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If a stroke occurs, a variety of symptoms are characteristic. The symptoms can often occur in combination with each other.

• (Unilateral) paralysis and/or sensory disturbance
  • Sudden paralysis or sudden numbness, usually only on one side of the body (face, arm and/or leg).
• Visual disturbance
  • Sudden blindness, visual disturbances in one or both eyes to the left or right or double vision.
• Speech disorders
  • Sudden loss of the ability to speak; inability to form words and sentences or difficulty understanding what is being said.
• Rotational vertigo
  • Long-lasting spinning vertigo, unsteadiness when walking, usually paired with other symptoms mentioned. Isolated dizziness ("vertigo") is not considered a stroke symptom.
• Headache
  • Sudden, unusual, very severe headache.

The symptoms can vary greatly depending on which area of the brain is affected. For example, those affected may not even perceive their symptoms as such.

A stroke can be a life-threatening emergency. Every minute counts! When certain treatments are used, there is only a short window of time available. That's why every minute that the patient gets to the hospital earlier is precious.with the FAST symptom check you can quickly recognize whether a stroke is present.

1. Face: Ask the person to laugh or show their teeth. Is the mouth crooked or are the corners of the mouth hanging down on one side?
2. Arm: Ask the person to stretch both arms horizontally forwards, raise them and turn their thumbs upwards. Does one of the arms hang or fall down?
3. Speech: Ask the person to speak. Is the speech slurred or difficult to understand?
4. Time: If one or more of these signs occur, do not hesitate to call the emergency number 144.

If stroke patients are hospitalized within three hours of the onset of symptoms, they have the best chance of being able to leave the hospital without permanent disability.

The onset of symptoms of a stroke is classified as a health impairment requiring urgent treatment. Accordingly, the patient is usually admitted to the University Hospital Basel via the Emergency Center, where the symptoms are recorded and initial clarification and immediate treatment steps are taken, which is where care in the so-called "Stroke Unit" begins. The term "stroke unit" refers to a comprehensive treatment process that includes special inpatient facilities and various measures that are used to care for patients with an acute stroke:

1. Determination of visible symptoms
2. ECG to clarify cardiac arrhythmia, arrhythmia
3. Computed tomography without and with contrast medium to localize the circulatory disorder
4. Three-dimensional, digital imaging of the vascular columns to localize arteriosclerosis or vascular occlusion
5. Ultrasound examination for detailed analysis of the vessel walls
6. Magnetic resonance imaging
7. Ultrasound examination of the heart to clarify sources of embolism

Treatment varies from case to case. The comprehensive diagnosis allows the specialists to make an optimal decision regarding suitable treatment options. In the case of vasoconstriction, it is important to dissolve it as quickly as possible. This is done either by injecting enzymes that dissolve the clots or by surgery.

Our care concept: the fastest possible clarification and state-of-the-art treatment

Supportive therapies such as physiotherapy, speech therapy, occupational therapy and other options complement our range of services for patients. These measures can achieve very good results in the long term and further improve quality of life. Relatives can also benefit from these services.

Social Services at the University Hospital Basel is an independent specialist group and part of the hospital's interdisciplinary treatment team. Our self-image is based on a holistic view of physical, psychological and social factors. This means that we work with you and your relatives to identify the respective problem situation and try to find a viable follow-up solution.

We can advise you on the following topics, among others:

• Outpatient support services
• Exit planning and rehabilitation
• Housing situation and homelessness
• Employment in connection with illness/disability
• Social insurance
• Financial problems and debt situation
• Child and adult protection law
• Dependence disorders
• Migration
• Violence and victim support

If you would like to talk to the social services, please contact your attending physician, the responsible nursing staff or contact us directly. We will be happy to assist you with our professional expertise.

Contact us

Medical Social Services

Thomas Rohrbach

Tel. +41 61 265 74 90

thomas.rohrbach@usb.ch

Stroke is characterized by an acute focal neurological deficit due to vascular pathogenesis. This definition includes events with permanent focal dysfunction of the central nervous system (usually the brain) associated with a disease affecting the cerebral circulation. If the symptoms are transient, it is referred to as a transient ischemic attack (TIA). A distinction is made between two types of stroke: The ischemic and the hemorrhagic.The ischemic stroke is more common i.e. seen in 85-90% of cases, while the hemorrhagic is seen in 10-15% of cases. Ischemic stroke is caused by a transient or permanent reduction or interruption of blood flow to a region of the brain. If unrestricted blood flow is not restored within the first few minutes or hours, metabolic processes (see below) occur, leading to necrosis of the brain tissue (cerebral infarction). If, on the other hand, an occluded artery reopens quickly and a consecutive improvement or normalization of blood flow is restored immediately, the tissue lesions are very minor and the underlying symptoms can manifest themselves in a transient TIA.

A focal neurological event whose symptoms and neurological deficits do not last longer than 24 hours is called a TIA. TIAs represent about 10% of all focal cerebral ischemic events. Approximately one third of TIAs herald an impending stroke and approximately one third of established strokes were preceded by a TIA. In most cases, the TIAs lasted no longer than a few minutes.

Hemorrhagic stroke is caused by hemorrhage with laceration of the brain parenchyma, edema and consecutive development of necrosis. The cause is usually the rupture of a small penetrating arteriole. In primary intracerebral hemorrhage, the hemorrhage may extend into the subarachnoid space. More rarely, blood can be detected in the ventricular system. However, intraventricular hemorrhage has an unfavorable effect on the prognosis of intraparenchymal hemorrhage. A secondary hemorrhagic infarction corresponds to a hemorrhage in a primarily ischemic zone. Sequential computed tomography scans show that in the course of up to one month after the onset of symptoms, up to one third of initial infarctions are accompanied by an ischemic hemorrhagic transformation. It is therefore sometimes difficult to distinguish between a primary intracerebral hemorrhage and a cerebral infarction with secondary hemorrhage. The diagnosis of subarachnoid hemorrhage is sometimes difficult to make in the absence of neurological deficits in the initial stage.

In Western countries, cerebral strokes are often caused by atherosclerosis of the cardiovascular system. In most cases, these are embolisms, whether arterio-arterial, cardio-arterial or aorto-arterial. Approximately a quarter of cerebral strokes are of cardiogenic origin. If cerebral angiography is performed early, i.e. within the first 24 hours after the onset of symptoms, distal occlusions of cerebral arteries can be detected in many affected patients. Cerebral microangiopathy, which occurs in association with hypertension or diabetes mellitus and leads to lacunar infarcts, is also common. Localized diseases of the cerebral arteries are a less frequent cause of cerebral strokes. Hemodynamic changes are a rare cause of stroke and occur, for example, in occlusion or high-grade stenosis of the internal carotid artery (ACI) and concomitant systemic hypotension. The ischemic lesions that occur in these situations are referred to as border sheath infarcts, i.e. infarcts localized at the border of two adjacent arterial territories. Considering the incidence of cerebral stroke causes, the following should be mentioned:

• Arteriosclerotic diseases of the carotid and vertebrobasilar arteries
• Cardioembolic causes
• Cerebral microangiopathy
• Other etiologies

The reduction in cerebral blood flow impedes cellular metabolism by interrupting the supply of oxygen and glucose and leads to the accumulation of lactate. Cells of the brain parenchyma are particularly susceptible to ischemia and the resulting metabolic changes. Occlusion of an artery leads to tissue damage, particularly ischemic in the center, from which an infarct develops. This region is surrounded by the penumbra zone, a less ischemic tissue with potentially reversible damage. The extent of this ischemic lesion depends on the duration of the circulation reduction. Cellular mechanisms of focal ischemia in brain tissue have become accessible for research since the development of corresponding animal models. Occlusion of the ACM in the rat has become the method of choice. The secondary cellular mechanisms of cerebral ischemia that lead to infarction can be described in several individual steps. The metabolic changes are partly brain-specific. The responsible components are the excitatory release of glutamate, the changes in the concentration of free calcium, the activation of proteases, the formation of free radicals and the mediation of a tissue inflammatory reaction with the migration of macrophages.

The central role of the excitatory transmitter substance glutamate lies in its release from ischemic cells through depolarization and the impossibility of reuptake from the intercellular space and the synaptic cleft. This results in a persistent depolarizing effect on neurons. Glutamate is transported from the extracellular space to the intracellular space with the help of Na-K adenosine triphosphate (ATP)ase. Neurons and astrocytes are able to perform this metabolic function. The extracellular glutamate concentration is normally 1-5 mmol/l, intracellularly 5-10 mmol/l (2000-fold gradient). In an early ischemic phase, synaptic glutamate release is responsible for the depolarization that occurs, but after loss of ATP-mediated transport functions, transmembrane, non-synaptic glutamate release along the concentration gradient can be assumed. Glutamate is released with a drop in cerebral blood flow to approx. 20 ml/100g/min. The uninhibited release of glutamate subsequently causes destabilization of calcium metabolism. The glutamate-dependent calcium channels allow free Ca2+ ions to enter the intracellular space in large quantities.

The depolarization associated with glutamate release triggers the opening of the voltage-dependent Ca channels. Calcium is also released from the endoplasmic reticulum and mitochondria by intracellular energy loss. The intracellular release of Ca2+ causes the activation of calmodulin and phospholipase A2. Calmodulin in turn activates nitric oxide synthetase, phosphocreatinine kinase C, cyclic adenosine monophosphate (AMP), the gene expression of these enzymes and that of various regulatory genes (c-fos, c-jun). Phospholipase A2 activates the formation of platelet aggregation factor and the formation of arachidonic acid. Arachidonic acid is metabolized by cyclooxygenases 1 and 2 to prostaglandins and leukotrienes.

Leukocytes can be detected in the ischemic tissue region as early as half an hour after the onset of ischemia. Several surface receptor molecules are activated: intercellular adhesion molecule-1 (ICAM-1) and CD11b/18. ICAM-1 is expressed on endothelial cells, induced by interleukin-1 and tumor necrosis factor alpha (TNF*).Cellular ischemia is also associated with the formation of free radicals, such as superoxides (O2-), peroxyl radicals (RO2-), nitric oxide (NO*) or hydroxyl (OH*). Free radicals are highly reactive molecules that can cause the formation of further free radicals in a cascade. For example, unsaturated fatty acids can become lipid peroxides, which in turn react as radicals. Lipid peroxidation is catalyzed by free iron (Fe2+, Fe3+) or iron chelates, which are released from hemoglobin. Cells have enzymes and free radical scavengers to protect themselves against the formation of or exposure to radicals. Such enzymes are superoxide dismutase (SOD), which catalyzes the superoxide radical to H2O2, catalase, which metabolizes H2O2 to O2 and H2O. The glutathione peroxidase requires glutathione as a cofactor for this step. The free radicals are *-tocopherol, *-carotene, ascorbic acid and free glutathione.

The clinical neurological examination is syndromic. The classification, based on the OCSP classification by Bamford et al, [Bamford J; Lancet 1992;339:400-2] has proved useful for the initial assessment, e.g. in emergency admissions. A distinction can be made on the basis of the neurological findings:

• Lacunar syndromes: These include one of the following possible syndromes: pure motor hemiparesis, pure sensory hemisymptomatics, sensorimotor hemiparesis, ataxic hemiparesis or rarer lacunar syndromes such as dysarthria-clumsy-hand (dysarthria and dysdiadochokinesia of one hand).
• Syndromes of the entire anterior carotid supply area: This includes the combination of: Cortical dysfunction (aphasia, acalculia, spatial sensory disturbance), vigilance reduction, contralateral homonymous visual field loss (hemi- or quadrant anopsia) and contralateral motor and/or sensory hemiparesis, where at least 2 regions (face, upper and lower limb) must be affected.
• Syndromes of a part of the anterior supply area: Here, only 2 of the 3 components from the complete anterior carotid syndrome are present or there is isolated cortical dysfunction such as aphasia, acalculia, spatial sensory disturbance, etc. Limited sensory and/or motor hemiparesis (face and hand only, monoparesis) and deficit syndromes are also included.
• Syndromes in the posterior/vertebrobasilar region: These include one or more of the following symptoms: ipsilateral cranial nerve palsy and contralateral motor and/or sensory, hemiparesis bilateral motor and/or sensory paresis (para- or tetrasymptomatic), dysconjugate eye movements, isolated hemianopsia or isolated cerebellar symptoms (without additional ipsilateral pyramidal tract signs).

The symptoms of ACI stenosis consist of ocular or focal cerebral ischemic syndromes of varying severity. Transient ischemic attacks (TIA), a focal neurological deficit with symptoms lasting less than 24 hours, often occur in atheromatosis of the carotid bifurcation. 50-75% of patients with atheromatous carotid disease and stroke also suffer TIA. In patients with strokes of other etiologies, the figure is around 10%. Hemispheric transient ischemic attacks usually last less than 15 minutes and manifest themselves only motorically, only sensory or combined with symptoms of the contralateral extremities and dysphasia. Neglect symptoms are rarely reported by patients as they are difficult to perceive. Patients with high-grade carotid stenosis may also experience involuntary, repetitive, cloniform or tremor-like, short-lasting movement disorders of an upper and lower extremity (so-called limb shaking TIA). They are triggered by rapid changes in position or hyperextension of the head and stop when sitting or lying down. These symptoms disappear completely after endarterectomy. Based on the clinical manifestation alone, the pathogenesis of a TIA cannot be attributed with certainty to a cardiogenic or arterial aetiology.amaurosis fugax (AF) is a monocular, short-lasting (up to 15, maximum 30 minutes) visual disturbance with the impression of blurred vision, foggy vision or a closing or lowering curtain. The occurrence of flashes, scintillations or altered color vision is usually an expression of migraine. Headaches are not part of the clinical picture of AF. AF is usually the result of thromboembolism in retinal arteries originating in the course of the carotid artery or in the heart. Only occasionally are fundoscopic changes seen, e.g. "Hollenhorst plaques", cholesterol crystals, which can often be detected in patients with generalized arteriosclerosis. Rarely, retinal ischemia in severe carotid stenosis can manifest itself as a visual disturbance when looking at a white light source or bright light, e.g. sunshine.

In focal cerebral ischemia syndromes with persistent neurological symptoms, it is not always possible to differentiate between hemodynamic lesions caused by reduced perfusion or embolic lesions on the basis of clinical findings alone. Indications of cerebral hypoperfusion include frequent previous TIAs and unilateral infarcts, mild motor symptoms emphasized in the lower extremities, restricted eye movements, transcortical motor and sensory aphasia, sensory aphasia, dyscalculia, constructive apraxia and grasping reflexes. In these situations, infarcts along the supply borders of the large cerebral arteries are visible on computed tomography; in embolic infarcts, the radiological findings correspond more to piomedullary territorial infarcts. The clinical symptoms are accordingly due to failure syndromes of the ACM, anterior cerebral artery (ACA) or its branches. Lacunar syndromes are not part of the clinical picture of ACI stenosis. Combined syndromes can occur if several neighboring arteries are affected.

Neuroradiology uses its methods to visually depict the areas of the brain affected by a stroke. Angiography can also be used to visualize the cerebral arteries and determine the origin of the disease in some patients.

It serves to coordinate the activities of the stroke unit between the departments and services involved. Permanent participants are the nursing managers of the departments, the representatives of the rehabilitation institutes, the neurology nursing consultants and the medical management of the stroke unit. Other specialists are invited depending on the topic. It meets at least 6 times a year.

The indications conference discusses cases that are eligible for surgical or neuroradiological interventional therapies. These are patients with carotid stenoses, occlusions in the vertebrobasilar circulation and intracranial occlusions and stenoses. (University of Basel course catalog no. 1537) Participants are representatives of neurology, neuroradiology, neurosurgery, vascular surgery and nuclear medicine.

Registration Tel. +41 61 265 41 85

Serves the further development of the Stroke Unit. All employees with an interest in research can exchange ideas here.

Rehabilitation after a stroke is carried out by the internal therapy institutes and coordinated by the nursing staff. Individual patients are also treated on an outpatient basis. Inpatient neurorehabilitation takes place at the Felix Platter Hospital, in special situations at the Rheinfelden Rehabilitation Clinic or Bruderholz Hospital (see also Partners).

As part of lectures and group lessons, medical students receive an introduction to cerebrovascular diseases and examination methods, among other things. (See also University of Basel course catalog no. 1418, 1444, 1244, 1606, 1608).

The cerebral arteries in the neck and inside the skull are examined using ultrasound technology. The examination provides information on the localization and severity of stenoses and occlusions. Patients with symptomatic cerebrovascular diseases are advised or followed up in the cerebrovascular consultation.