result of oozing from injured venous vessels, rarely from ruptures of small cortical arteries (Delank, 1991; Soyka, 1991).

35 Such hematomas develop more slowly than epidural hematomas, so the symptoms often only appear after weeks or months (Delank, 1991; Soyka, 1991). There is an increasing clouding of consciousness, the development of hemiparesis, possibly focal seizures and, as in the case of an epidural hematoma, also the development of a unilateral mydriasis due to pressure paralysis of the parasympathetic oculomotor fibers at the tentorial slit. (Soyka, 1991, p.). According to Delank and Gehlen (2004) the symptoms show up as slowly progressing organic psychosyndrome and hemisphere symptoms. According to Rothenberg (1995), a subdural hematoma is associated with very high mortality even with immediate treatment. A chronic subdural hematoma is when the hematoma occurs four weeks or later after the trauma (Berlit, 2000). It is defined as recurrent venous bleeding into the subdural space. (Berlit, 2000, p. 326) The predisposing factors for a chronic subdural hematoma include older age (over 50 years), coagulation disorders and alcohol abuse (Berlit, 2000). The clinical symptoms are often unspecific and include, in addition to a fluctuating disturbance of consciousness, confusion, headaches and variable focal signs (Berlit, 2000). A traumatic intracerebral hematoma is found mainly in the temporal or forehead area and shows neurological focus symptoms according to its location (Delank, 1991; Delank & Gehlen, 2004). Acute intracerebral hematomas lead to mass displacements and a penetration into the ventricular system (Berlit, 2000). If this only affects individual cerebral lobes and there is rapid relief, the consequences can be minimized. Brain edema The brain edema is another triggering event for an increase in intracranial pressure (Delank & Gehlen, 2004). Edema production is promoted by compression of the brain tissue, which can lead to hypoxia as a result of insufficient blood flow (Delank, 1991; Delank & Gehlen, 2004). The traumatic edema forms mainly in the medullary bed, which leads to a more or less extensive medullary shrinkage (Delank and Gehlen, 2004).

36 This increase in pressure, triggered by edema, can lead to entrapment symptoms and thus to midbrain or bulbous brain syndrome, which significantly worsen the prognosis (Soyka, 1991) Inflammatory complications After a basic fracture with rupture of the dura, fluid fistula can develop, most often in the nasal cavity, come. When the head is bent forward, slightly bloody fluid is discharged into the nasal cavity (Mumenthaler & Mattle, 1997). Liquor fistulas, which usually occur after fractures of the anterior cranial fossa or the temporal bone, usually lead to nasal liquorrhea or to CSF ​​drainage from the external auditory canal, but can also be identified radiologically by spontaneous pneumocephalus. (Delank, 1991, p. 192f) As an additional complication of such a fistula formation, ascending purulent meningitis, mostly recurrent and caused by pneumococci, can occur. However, this is only possible a few years after the trauma experienced. A brain abscess can develop as a result of a penetrating injury, but in principle by the same route (Delank, 1991). Since open brain wounds are always infected, the potential for inflammatory complications is particularly high in the early phase.They all require neurosurgical care. (Delank, & Gehlen, 2004, p. 284) 2.5. Late complications and long-term consequences After severe substance damage to the brain, permanent physical or psychological damage can remain. But not every damage to the brain substance must lead to a permanent, tangible functional disorder or result in permanent complaints (Poeck & Hacke, 1998). The following defect states occur frequently:

37 Tab. 1.

38 Post-traumatic late-stage epilepsy In the case of covered brain injury with substance damage, the development of traumatic epilepsy is common (Poeck & Hacke, 1998). Posttraumatic late epilepsy is when seizures occur with an interval of more than 3 months after the TBI. (Berlit., 2000, p. 326) The probability of developing epilepsy after traumatic substance damage to the brain is 3-4 times higher than in the general population (Poeck & Hacke, 1998). According to Berlit (1992), post-traumatic late epilepsy can be expected in up to 10% of all moderate and severe traumatic brain injuries. Remschmidt and Stutte (1980), on the other hand, assume a risk probability for this complication of 10-30%. The risk of developing post-traumatic epilepsy after trauma is significantly increased, especially in children who have had early seizures (Poeck & Hacke, 1998). According to Delank (1991), post-traumatic late-stage epilepsy occurs as a result of scarring on meninges and brain tissue after open brain injuries than after covered brain damage. Poeck and Hacke (1998) give the incidence of epilepsy as a late complication of a traumatic brain injury in closed brain injuries at around 5%. After an open brain injury, post-traumatic late-stage epilepsy can be expected in up to a third of cases (Delank, 1991). Poeck and Hacke (1998) also give a similar value with 35% and consequently call for a preventive prescription of anti-epileptic drugs. Post-traumatic late-stage epilepsy occurs in 50% of patients in the first year and in 70-80% in the first 2 years after the trauma (Poeck & Hacke, 1998). For the next 10 years Poeck and Hacke (1998) estimate 3-5% first-time epilepsy. According to Berlit (1992), every second post-traumatic late epilepsy manifests itself by the end of the first year and in 95% of cases the first attack occurs before the end of the second year after the traumatic event.

39 Chronic cognitive deficits A number of studies (e.g. Fleminger et al., 2003; Mehta et al., 1999; Plassman et al., 2000; Salmond et al., 2005) deal with the long-term effects of a brain injury on the cognitive system. Patients with traumatic brain injury show a neuropsychological profile that resembles a chronic cholinergic deficit. The patients' attention span, association learning, and reaction time were particularly affected (Salmond et al., 2005). The authors call for drug treatment of the cholinergic system in order to achieve a significant improvement in the subsequent sequelae of a craniocerebral trauma. Fleminger et al. (2003) report a dysfunction of the cholinergic system as a risk factor for Alzheimer's disease. Acethylcholine is seen to be of particular importance for the late sequelae of craniocerebral injuries. Plassman et al. (2000) were able to show that traumatic brain injury at an early age increases the risk of dementia and Alzheimer's disease. A particularly increased risk was found in moderate to severe cranial brain injuries (Plassman et al., 2000).

40 2.6. Diagnosis With the help of the Glascow Coma Scale, a disturbance of consciousness can be recorded (Berlit, 2000). This method makes it possible to quickly quantify states of impaired consciousness and to display their progress in a clear and comparable manner. Three different reactions of the patient (opening eyes, verbal and motor reactions) are checked and evaluated with the given number of points. The sum of the three scores obtained then gives a numerical value that can range from 3 to 15 and represents an indicator for the degree of brightness of the state of consciousness (Delank & Gehlen, 2004). In an awake, clinically and neurologically normal patient with a traumatic craniocerebral injury, an X-ray overview of the skull or a computed tomography must always be taken first. If the findings are not clear or if there are corresponding clinical symptoms, special images of the base of the skull, the occiput, the petrous bones and the orbit must be taken (Berlit, 2000). Immediate CT is indicated especially if the patient shows secondary clouding or deterioration of the neurological findings (epidural hematoma), or if there is a lateral brainstem syndrome in the admission situation, as well as in the presence of coagulation disorders or temporal skull fractures (Berlit, 2000). An EEG reveals a history of a fleeting disturbance of consciousness as an expression of slight brain damage (Berlit, 2000). In the case of commotio cerebri, the EEG only shows general or, rarely, focal changes in the very fresh stage, i.e. within the first hours after the trauma ( Poeck & Hacke, 1998). However, this does not allow any conclusions to be drawn about morphological changes in the brain tissue (Poeck & Hacke, 1998).

41 According to Poeck and Hacke (1998, p. 551), in the computed tomographic examination of a contusio cerebri with hemispherical contusion, hypodense, non-vascular-dependent lesions are typically found near the cortex or deep into the medullary bed, in which very differently sized, blood-isodense areas are interspersed also confluent to large hemorrhages. In the acute stage of the trauma, the contusion can only be recognized if several small bleeding foci are present at the same time. Without bleeding, small to medium-sized contusions can only be seen after hours on CT (Poeck & Hacke, 1998). Therefore, in the acute stage, CCT is the method of choice for radiological recording of contusion foci, but MR tomography usually offers better detection options (Delank & Gehlen, 2004). According to Poeck and Hacke (1998), the EEG is slowed down in the acute stage and can show a focal finding. However, the basic rhythm can accelerate again within a few weeks and the focal findings recede. The EEG changes usually normalize within 6 months (Poeck & Hacke, 1998).

42 2.7. Therapy Poeck and Hacke (1998) criticize the unnecessary and mostly irrelevant practice of prescribing bed rest for 2-3 weeks in the therapy of concussions. According to Delank and Gehlen (2004), stabilization of the orthostatic circulatory regulation after a concussion usually only requires bed rest for a few days. Subsequent circulatory training can often achieve complete freedom from symptoms and work ability after just a few weeks (Delank & Gehlen, 2004). Careful primary care and intensive treatment of all severe brain injuries should begin in the acute phase as early as possible at the scene of the accident. Delank and Gehlen (2004, p. 279) call for the following measures: keeping the airways free (risk of aspiration pneumonia!); intubation is generally indicated in the case of persistent unconsciousness, breathing disorders and extensive facial skull injuries; Rapid stabilization of circulatory conditions (if necessary with plasma expander); Stabilization of vegetative regulations; Edema prophylaxis (administration of 100 mg dexamethasone iv) Continuous monitoring of the intracranial pressure in unconscious patients after a traumatic brain injury (Berlit, 2000) The therapy of epidural hematoma, which is always an acutely life-threatening complication of recent traumatic brain injuries, requires surgical removal of the hematoma as quickly as possible (Delank & Gehlen, 2004). The time of the operation has a great influence on the mortality of the epidural hematoma, which is why no time should be lost in making a diagnosis (Berlit, 2000). Intracerebral hematomas are only treated surgically in the event of secondary deterioration or if the increase in intracranial pressure cannot be influenced in any other way (Berlit, 2000). The treatment of subdural hematomas consists of surgical pressure relief or hematoma removal (Delank & Gehlen, 2004).

43 3. Stroke 3.1. Definition A stroke describes a clinical picture that occurs acutely to subacute and is associated with focal neurological symptoms that depend on the affected areas of the brain. (Diener & Forsting, 2002, p. 2). It is an acute and threatening event and requires emergency care as quickly as possible. Rothenberg (1995) describes a stroke as the sudden failure of certain brain functions as a result of an acute interruption of the blood supply to a brain area (p. 709). The term stroke is not used consistently. Previously used but no longer current synonyms for stroke include apoplexy, cerebral or apoplectic insult, cerebral infarction and stroke (Diener & Forsting, 2002) Epidemiology Stroke is a widespread disease and is the third most common disease in industrialized nations, accounting for 15% of all deaths Cause of death after heart disease and malignant tumors (Bundesarbeitsgemeinschaft für Rehabilitation, 1994; Diener & Forsting, 2002). In Germany, the number of new cases of stroke each year is between and (Bundesarbeitsgemeinschaft für Rehabilitation, 1994). At least humans suffer from the consequences of a stroke (Diener & Forsting, 2002). However, there has been a general decline in new cases for some years. This is attributed in particular to improved treatment options and greater health awareness, especially with regard to possible risk factors for stroke (Diener & Forsting, 2002). Furthermore, the number of new annual strokes shows a clear differentiation in terms of age. They increase with age.

44,300 of people between the ages of 55 and 64 suffer a new stroke every year, while among the 65 to 74 year olds there are already 800 of people (Diener & Forsting, 2002). While Diener and Forsting (2002) assume that 20% of those who survive a stroke will need care, the Federal Association for Rehabilitation (1994) estimates that over 40% of patients discharged from hospital become dependent on the care of others. Only about a third of stroke survivors can continue a life without restrictions or outside help (Poeck & Hacke, 1998). Lethality, a measure of the fatality of a disease, is around 20% in the first three months after a stroke (Diener & Forsting, 2002).

45 3.3. Neurophysiological basis of cerebral blood flow. Brain metabolism The brain metabolism almost exclusively requires glucose as an energy supplier. The daily requirement for glucose is 115g (Mumenthaler & Mattle, 1997). Since the brain does not build up any nutrient reserves, it depends on a constant supply from the blood. The cerebral blood flow is the basis for the supply of oxygen and nutrients to the nerve cells of the brain. The human brain uses about 20% of the body's total oxygen requirement (Poeck & Hacke, 1998). Although the brain makes up only about 2% of the total body weight, about 14% (about 1.2 liters) of the cardiac output flow through the brain and its surrounding tissue in healthy adults. This corresponds to around 700 ml of blood per minute. In relation to 100 g of brain tissue, the average size of the blood flow is 55 ml / min (Soyka, 1991). Clinical symptoms occur when the blood supply falls below 22 ml / 100 g brain tissue / minute (Mumenthaler & Mattle, 1997). If the blood flow is reduced below the functional threshold, the evoked potentials can fail and the EEG flattens out (Mumenthaler & Mattle, 1997). When blood flow to the tissues returns to normal, electrical and clinical functions may return to normal. If, on the other hand, the perfusion falls below values ​​of 8-10 ml / 100 g brain tissue / minute, irreversible damage ensues (Mumenthaler & Mattle, 1997). This focal or global reduced blood flow ultimately leads to an insufficient supply of oxygen and glucose and the neurons of the affected environment can no longer carry out their activity (Mumenthaler & Mattle, 1997). If the infarct threshold is not reached, the cells can no longer survive and die (Poeck & Hacke, 1998).

46 Regulatory Mechanisms The security of the cerebral blood flow is guaranteed by multiple protective mechanisms. These mechanisms include physiological perfusion well above the infarct threshold and collateral circulation such as the Circulusus arteriosus Willisii. Autoregulation is another protective mechanism. The brain minute volume depends primarily on the factors blood pressure and vascular resistance. The cerebral perfusion pressure is influenced by the cardiac output, the mean arterial pressure, the peripheral vascular resistance and the intracranial pressure. The cerebral blood flow (CBF) can also be regulated by controlling the vascular resistance. It corresponds to the quotient of perfusion pressure and vascular resistance (Poeck & Hacke, 1998). In order to keep the cerebral blood flow constant, the vascular resistance must increase at the same time in the case of an increase in blood pressure, and the vascular resistance must be decreased in the case of a decrease in pressure. If the systemic blood pressure rises, the cerebral vessels contract; if the pressure drops, they expand, thereby keeping the cerebral blood flow constant. This mechanism is called the Bayliss effect (Soyka, 1991, p. 242). As a result of the autoregulation, the cerebral blood flow remains largely independent of the arterial blood pressure in a broad physiological range (Poeck & Hacke, 1998). The Bayliss effect only works with blood pressure values ​​between 70 mm Hg and 200 mm Hg systolic and with an oxygen saturation of the arterial blood over 60% (Poeck & Hacke, 1998). These regulatory mechanisms ensure an adequate supply of oxygen and nutrients to the brain within wide limits (Mumenthaler & Mattle, 1997). Normally, the cerebral minute volume remains largely stable. With increasing age, however, the minute volume generally decreases somewhat. Under pathological conditions there can even be very significant changes. The cerebral disorders only become clinically manifest when the blood flow is reduced to about half (Soyka, 1991).

47 Pathophysiology of Stroke Despite a narrowed vascular site, the brain can be adequately supplied with normal blood pressure and good cardiac output, as it is largely secured by a considerable margin of safety. By increasing the use of the available oxygen, the brain can compensate for a decrease in blood flow to around 50% of the norm. If the oxygen supply falls below 50% of the norm, there is initially a reversible functional failure. Only a further reduction to 15-20% leads to irreversible damage and cell death. However, with regard to such a development, the time factor also plays a decisive role (Mumenthaler & Mattle, 1997). After the onset of a clinically relevant oxygen shortage in the brain, there is initially a time window in which recovery is possible as long as the oxygen supply returns to normal within this range. The disturbed functions then return after a recovery latency (Soyka, 1991). Only when the oxygen shortage persists beyond this resuscitation period does irreversible tissue damage result (Soyka, 1991). In the event of a complete interruption of the oxygen supply, i.e. anoxia, the functional disorders of the brain set in very quickly. After 2-8 seconds, there is no longer any free oxygen in the affected areas, as the brain has almost no oxygen and glucose stores. EEG changes occur. After 12 seconds the patient loses consciousness, after seconds the bioelectrical activity of the cortex disappears and no electrical activity can be detected in the EEG. The resuscitation time is only a maximum of 3-4 minutes under these extreme conditions. After this time, histologically detectable, irreversible necroses of the brain tissue are found (Mumenthaler & Mattle, 1997). If the anoxia persists, irreversible tissue necrosis occurs (Soyka, 1991).

48 3.4. Classification Basically, the classification of a stroke in the literature is based on two different ways of looking at the occurrence of the insult. On the one hand, the classification can be based on a dynamic and prognostic approach, on the other hand, according to pathogenetic aspects. Nowadays, classification based on pathogenetic criteria is preferred. A distinction is made between the following types of stroke (e.g. Diener & Forsting, 2002; Krämer, 1993): Micorangiopathies (lacunar infarcts) Macroangiopathies (hemodynamically induced infarcts and territorial infarcts) According to symptoms that occur during a stroke, the following types of stroke can be distinguished (e.g. Diener & Forsting, 2002; Krämer, 1993): asymptomatic stage transistor ischemic attacks (TIA) reversible ischemic neurological deficits (RIND) progressive insults complete insults

49 Classification according to pathogenetic aspects Pathogenesis describes the development of a disease or the course of a pathological process leading to a disease. It is based on neuroimaginative methods such as computed tomography or magnetic resonance tomography to record the occurrence of the insult. This classification is more preferred today. One speaks of cerebral microangiopathy when the small penetrating cerebral arteries are affected, which arise almost at right angles from the large arteries running in the subarachnoid space. (Diener & Forsting, 2002, p. 18). When these cerebral arteries are blocked, so-called lacunar infarcts occur. Lacunar infarcts are mostly multiple, subcortical lesions in the supply area of ​​small and tiny intracerebral arteries in the basal ganglia, medullary bed and brain stem (Berlit, 1992). According to Berlit (1992), the cause of lacunar infarcts is the interplay of arteriosclerosis, hypertension and thrombosis. The term macroangiopathy includes circulatory disorders of the large extra- and intracranial supplying vessels of the carotid area and the vertebrobasilar system, but also embolic, vasulitic and other diseases-related occlusions of large vessels (Diener & Forsting, 2002). In macroangiopathies, different subspecies are differentiated: Territorial infarcts most frequently affect the supply area of ​​the middle cerebral artery (Krämer, 1993) and usually arise from embolic or local thrombotic closure of terminal branches, branch groups or main trunks of larger cerebral arteries (Mumenthaler & Mattle, 1997). Terminal infarcts occur in areas where the long medullary arteries spread, which do not have collateral circulation (Poeck & Hacke, 1998). Border zone infarcts affect the border between the supply areas of two or more cerebral arteries (Diener & Forsting, 2002; Berlit, 1992).

50 Classification according to the course of time As can be seen in Fig. 2, the individual forms of stroke differ in the duration of the symptoms and the severity of the neurological deficit. Combining these variables results in five different types of stroke: asymptomatic strokes, transient ischemic attacks, reversible ischemic neurological deficits, progressive infarcts, and complete infarctions (Diener & Forsting, 2002). Fig. 2. Classification of the infarct type based on the course of the symptoms (from Diener & Forsting, 2002, p. 5)

51