What is the midbrain activation technique

Ruhr University Bochum Prof. Dr. med. Sylvia V. Kotterba Place of employment: Ammerland Clinic Department of Neurological Clinic


1 Ruhr University Bochum Prof. Dr. med. Sylvia V. Kotterba Place of employment: Ammerland Clinic Dept. Neurological Clinic Risk of accidents after acute cerebral circulatory disorders - Importance of driving simulator examinations Inaugural dissertation for obtaining the doctoral degree in medicine from a high medical faculty at the Ruhr University Bochum, presented by Stefan Brylak from Gelsenkirchen 2008

2 Dean: Prof. Dr.med. G.Muhr Speaker: Prof. Dr. med. S. Kotterba Coordinator: PD Dr. med. B. Henning Oral Examination Day:

3 I dedicate this work to my parents, Ingrid and Franz Brylak.

4 1 Table of contents Table of contents ... 1 List of abbreviations ... 5 List of tables ... 6 List of figures Introduction Cerebral circulatory disorders Definition of vascular supply to the brain Pathophysiological principles Risk factors for ischemic insults Functional disorders according to vascular assignment Time course Infarct morphology Diagnostics Medical history Clinical examination findings Technical laboratory and device examinations Therapy Stroke- Unit treatment in the acute phase ... 25

5 Treatment in the subacute phase Prophylaxis Neuropsychological tests Driving simulator examinations Driving and stroke Legal basis Questions Methodology Patients and test persons Questionnaire on driving behavior Questionnaire for recording daytime sleepiness Neuropsychological profile Reaction test Vigilance test Driving simulation in the CAR driving simulator The simulator Course of the journey The evaluation Statistical processing Results First examination phase Test) Questionnaire on driving behavior ... 51

6 Questionnaire for recording daytime sleepiness (ESS) Simple attention in the reaction test Vigilance test Driving simulation Second phase of investigation (retest) Questionnaire on driving behavior Questionnaire for recording daytime sleepiness (ESS) Simple attention in the reaction test Vigilance test Driving simulation Relationships between accident frequency / concentration errors, neuropsychological test results and ESS Discussion Causes increased accident risk in patients with cerebral circulatory disorders Driving experience and fitness to drive in patients with cerebrovascular deficits Questionnaire on daytime sleepiness (ESS) Neuropsychological profile Simple attention Vigilance test Driving simulator examination Dangered distance / speed Reaction deer

7 Frequency and type of accidents Accident rate over time Frequency and type of concentration errors Concentration errors over time Driving errors in the driving simulator according to weather conditions Summary evaluation of the driving simulator test Use and value of driving simulator tests Follow-up tests in patients with cerebrovascular deficit Clarification of the questions Summary of references

8 5 List of Abbreviations A. Arteria Aa. Arteriae CBDI Cognitive Behavioral Drivers Inventory CBF Cerebral Blood Flow CCT Cranial Computed Tomography EEG Electroencephalogram EKG Electrocardiogram ESS Epworth Sleepiness Scale MEZ Mean decision time MMZ Mean motor time MRI Magnetic resonance imaging MRZ Mean reaction time PRIND Ischemic neurological vein deficiency

9 6 List of tables Table 1: Inclusion and exclusion criteria of the test persons Table 2: Driving conditions in the simulated driving situation Table 3: Type of accidents Table 4: Type of concentration errors Table 5: Results of the questionnaire on driving behavior (test) Table 6: Mean values, standard deviations and case numbers for the ESS Table 7: Mean values, standard deviation and number of cases in the reaction test Table 8: Mean values, standard deviations and number of cases in the vigilance measurement ..

10 Table 18: Mean values, standard deviations and case numbers of all subjects who participated in both phases of the investigation: Driving simulator (retest) Table 19: Average values, standard deviations and number of cases of all subjects who took part in both phases of the investigation: Driving simulator (test)

11 8 List of Figures Figure 1: C.A.R.

1284 Figure 29: Significant differences in concentration errors during the day (media left, media right, vertebrobasilar) in the initial test Figure 30: Driving experience of the patient groups (km / year) in the last 3 years (retest) Figure 31: Simple attention in milliseconds ( Retest) Figure 32: Percentage ranks with pathological performance compared to athletes (retest) Figure 33: Percentage ranks with pathological leads compared to organic chemists (retest)



15 12 1 Introduction In patients with acute cerebral ischemia, motor and sensory deficits as well as cognitive dysfunctions (impairment of recognition) can be detected to varying degrees. These can have a negative impact on everyday life. In the context of rehabilitation after acute cerebral ischemia, an assessment of the occupational ability and fitness to drive is necessary. In addition to imaging procedures and clinical experience, the attending physician needs various measuring instruments in order to be able to objectively assess the extent of the illness-related restrictions. The literature shows that clinical assessment is insufficient for this. However, there is still controversial discussion about which measuring instruments are suitable. A distinction must be made between neuropsychological tests, questionnaires, driving aptitude tests in road traffic and on secured terrain, as well as driving simulator examinations. 1.1 Cerebral circulatory disorders Definition The ischemic stroke describes an acute focal neurological deficit due to a circumscribed circulatory disorder of the brain. The term stroke is also used as a synonym. Cerebral infarction describes the morphological correlate of cerebral parenchymnecrosis, which today can already be demonstrated intravitally by imaging methods [41, 47]. Most strokes (up to 85%) are ischemic. The rest is caused by intracerebral (approx. 10-12%) and subarachnoid (up to 8%) bleeding [80]. You can

16 13 manifest themselves in the form of transient ischemic attacks, so-called TIAs, reversible ischemic deficits or as permanent neurological deficits. 2/3 of all ischemias affect the carotid or medial flow area and 1/3 affect the vertebrobasilar area. The main causes are extracranial macrooangiopathy (arteriosclerosis, vascular stenosis) and cardiogenic embolism. They typically lead to territorial infarcts. Lacunar infarcts, on the other hand, are caused by microangiopathies, which arise in the context of systemic diseases through changes in the smaller arterial vessels [90]. Strokes in younger patients are often based on traumatic vessel dissection [85]. With 9.3%, cerebral insults are the third most common cause of death in Germany after heart attacks and tumors [41, 105]. They most frequently lead to permanent disability and comprise the most expensive disease group in the western industrialized countries [80, 85, 123]. Half of the follow-up costs result from the loss of productivity of those affected [5]. Every year between and strokes occur in Germany [120]. The annual incidence is on average at / inhabitant [47] and increases in 65-74 year olds to / inhabitant [80]. In contrast, the incidence of short-term circulatory disorders is only 50 per inhabitant [47]. The prevalence of a stroke is approx. Per inhabitant [47, 120]. Epidemologically, there are higher case numbers among Japanese, Finns and Scots compared to Central Europeans or white North Americans [80]. Furthermore, men are affected approx. 30% more often than women [41]. About 15-20% of patients die within the first 4 weeks. Only about a third of the survivors recovered without permanent restrictions. Another third can carry out simple activities independently, but a professional activity is no longer feasible. The last third of the surviving patients remain in need of permanent care.

17 Vascular supply to the brain The arterial blood supply to the brain is provided by the two Aa. carotides internae and Aa. vertebral. Collateral circuits between the vertebrobasilar and carotid flow areas serve as additional security for the arterial brain supply. The Circulus arteriosus Willisi, which runs over the Aa. communicantes anteriores and posteriores connects the large arteries supplying the brain at the base of the brain. The venous outflow is made possible by the drainage of blood from the cortical cerebral veins into the dural sinus (sinus sagittalis superior and inferior). Via the sinus transversus, sigmoideus, rectus and cavernosus, the blood finally reaches the two veins. Pathophysiological principles Autoregulation Autoregulation enables an adequate oxygen supply to the brain with constant cerebral blood flow (CBF) when the perfusion pressures fluctuate [14]. However, this autoregulation mechanism only works within certain blood pressure limits (mean pressure threshold between 70 mmhg and 160 mmhg). Autoregulation ceases to exist beyond these threshold values ​​for arterial blood pressure. In hypertensive patients, this mean pressure range is shifted considerably upwards (between mmHg). For this reason, patients with chronic arterial hypertension with regard to cerebral blood flow tolerate a rapid decrease in blood pressure far more poorly than the normotensive person [44].

18 Ischemic brain edema After the onset of ischemia in the infarct area, brain edema develops. The energy-related failure of the sodium / potassium pump causes the cells to swell and form cytotoxic brain edema. After the blood-brain barrier has broken down, osmotically effective plasma components flow into the brain tissue. This results in extracellular vasogenic brain edema with an increase in intracranial pressure [44]. This can lead to the top or bottom pinching. Furthermore, the perfusion of the penumbra is reduced, which can ultimately enlarge the infarct area. Ischemia thresholds and penumbra When the cerebral blood flow is reduced, functional metabolism is initially disturbed and then structural metabolism is further down the line [14]. Too long falling below the functional threshold leads to irreversible damage for individual neurons, e.g. for the neurons of the hippocampus [80]. If the infarction threshold is not reached, irreversible structural damage occurs. The area between the functional and infarction threshold is called the penumbra. It surrounds the irreversibly damaged part of the brain and is initially only impaired in the functional metabolism [45,80]. Their fate depends on whether or not recirculation can take place [14]. Stenoses and vascular occlusions The most common cause of stenoses and vascular occlusions is arteriosclerosis [14], which mainly arises from vessel bends and arterial branches. It then leads to intravascular wall thickening (plaques) and thrombus formation with partial or complete vascular occlusions. The changed wall structure can also cause aneurysms [80]. 20% of all vascular occlusions result from embolisms of cardiogenic or arteriogenic origin. An arterial dissection (especially in younger people) results from bleeding into the vascular wall between the intima and media. As the cause

19 Trauma (whiplash injuries, chiropractic manipulations) or congenital wall changes (Ehlers-Danlos syndrome) discussed risk factors for ischemic insults Chronic arterial hypertension is the most important risk factor for cerebrovascular disease, as it leads to premature arteriosclerosis / arteriosclerosis due to changes in the vascular wall. This creates the possibility of a cerebral infarction and hypertensive mass bleeding [14, 40, 80]. Furthermore, cardiogenic pre-existing conditions such as Vitien, endomyocarditis, atrial fibrillation or heart attacks as a source of embolism also lead to brain insults. Increased blood viscosity such as polyglobulia or coagulopathy can also cause cerebral ischemia due to the possible formation of thrombus [14]. Other risk factors are metabolic diseases such as diabetes mellitus, alcohol and cigarette consumption, and hyperlipidemia [40]. Vascular inflammatory diseases are rare causes of cerebral circulatory disorders. They occur in bacterial meningitis, vascular syphilis, neuroborreliosis or lupus erythematosus visceralis [14] Functional disorders according to vascular assignment Disorders in the medial flow area Internal carotid artery The internal carotid artery is most affected by stenoses and vascular occlusions of all intracerebral arteries [90]. The main cause is atherosclerosis of the carotid bifurcation and the carotid siphon. The internal carotid artery syndrome is often preceded by transient ischemic attacks. The deficits mainly include sensorimotor dysfunctions in the medial flow area with brachiofacially accentuated hemiparesis of the opposite side and transient speech disorders. The oculocerebral syndrome with complete carotid occlusion is very rare due to the good collateralization [80].

20 17 A. ophthalmica Circulation disorders of the A. ophthalmica lead to monocular visual disturbances and amaurosis [80]. Amaurosis fugax (retinal TIA) is a short-term, recurrent visual loss in one eye that usually spreads vertically from top to bottom. [85]. A. cerebri media Among all intracranial cerebral artery occlusions, those of the A. cerebri media are the most common [14, 85]. The main causes are cardiogenic embolisms or atheromatous plaques on the carotid fork [14]. The main symptoms of territorial infarction are contralateral facio-brachio-crural hemiparesis, hemisensitive deficits and homonymous visual field defects with paresis to the opposite side. In the case of lesions on the language-dominant side, there are additional aphasia and apraxia as well as spatial processing disorders in the case of right-hemispheric lesions [80]. In the acute stage of the hemisndrome, muscle tone is usually reduced, resulting in flexion spasticity in the affected arm and extension spasticity with circumduction in the leg (Wernicke-Mann gait) [14, 80]. In subcortical ischemia, disruption of the basal ganglia leads to a functional inhibition of the neighboring cortical parts. An early spastic hemiparesis results, which is accompanied by sensory disturbances. In addition, the central visual pathway can be affected and lead to hemianopia [85]. Distal media occlusions lead to superficial cortical infarction with weaker sensorimotor hemisphere symptoms or motor aphasia [14]. When the upper anterior main branch of the A. cerebri media is closed, especially the frontal lobe (with motor disorders) is infarcted. When the lower rear main branch is closed, however, sensitive hemisndromes with additional homonymous visual field defects or spatial processing disorders such as neglect occur [80]. Occlusions of the lenticostric arteries lead to lacunar infarcts of the

21 Basal ganglia and the internal capsule. As a result, they can also cause extrapyramidal motor disorders [80]. 18 A. choroidea anterior In the rare inflow disorders of the A. choroidea anterior, the basal ganglia, the visual radiation and the posterior leg of the internal capsule are partially affected. This can result in homonymous hemianopia, contralateral hemiparesis, and extrapyramidal disorders [85]. Anterior cerebral artery Isolated stenoses and occlusions of the anterior cerebral artery are very rare overall (<5%). Atherosclerotic processes are again the cause [14, 85]. Vascular spasms such as subarachnoid hemorrhages or the iatrogenic cliffs of aneurysms can trigger a bilateral anterior infarction: This leads to spastic paraparesis of the legs with bladder emptying disorders and akinetic mutism [14, 85] Disorders in the vertebrobasilar flow area The infarcts in the supply area of ​​the Aa. vertebrales or the basilar artery are also preceded by several transitory ischemic attacks with temporary symptoms such as vertigo, double vision or visual field and hearing disorders. So-called drop attacks with lightning-like falls and short-term impairment of consciousness (lightning syncope) often occur [14]. A. vertebralis The primary cause of the obstruction of the flow path in the A. vertebralis is again the arteriosclerosis especially at the branch from the A. subclavia. In addition, however, there are also degenerative changes in the cervical spine with vascular compression as well as system disorders and abnormal vascular kinks in the vertebral arteries [14]. The clinical result is a brainstem or cerebellar infarction. However, the unilateral occlusion of the vertebral artery can often be tolerated without symptoms [85].

22 19 A. cerebelli inferior posterior It supplies about 2/3 of the ipsilateral cerebellum and, if occluded, leads to cerebellar hemisphere infarction. The typical cerebellar symptoms with ataxia, dysmetria, rotating spontaneous nystagmus and rebound phenomena are shown ipsilaterally [85]. Cerebellar infarctions usually occur in conjunction with lateral ponsin infarctions [14]. Extensive cerebellar infarctions can cause compression of the ventricular system or life-threatening brain stem dysfunction. Early symptoms are changes in the level of consciousness, hiccups, vomiting and / or double vision due to abdominal paralysis.Finally, there is a risk of entrapment of the medulla oblongata. The vascular supply of the dorsolateral part of the medulla oblongata arises in approx. 50% of the cases from the A. cerebelli inferior posterior or, on the other hand, directly from the A. vertebralis. The embolic or local thrombotic closure of these small vessels leads to Wallenberg syndrome. Symptomatic symptoms are a contralateral dissociated sensitivity disorder for temperature and pain, ipsilateral Horners syndrome and soft palate paresis, as well as ipsilateral hemiataxia [85]. Basilar artery Occlusions of the basilar artery and its branches lead to a variety of symptoms, depending on the respective brain stem area (e.g. pons, midbrain and cerebellum). This can result in ipsilateral cranial nerve paralysis and contralateral symptoms of the long ducts. The motor function of the eye is often impaired in marked brainstem infarcts with paresis of the abdomen, unilateral or bilateral internuclear ophthalmoplegia or oculomotor paresis. If the cerebellum is involved, there is often an ocular tilt reaction with the head tilted towards the damaged side and skew deviation of the eyes [85]. Acute closure in the context of a basilar thrombosis can be life-threatening and infarcts the medulla oblongata, pons and cerebellum [80]. If the medulla oblongata is infarcted, the picture of Wallenberg's syndrome appears. In contrast, infarction of the pons within the framework of the middle basilar artery occlusion forms a complete tetraplegia with pseudobulbar paralysis. This can be from cardiac

23 20 arrhythmias are accompanied [14]. The full image corresponds to the locked-in syndrome, in which the patient is only able to communicate through vertical eye movements. With embolic closure of the basilar tip, in addition to premature unconsciousness, there is finally oculomotor paresis with cortical blindness. A. cerebelli inferior anterior The symptoms of occlusion of the A. cerebelli inferior anterior are uncharacteristic. Pointing ataxia, horizontal nystagmus to the opposite side, ipsilateral Horner syndrome and a contralateral dissociated sensory disorder are described [85]. A. cerebelli superior The occlusion of the upper cerebellar arteries leads to cerebellar worm infarction with gait disorders and, more rarely, ataxia [85]. A. cerebri posterior From the proximal part of the A. cerebri posterior arise the A. choroidea posterior, Aa. thalamoperforantes anteriores and posteriores [85]. About the Aa. communicantes posteriores is connected to the carotid flow area. Occlusion of the left artery results in alexia and agraphia, a transcortical sensory aphasia. Color and finger agnosia as well as constructive apraxia are also described. In the case of right-sided circulation disturbances, however, there are again disturbances of the sense of space such as visual neglect. If both sides of the posterior cerebral artery are affected, vertical hemianopia, cortical blindness (Anton syndrome), and severe memory impairment appear [80]. Thalamic infarction The thalamus is supplied by vessels from the posterior communicating artery and the posterior cerebral artery. Infarction results in a contralateral sensitive hemisndrome, usually associated with mild hemiparesis and hemiataxia. At

24 left-sided infarcts can be combined with aphasia, in the case of right-sided with spatial impairment [80] Temporal course Another classification of ischemic insults is based on the temporal course of the insult. Transient ischemic attack (TIA) The TIA describes a mild, neurological dysfunction which is completely reversible after 24 hours at the latest. The individual attacks usually last less than 30 minutes [41]. The diagnosis is made more difficult because the TIA can usually only be discussed retrospectively based on anamnestic and objective findings are mostly missing. The symptoms are mainly contralateral sensorimotor hemisndromes, as well as the above-mentioned amaurosis fugax [14]. The cause of a TIA can often only be determined imprecisely. Short-term cardiac arrhythmias with flooding of embolic material are mainly found [80]. TIAs can recur for a short time and are also often the harbingers of a massive cerebral infarction. Today, not least due to improved imaging, demarcated ischemia zones can often be found in CCT or diffusion-weighted MRI [12, 47]. (P) BOVINE If the clinical symptoms of an ischemic insult subside even after 24 hours, it is referred to as a prolonged reversible ischemic neurological deficit (PRIND) [14, 80, 85]. Progressive insult In a progressive insult, the symptoms continue to increase for hours. There are courses with fluctuating symptoms, with remissions (crescendo-TIA) and with continuous progressive deterioration of the neurological deficits [85].

25 22 Completed infarct The characteristics of a completed infarct are neurological deficits that have stabilized and persist over time. In up to 50% of complete infarcts with extensive functional disorders, TIAs or reversible insults with a slight deficit were preceded in the same river area. Sometimes the complete infarct with severe failures comes at the end of the progressive insult [80, 85]. Infarct morphology Morphological findings from CCT and MRI provide information about the size of the occluded vessel as the cause of the ischemic infarct [85, 90]. Territorial infarcts Territorial infarcts result from embolic or local thrombotic occlusion of arteries on the surface of the brain. They are often wedge-shaped and limited to the supply area of ​​the affected artery [85, 90]. Radiologically, hypodense areas can be found in the supply area of ​​the large cerebral arteries (pia arteries) or their branches [14]. End current infarcts These are small hemodynamically caused infarcts in the distal area of ​​spread of the penetrating arteries (last meadow). Radiologically, hypodense subcortical areas of different sizes can be seen in the terminal supply area of ​​the long, penetrating medullary arteries [80, 85]. Border zone infarcts These are infarcts in the supply areas of several large vessels. They are almost always based on high-grade, haemodynamically effective stenoses of the extra- or intracranial vessels. In addition to the arteriosclerotic etiology, dissections are also possible [90]. Radiologically, there are hypodense areas on the watershed of two vascular territories [14].

26 Diagnosis Anamnesis Since the first few hours of a stroke are decisive for thrombolysis, the anamnesis of the patient is very important, especially with regard to the symptoms. In addition to the personal history, the external and family history is also indicative psychological findings are adequately examined and recorded [41]. General physical examination findings The general physical examination findings for checking organ function are also part of the diagnostic assessment. In particular, signs of cardiac insufficiency, arrhythmias, valve defects, signs of desiccosis and pulmonary ventilation disorders should be observed [41] Technical laboratory and device examinations The first standard examinations (e.g. pulse oximetry, ECG monitoring, blood sugar and temperature determination) should be carried out immediately after the clinical examination. . In addition, laboratory diagnostics are carried out to assess the risk of arteriosclerosis and determine organ dysfunctions. The additional CSF examination is used to diagnose inflammatory changes (meningitis, encephalitis) or disorders of the blood-brain barrier [80]. This is followed by a rapid radiological examination with the help of CCT or MRT angiography. This is where the vascular occlusions and abnormalities

27 24 localized accordingly. By making diffusion- and perfusion-weighted MRI images, the full extent of the infarct area and also the surrounding penumbra (mismatch between the ischemic lesion in the diffusion and the less perfused image) becomes clear at an early stage [17, 45]. As a further method, digital subtraction angiography (DSA) can be used to better assess the extent and morphology of a stenosis. A DSA is also performed before carrot surgery. Due to the rapid development of Doppler and duplex sonography, this vascular examination as a non-invasive method can hardly be replaced nowadays. When the patient is admitted, extracranial and transcranial examinations of the vessels can already reveal high-grade stenoses, occlusions or dissections, e.g. internal carotid artery or vertebral artery can be recognized. Due to the frequent cardiac embolisms, special cardiological diagnostics are necessary, especially in younger stroke patients. In addition to the short-term ECG and blood pressure measurement, a long-term ECG and blood pressure measurement should also be carried out to rule out arrhythmias or hypertensive derailments. The additional implementation of a transthoracic and transesophageal echocardiography to assess the heart valves and cavities and to exclude cardiogenic sources of embolism is essential [80]. Targeted neuropsychological tests and the Aachen aphasia test are suitable for the qualitative and quantitative recording of language disorders and cognitive performance losses, even during the course. These procedures are used particularly in rehabilitation [85].

28 Stroke unit therapy An acute stroke is a vital emergency and should therefore be treated either in a stroke unit or in an intensive care unit [14, 17, 80, 85, 106]. According to Wiborg et al. In rural areas, telemetry can improve the care of stroke patients [121]. Furthermore, according to Diener et al. a significantly better outcome after treatment on a stroke unit compared to the normal ward [17]. However, this could neither shorten the hospital stay nor lower the overall costs with increased diagnostic and therapeutic effort [121] Treatment in the acute phase The goals of basic therapy in the stroke unit are to preserve the structural penal tissue and to avoid and treat complications [17]. In the acute phase, in addition to basic monitoring (O2 saturation, ECG, blood pressure and temperature measurement), there is a close-knit fluid balance and laboratory control (glucose level). Fever, hyperglycaemia, arrhythmias and hypertension can significantly worsen the patient's outcome [14]. Space-consuming brain edema, epileptic seizures, aspiration and stress ulcerations are described as complications. Thrombosis, pneumonia and decubitus prophylaxis (low dose heparinization, breathing exercises, alternating pressure mattresses) should be used. If a cardiac source of embolism is suspected, therapeutic heparinization is followed by marcoumarization [41]. For recanalization of closed vessels, thrombolysis should be carried out in the 3-hour time window [45]. A distinction is made between systemic thrombolysis with a plasminogen activator (recombinant tissue plasminogen activator) and local lysis with urokinase [85].

29 Treatment in the subacute phase The subacute phase begins after the first day. On the one hand, further drug treatment of cardiac disorders and blood pressure control as well as adequate platelet aggregation inhibition or anticoagulation are aimed for [14, 41]. In addition, there is consistent early abilitation with physiotherapy and occupational therapy. The effectiveness of motor rehabilitation in relation to a better treatment outcome has now been reliably proven [17]. The development of spasticity can be prevented through special positioning and activation techniques. Training in handling personal aids (e.g. glasses, hearing aids, dentures) is also included [85]. Early speech therapy is also recommended, even if the effectiveness is worse than for motor rehabilitation [15, 17, 85]. After the end of acute therapy, early care should be sought in a rehabilitation facility. Physiotherapy, occupational therapy and speech therapy measures can be intensified. The question of fitness to drive is also often raised here and should be able to be answered by the multidisciplinary team [81]. 1.4 Prophylaxis The prophylaxis of ischemic insult mainly comprises the elimination and treatment of risk factors as well as surgical and medicinal measures. In addition to abstinence from nicotine and alcohol, the aim is to eliminate obesity and hyperlipidemia through conscious nutrition and physical activity. Furthermore, the therapy of hypertension or cardiac diseases such as e.g. Pay attention to atrial fibrillation [14, 15]. Primary prevention tries to avoid cerebral ischemia or transitory attacks (TIAs) through close risk management. The

30 27 Secondary prevention serves to avoid recurring cerebral ischemia after the first event [17, 18, 47]. The recommendations regarding primary and secondary prophylaxis by the German Society for Neurology (DGN) and the German Stroke Society (DSG) are subject to constant changes based on the current study situation [17, 47]. 1.5 Neuropsychological tests A number of studies have dealt with the measurement of neuropsychological deficits in stroke patients. Disturbances of attention in the acute phase are leading. Attention is made up of a large number of specific sub-functions of the cognitive system. Treisman et al. describe attention as functions through which the stream of experience and thoughts are given an orderly structure in terms of content and time [110]. According to Zimmermann et al. provide a bridge to connect emotional and motivational processes with selective information intake and to structure them hierarchically [124]. However, the effectiveness of this function varies with the state of wakefulness and the performance of the cognitive system [124]. Attention was characterized by a three-component model by Posner and Boies and Posner and Rafal [86, 87]. In addition to divided attention, a distinction is made between selective attention and vigilance (sustained concentration). Divided attention describes the ability to process many different stimuli at the same time (e.g. driving a car). Selective attention, on the other hand, includes the possibility of filtering out the most important of many different stimuli and reacting to them accordingly. Finally, the ability to remain attentive over a longer period of time with relative stimulus monotony (driving at night, driving on the motorway) is referred to as vigilance [11, 119]. This complex process also describes the effort to counteract fatigue.

31 28 With the help of the variables speed, accuracy and constancy of an attentional performance, an attempt is made to measure individual abilities by means of appropriate reaction tests [92]. During the vigilance test, monotonous stimulus conditions should be created for at least 30 minutes and irregular reaction processes should be queried at the same time. Zimmermann et al. emphasized the complexity of the attention system, which extends over all brain areas of the cortical and subcortical systems and is therefore very vulnerable (e.g. in the event of a stroke) [124]. Various test methods (intelligence tests, paper-and-pencil tests, electronic equipment) have been developed to record neuropsychological deficits in patients suffering from a stroke. The Cognitive Behavioral Driver s Inventory (CBDI) was published by Engum, Lambert et al. developed [20, 21, 65]. It consists of 27 subtests, which are derived in particular from the visual aspects of driving. The tests are mainly carried out on computer-controlled devices, but also in writing as paper-and-pencil tests. Concentration, visual attention, reaction time and quick decision-making are recorded. The entire test phase takes up to 1.5 hours. The evaluation is carried out using a point system [18, 19, 20, 21, 22, 65]. However, this test procedure showed weaknesses in the assessment of driving behavior on the device and in the practical driving test [8]. In Lambert and Engum et al. In a comparison of the CBDI with the on-road assessment, driving differences were found, especially in older patients (better driving with the device) and in young drivers after traumatic brain damage (driving worse on the device) [65]. In the opinion of the developers, it is therefore still necessary to carry out a practical test drive. Another experimental set-up shows testing using the Dynavision Performance Assessment Battery (DPAB) by Klavora et al. [53, 54, 55, 56]. It is a construction with an LED light in the center, which is surrounded by different lamps like a ring. When these lamps light up, the test person reacts with them

32 29 Push of a button. At the same time, numbers are shown in the center, which must also be mentioned or noted. This also determines visual perception and attention in connection with motor reaction time [56]. Many stroke patients show weaknesses in terms of cognitive functions.In various neuropsychological studies, deficits were found particularly in information processing, in visual memory and in attention [91]. Differentiating cognitive impairment in stroke patients from vascular dementia is often difficult, since the patterns of neuropsychological deficits are often similar and only differ in intensity. Both Sachdev et al. as well as Kurz et al. therefore assume that the boundaries to incipient dementia are fluid [64, 91]. The literature frequently mentions that it is less physical disabilities than cognitive disorders that can lead to a deterioration in driving behavior [4, 102]. Thus, a large number of neuropsychiological tests deal with the measurement of driving ability after cerebral ischemia. Kumar et al. used various paper-and-pencil tests to record cognitive dysfunction when driving a car [63]. They were able to show that patients with special theoretical and practical driver training after cerebral ischemia performed better than patients without driver training after an insult. Sundet et al. used not only simple paper-and-pencil tests but also a whole battery of tests (perimeter, REAKT computer test and tachistoscope to determine neglect) to discriminate whether they were fit to drive in stroke patients and a control group [107]. The assessment of the ability to perceive, the spatial-visual attention and the cognitive processing speed came about. Symptoms such as hemianopia, spatial-visual neglect, aphasia and apraxia were also included in the assessment. There were significant differences between the group of stroke patients and the control group in terms of fitness to drive. The stroke patients were additionally based on the affected side again

33 30 differentiated. Despite different symptoms (e.g. neglect, aphasia), there were no differences in driving performance between the left and right hemisphere. At Tant et. al. hemianoptic patients were examined after exclusion of a neglect using neuropsychological tests and a driving test [109]. The following tests had a good validity with the driving test: Gray Scale Task Test, Trailmaking Test, Bells Test and Hidden Figures Test. In Schulte et al. however, patients with visual field defects were tested on a driving simulator [93]. There were no significant differences in driving performance between the control group and the patient. Brouwer et al. found out through neuropsychological tests that higher-order cognitive deficits have a particularly negative impact on the safety and fluency of driving [9]. Smith-Arena et al. discovered a good validity of the Mini-Mental-State-Examination and the Motricity Index Score regarding the fitness of stroke patients to drive [104]. 1.6 Driving simulator studies Some studies come to the conclusion that there is no alternative to driving a test in road traffic when assessing fitness to drive after brain damage [43]. However, it has been mentioned in several studies that practical tests of fitness to drive can be costly and dangerous [35, 66]. Neuropsychological tests alone, however, are only of limited informative value [35, 56, 61, 84]. Driving simulators were specially developed, which showed sufficient validity in direct comparison with practical driving activity [66]. George et al. used the DADT (divided attention driving test) simulator [31, 35]. It consists of a screen and a steering column with buttons. During a 30-minute test drive, the test person should try to keep a digital cross on the monitor in a target box while driving (tracking). In addition, numbers appear on the screen, after which the buttons provided must be pressed (visual search). Evaluation criteria are variability in road behavior, average response time and the number of correctly recognized digits.

34 31 Findley introduced driving simulator testing using Steer clear in 1989 [25]. The patient sits in front of a PC and drives a car on a two-lane motorway. During the 30-minute test drive, he has to avoid 787 obstacles by pressing a button. Finally, the total errors are determined [23, 24, 25, 26]. Another computer-aided, more complex driving simulator is the STISIM (3M Company of St. Paul, Minnesota, on the screen with authentic background noise different traffic situations are shown (differences in light conditions, weather conditions, other road users). The test person sits in a detailed driver's cab. Galski et al used the Doron L225 Driving System / Analyzer (manufactured by Doron Precision Systems, Inc., PO Box 400, Binghamton, New York 13902) in their investigations [33, 34, 37] undertakes a one-hour test drive. There are various realistic driving programs that show, for example, the normal traffic situation, the busy traffic situation or dangers due to the misconduct of other road users. A test leader observes the test subject specifically for distractibility, inattentiveness or mental slowdown. Lings et al used driving simulators ators with subtasks [71]. Visual impulses are given via a three-phase traffic light and directional arrows. This determines the subject's journey accordingly (red: brake, green accelerate, arrow to the left: steer to the left, arrow to the right: to steer to the right). Sound signals also create realistic driving situations (airflow, driving noises). The driving simulator can measure visual and motor reaction times and determine incorrect reactions. A major disadvantage, however, is that the test subject does not get a feel for the direction when maneuvering. Akinwuntan et al. used a driving simulator with everyday weather and traffic situations in their studies of stroke patients [1, 2]. Number of collisions, accidents with pedestrians, exceeding speed limits, traffic light errors