StrokeI63.0-9 und I61.0-9

The first person to describe transient ischemic attacks (TIA) was Hippocrates, who described attacks of numbness and numbness as a sign of an impending stroke around 230 BCE (Limroth 2019).

Motor aphasia was first described by P. Broca (1824 - 1880) as the brain region in the frontal lobe of the dominant cerebral hemisphere and named after him as "Broca's aphasia". Cortical sensory aphasia, which exists despite an intact Broca's language center, was discovered by C. Wernicke in 1874 (Gerabek 2007).

The recombinant tissue plasminogen activator alteplase was approved in the USA in 1996 and is so far the only drug to show good healing results in patients with early-stage ischemic stroke (Lee 2022).

Apoplexy is primarily defined clinically as a sudden syndrome with focal neurological deficit(s) resulting from a vascular cause (Herold 2023).

Apoplexy has the highest incidence in the industrialized countries, especially the Eastern Bloc countries and Germany. It is 300 / 100,000 / year in 55 to 64 year olds and 800 / 100,000 / year in 65 to 74 year olds. The lifetime prevalence, which is around 15%, increases significantly after the age of 60. Overall, more men than women are affected (Herold 2023). From the age of 55 to the age of 75, for example, the risk of men suffering a stroke is twice as high as that of women (Gehring 2023).

At around 80%, ischemic strokes occur much more frequently than hemorrhagic strokes, which are the cause of apoplexy in only 20% of cases (Herold 2023). Primary cerebral hemorrhages occur in approx. 10 - 12 %, subarachnoid hemorrhages in only 3 % (Mader 2020).

In patients with chronic atrial fibrillation - without thromboembolism prophylaxis - the risk of suffering a cerebral embolism is 6 % / year (Herold 2023).

In apoplexy, a distinction is made between an ischemic and a hemorrhagic insult in terms of etiology:

I. Ischemic insult:

• Ia. Macroangiopathy

Macroangiopathy causes up to 50 % of all strokes. These are arterio- arterial embolisms or hemorrhagic infarcts in the area of extra- or intracranial arteries. The most important risk factor is arterial hypertension , whereby the systolic blood pressure value is typically the most significant (Herold 2023).

Around 75% of stroke patients have arterial hypertension. Hypertensive patients have a 4-fold higher risk of suffering a stroke compared to normotensive patients. With an increase in systolic blood pressure of just 10 mmHg, the risk of stroke rises to around 30%. Other risk factors are: first-degree relatives who suffered an apoplexy before the age of 60, age, existing CHD and cardiovascular risk factors such as smoking, diabetes mellitus, estrogen-containing contraceptives, migraine with aura and high alcohol consumption (Herold 2023).

• Ib. Microangiopathy

Microangiopathy as a cause occurs in approx. 25 % of apoplexy patients. Small perforating vessels with status lacunaris and subcortical vascular encephalopathy (SVE) are affected (Herold 2023).

• Ic. Proximal emboli

Proximal emboli account for approx. 20 % of all cerebral infarctions. Two sources of embolism play a role here

• Ic.1 Cardiac

These originate from the left atrium in cases of e.g. atrial fibrillation, myocardial infarction, aortic and mitral valve vitis, bacterial endocarditis, cardiac wall aneurysm, cardiac catheter manipulation (Herold 2023).

• Ic.2 Proximal to the aorta

Here the thrombi originate from a portion of the proximal aorta and occur predominantly in aortic sclerosis (Herold 2023).

• Id. Other causes

The remaining causes affect approx. 5 % of all stroke patients. Younger people are particularly affected. The causes can be, for example: dissection of the extracranial cerebral arteries (e.g. after chiropractic maneuvers), inflammatory and non-inflammatory (e.g. moyamoya angiopathy) vascular wall disorders (e.g. vasculitis), paradoxical embolisms in right-left shunts (e.g. in ventricular and cerebrovascular accidents). ventricular and atrial septal defects including pulmonary AV shunts and persistent foramen ovale), antiphospholipid syndrome, cocaine or amphetamine use, genetic and hereditary diseases (e.g. Osler's disease, Fabry's disease, CADASIL, etc.) (Herold 2023).

According to TOAST criteria, ischemic strokes can be divided etiologically into:

- Approx. 25 % cardiac embolism

- Approx. 20 % macroangiopathy

- Approx. 20 % microangiopathy

- Approx. 10 % other causes to be identified

- Approx. 25 % cryptogenic (Litmathe 2016)

II. Hemorrhagic insult

A meta-analysis has shown that there is a linear increase in the risk of hemorrhagic infarction with increasing alcohol consumption (Mader 2020).

• IIa. Spontaneous intracerebral hemorrhage (ICH), also known as primary intracerebral hemorrhage.

It accounts for approx. 15 % of all strokes. The main risk factor is arterial hypertension, which can lead to a rupture of the vessels at a typical location in the subcortical medullary layer or the pons (Herold 2023).

• II. b. Secondary intracerebral hemorrhage

This can be caused by e.g. anticoagulants, malformations, coagulation disorders, amyloid angiopathy or vasculitis etc. (Herold 2023).

• II. c. Sympathomimetic drugs

These include cocaine, amphetamines, crack, pseudoephedrine, etc. (Litmathe 2016). Cocaine in particular can lead to intracerebral, intraventricular and subarachnoid haemorrhages (Kraft 2020).

The energy requirement of the brain is 20 % of the cardiac output, although it only accounts for 2 % of the total body weight. The brain cannot store energy, but it can autoregulate blood flow to the brain and collateralize via the cerebral artery (Litmathe 2016).

- Ischemic infarction

In ischemic infarction, the ability to autoregulate is limited (Litmathe 2016).

A decrease in cerebral blood flow to zero results in the death of brain tissue within 4 - 10 minutes. With a blood flow to the tissue of < 16 - 18 ml / 100 g, an infarction occurs within an hour. With blood flow values of < 20 ml / 100 g, this results in ischemia without infarction unless it lasts for hours or several days (Kasper 2015).

A focal cerebral infarction can occur in two ways:

1. necrotic

This involves the rapid breakdown of the cellular cytoskeleton. The result is a loss of energy in the cell (Kasper 2015)

2. apoptotic

In the apoptotic pathway, the cells are pre-programmed for death. Ischemia leads to necrosis by depriving the neurons of glucose and oxygen, so that the mitochondria can no longer produce ATP and the intracellular calcium increases (Kasper 2015).

Penumbra

An ischemic zone, also known as the "penumbra", is found around the core area of the infarct. This area is reversibly dysfunctional and can be visualized as a penumbra using imaging (see above) (Kasper 2015).

- Hemorrhagic infarction

This usually results from a spontaneous rupture of a small penetrating artery deep in the brain. The basal ganglia, in particular the putamen, the thalamus, the pons and the cerebellum are most frequently affected. If blood penetrates into the ventricular cavity, this significantly increases mortality or can cause hydrocephalus (Kasper 2015).

Hypertensive intracerebral hemorrhages (ICH) usually develop within 30 - 90 min. ICH under anticoagulation therapy, on the other hand, takes up to 24 - 48 hours to develop. Within 48 h, the macrophages begin to phagocytose the outer surface of the hemorrhage. If the patient survives, the hemorrhage resolves within 1 - 6 months and a cavity forms, which is lined with glial scars and hemosiderin-laden macrophages (Kasper 2015).

A distinction is made between 3 stages of occlusive disease of the extracranial cerebral arteries:

- Stage I:

This corresponds to the asymptomatic stage (Herold 2023).

- Stage II:

Transient ischemic attacks (TIA) are found in this stage. These are short-term neurological deficits that are reversible within 24 hours. There is no evidence of diffusion restrictions on MRI. Nevertheless, TIA must be considered an emergency, as 20 % of strokes are heralded by a TIA. After a TIA, the risk of stroke is 12 % within one month and 20 % within one year (Herold 2023).

- Stage III:

In stage III, a so-called cerebral infarction occurs with only partial or no recovery of the neurological deficits (Herold 2023).

Themain symptoms of the stroke are:

- Motor hemiparesis symptoms

- Sensory hemiparesis symptoms

- Motor speech disorders

- Sensory speech disorders

- Visual field defects (Herold 2023)

The clinical picture gives no indication of the cause of an apoplexy, but the symptoms are determined by the localization of the occlusion:

I. Occlusion of extracranial cerebral arteries:

They cause about 20 % of all strokes and are divided into:

- 1. carotid type

This is an occlusion of the internal carotid artery (ACI), most frequently in the area where it leaves the brain. If there is good collateralization, unilateral occlusions can be asymptomatic.

A unilateral amaurosis fugax is typical of a unilateral ACI occlusion. There may be contralateral sensorimotor hemipareses, which are usually brachiofacial in nature. An infarction in the dominant (predominantly left) hemisphere results in aphasic speech disorders. If it is a large infarct, there are also disturbances of consciousness with a possible turning of the head or gaze to the side of the infarct (Herold 2023).

- 2. vertebral artery type

The vertebral artery type is characterized in particular by the following symptoms: nystagmus, vomiting, paresis, visual disturbances, etc. Occlusion of the inferior posterior cerebellar artery leads to the so-called Wallenberg syndrome with ipsilateral pharyngeal, palatal and vocal cord paresis, subclavian steal syndrome, Horner syndrome, nystagmus, trigeminal nerve loss, dysmetria (failure to estimate distance), limb ataxia, contralateral dissociated sensory disturbance for pain and temperature from the cervical region (Herold 2023).

- 3. subclavian steal syndrome

This is very rare. Occlusion of the subclavian artery proximal to the vertebral artery leads in most cases to a predominantly asymptomatic reversal of flow, the so-called subclavian steal phenomenon. Visual disturbances and dizziness may only occur when the arm works on the same side (Herold 2023).

II Occlusion of intracranial cerebral arteries

- 1. aneurysmal subarachnoid hemorrhage

- 2. hypertensive intracerebral hemorrhage (Kasper 2015)

Occlusions of this type usually affect the flow area of the middle cerebral artery (ACM). The symptoms are similar to those of an ACI occlusion with the difference that amaurosis fugax is absent (Herold 2023). The following symptoms may occur: hemiplegia of the opposite side, paresthesias of the opposite side, speech disorders and word-finding disorders (in the case of lesions in the dominant hemisphere), gaze deviation towards the focus, visual field defects if the occipital region is affected (Litmathe 2016).

In rarer cases, the anterior cerebral artery (ACA) may also be affected. In this case, there is a leg-accentuated contralateral hemiparesis (Herold 2023).

Occlusion of the posterior cerebral artery (ACP) with hemianopsia is also less common (Herold 2023).

If there is occlusion of the basilar artery, there is, for example, a progressive impairment of consciousness, possibly visual disturbances due to oculomotor and pupillomotor disorders, dysarthria, hemiparesis, ataxia and dizziness (Herold 2023).

The medical history and clinical symptoms play a major role in the diagnosis.

Initially, the FAST test (Face, Arms, Speech, Time test) should be carried out:

- 1. facial paresis (grimace, laughter, frown)

- 2. arm paresis (holding arms stretched forward, handshake)

- 3. speech and language (naming things, repeating sentences)

- 4. time - further measures should be initiated immediately (Litmathe 2016)

If the FAST test proves positive (at least one positive pathology), the emergency doctor must be informed immediately. The FAST test has an 80 % sensitivity (Herold 2023).

If the FAT test is negative, 4 further functions should be checked:

- 1. gaze palsy (check eye movement to the right and left)

- 2. leg paresis (when lying down, have each leg raised outstretched forwards)

- 3. visual disturbance (check right and left visual field)

- 4. hemihypesthesia (check sensation of touch in the face, arms and legs)

(Herold 2023)

In addition, the blood pressure should be measured on both arms (the subclavian steal phenomenon is diagnosed by measuring the blood pressure of both arms as soon as there is a difference of > 20 mmHG) and the pulse (atrial fibrillation) should be measured with auscultation of both carotid arteries (Herold 2023).

Immediate imaging is mandatory in cases of suspected stroke, as the guiding principle is "time is brain". Further diagnostic investigations into the aetiology of the stroke are also obsolete (Herold 2023).

CCT

Hemorrhagic infarcts can be reliably detected immediately (Herold 2023).

Ischemic infarcts, on the other hand, show an unremarkable result in the first 4 hours, after which the infarct region appears hypodense (Herold 2023).

MRI

This also allows hemorrhagic infarcts to be reliably detected immediately (Herold 2023).

In the case of ischemic infarcts, an insult can be detected in the DWI weighting after just 30 minutes (Herold 2023).

Perfusion imaging CT and MRI

This allows a differentiation to be made between vital, infarcted and valvularly supplied areas (penumbra). This is important for possible lysis, as the area of the penumbra can still be saved by rapid lysis (Herold 2023).

Imaging of extracranial and intracranial vessels

This is performed with:

- Duplex sonography of the carotid and vertebral arteries

- Transcranial color duplex sonography of the intracranial vessels

- MR or CT angiography (Herold 2023)

In the case of a severe apoplexy, vascular diagnostics should be performed immediately with the question of a proximal occlusion. A DAS, on the other hand, is only recommended for planned invasive measures (Herold 2023).

Cardiac diagnostics

The following should be performed to rule out a cardiac source of embolism: ECG, long-term ECG, event recorder with the question of atrial fibrillation, transthoracic and esophageal echocardiography.

Contrast-enhanced TEE (transesophageal echocardiography) and / or contrast-enhanced TCD (transcranial Doppler sonography) are recommended to rule out a cardiac right-to-left shunt (Herold 2023).

Dysphagia screening

Up to 50 % of stroke patients initially experience dysphagia and the associated risk of aspiration pneumonia. As aspiration pneumonia is an important mortality factor, dysphagia screening is mandatory in the acute phase.

For this purpose, an inspection of the mouth and throat should be carried out with the question of a saliva lake. Tongue and pharyngeal motor function, the gag reflex and the cough reflex should also be checked. If these examinations are inconspicuous and the patient shows sufficient vigilance, a swallowing test with a few ml of water is recommended (Herold 2023).

In the acute situation, the following parameters in particular should be determined:

- CBC

- Electrolytes

- Coagulation parameters such as INR, prothrombin time, aPTT thrombin time

- Blood sugar

- GFR

- Troponin

The troponin value is of particular importance with regard to the prognosis. The higher the value rises in the first hours or days after the stroke, the worse the prognosis (Gehring 2023).

The differential diagnosis of a stroke should exclude:

- Hypertonic encephalopathy

- Neurosyphilis

- Space-occupying brain processes

- Intoxications

- Epileptic seizure

- Reversible cerebral vasoconstriction syndrome (RCVS)

- Migraine attack

- Subdural hematoma

- Craniocerebral trauma

- Hypoglycemic shock

- Encephalitis disseminata

- Meningoencephalitis (Herold 2023)

- Transient global amnesia

- Functional disorders (Litmathe 2016)

The complications of an apoplexy are numerous. These include, for example:

- Respiratory regulation disorders

- Urinary tract infections if a urinary catheter is inserted

- Swallowing disorders with the risk of aspiration pneumonia (this is the most common complication)

- Epileptic seizures

- Incontinence of urine and stool

- Repeated apoplexy

- Decubitus ulcers

- Deep vein thrombosis with the risk of embolism (this causes up to 25% of deaths after apoplexy)

- Falls with the risk of fractures

- Dementia

- Depression

- Psychosocial problems (Herold 2023)

Pre-hospital:

If an apoplexy or TIA is suspected, the patient should be admitted to a stroke unit immediately (Herold 2023).

The therapeutic measures depend on the cause of the stroke and differ significantly. As it is not possible to distinguish clinically between an ischemic and a hemorrhagic insult, treatment is only possible after precise diagnosis by imaging examinations and must never be initiated pre-hospital (Herold 2023).

- Neither heparin nor ASA should be administered pre-hospital, nor should i.m. injections be given (Herold 2023).

- Peripheral access should be placed on the non-paretic arm if possible

- The upper body should be positioned high (Herold 2023) = positioning to avoid intracranial pressure (Litmathe 2016)

- If hypoxemia is < 95% (Mader 2020), administer oxygen via the nasogastric tube until O2 saturation is > 95%.

- Particular care should be taken to ensure that no time is lost, as the time window for possible lysis is max. 4.5 h (Herold 2018)

- Blood glucose measurement: From a BG < 60 mg / dl, glucose should be administered i.v. and from a BG > 200 mg / dl, insulin should be administered (Litmathe 2016).

- Blood pressure measurement:

- From a systolic value < 120 mm Hg, a crystalloid infusion should be administered

- With systolic RR values of ≥ 220 mm Hg, the blood pressure can be reduced by approx. 15 % through careful titration with medication (Mader 2020)

Inpatient:

The aim here is to

- Securing the vital functions

- Checking breathing with determination of blood gas values and any necessary intubation or controlled ventilation. Hypoxia and / or hypercapnia should be avoided at all costs.

- Control of water and electrolyte balance including blood glucose measurement

- Tube feeding or parenteral nutrition:

- Patients with dysphagia and / or impaired consciousness should be fed by tube or parenteral nutrition

- Control of bladder and bowel function:

- If necessary, a urinary catheter should be inserted

- Bowel function should be monitored regularly.

- Thromboembolism prophylaxis:

- Low-dose heparinization is required for immobile patients. This applies regardless of the cause of the apoplexy. Exercise should also be performed at an early stage (Herold 2018)

- Blood pressure:

- Ischemic insult

High-normal or slightly elevated blood pressure values should be aimed for in the acute phase, as hypertension is usually reactive in this phase. Constant RR checks are obligatory. There is only a medical need to lower blood pressure in the case of values >220 / 120 mmHg and in the case of a hypertensive emergency with the risk of hypertensive encephalopathy, pulmonary edema or angina pectoris. Blood pressure should always be lowered gently and not by more than approx. 20 % compared to the initial value. The following are particularly suitable for intravenous blood pressure lowering: captopril, metoprolol and urapidil (Herold 2018).

- Hemorrhagic insult:

In the case of a hemorrhagic insult, it is recommended to lower the systolic blood pressure to values of 140 - 179 mmHg.

- Therapy of any existing concomitant diseases

- Rehabilitation

- Early rehabilitation should be initiated in the hospital in the form of physiotherapy, respiratory gymnastics and speech therapy.

- Further rehabilitation then takes place in appropriately equipped clinics (Herold 2018)

- Ischaemic insult

As soon as there is evidence of an ischemic infarction, platelet aggregation inhibitors should be used, e.g. 100 - 300 mg ASA / d orally. If swallowing is impaired, the dose should be administered intravenously (Herold 2018). If medication is possible within 3 h of the event, the neurological symptoms usually improve. However, this therapy has no influence on mortality (Kasper 2015).

Any fever that occurs should be reduced with medication, e.g. with paracetamol (Litmathe 2016), as fever significantly worsens brain damage. The same applies to hyperglycemia from a glucose value of > 11.1 mmol / l or > 200 mg / dl (Kasper 2015).

- Reperfusion measures:

The effectiveness of systemic thrombolysis (i.v. rtPA) with e.g. alteplase was demonstrated in randomized, controlled trials in 1995 and that of mechanical neurothrombectomy in 2014. However, these are complementary treatment methods, as combined or bridging procedures are always preferred where possible. In Germany, approx. 10 % were treated with i.v. rtPA in 2010; the target value is 30 % (Litmathe 2016).

- Endovascular thrombectomy (EVT)

Another treatment method for ischemic stroke is EVT (Jorgensen 2018). In a study by Wee (2017), up to 61.7 % of patients showed a significant neurological improvement within 24 hours of undergoing EVT, while mortality during the inpatient stay was 7.1 %.

- Hemorrhagic insult

- Increased intracranial pressure

If an intracerebral hemorrhage (ICB) is detected, particular attention should be paid to the intracranial pressure. If necessary, this can be treated conservatively or surgically.

Conservatively by elevating the body by approx. 30°, positioning the head in a frame and possibly intubation. Long-term hyperventilation should be avoided in particular, as this can worsen cerebral perfusion. Osmotherapy with e.g. mannitol 50 mg i.v. every 6 h is also recommended (Herold 2018).

Neurosurgical treatment includes a decompression craniotomy in the presence of a large medial infarction or brain stem decompression in the case of a large posterior fossa infarction. In the case of a cerebellar infarction with occlusive hydrocephalus, temporary ventricular drainage is recommended (Herold 2018).

- Minimally invasive surgery

An attempt is made to remove the hematoma in a minimally invasive manner (Gil-Garcia 2022).

The risk of a re-infarction can be estimated using the Essen Stroke Risk Score.

1 point is awarded for:

- Age 65 - 75 years

- Diabetes mellitus

- Arterial hypertension

- Z. n. TIA or ischemic stroke

- PAD

- CHD

- Z. n. ACVB

- Z. n. myocardial infarction

- Nicotine abuse

And 2 points for:

- Age > 75 years

Assessment:

With < 3 points, the risk is < 4 % / year

With ≥ 3 points, the risk is the risk is the risk is ≥ 4% / year (Herold 2018)

In Germany, around 200,000 people suffer an apoplexy for the first time and 70,000 for the second time. Of these patients, between 25 - 33 % die within the first year after the event Of those who survive, up to 40 % suffer significant functional limitations (Mader 2020).

In the case of a hemorrhagic infarction, particularly due to ICH, there is a disproportionately high risk of death (the mortality rate is 40% [Gil-Garcia 2022]) or long-term disability (Montano 2021).

The prognosis of cocaine-induced intracerebral hemorrhages is generally worse than that of cerebral hemorrhages triggered by other causes (Kraft 2020).

- Hormone therapy

Premenopausal women who have already suffered a stroke should refrain from combined oral contraception. After suffering a stroke, in- or postmenopausal women should discontinue any ongoing hormone replacement therapy, taking into account the risk-benefit ratio (Mader 2020).

- Arterial hypertension

In hypertensive patients, blood pressure should be lowered to values < 140 / 90 mm Hg with medication (Mader 2020).

- Diabetes mellitus

People with diabetes mellitus already have a high risk of stroke. After an apoplexy, they should be advised in accordance with the DEGAM S3 guideline on cardiovascular prevention (Mader 2020).

- Platelet aggregation inhibitors

The patient should be offered treatment with ASA 100 mg/d or clopidogrel 75 mg/d for secondary prophylaxis after apoplexy, provided there is no indication for oral anticoagulation (OAC). However, ASA 100 mg/d is not recommended for primary prevention (Mader 2020).

- Lipid management

For secondary prevention, patients should be offered a statin after an apoplexy, as well as advice on a lifestyle with favorable effects on lipid metabolism (Mader 2020).

- Atrial fibrillation

For primary prevention, patients with atrial fibrillation should be offered OAC therapy; as secondary prevention, long-term treatment with OAC is indicated (Mader 2020).

Stroke prevention includes:

- Dietary advice (Mediterranean or Nordic)

- Reduction of salt intake in patients with arterial hypertension

- At least 2 x strength training sessions per week for all major muscle groups

- At least 75 minutes of intensive or at least 150 minutes of moderate physical activity per week

- If overweight, help with weight reduction

- Limit alcohol consumption

- For smokers, help to stop smoking (Mader 2020)

In Germany (Mader 2020) and worldwide, apoplexy is the second most common cause of death (behind CHD/myocardial infarction) and the first most common cause of disability in old age. Aspiration pneumonia is an important mortality factor (Herold 2018).

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