Ischemic stroke: a brief overview

Ischemic stroke is an acute disruption of blood supply to a portion of the brain caused by a blockage of an artery by a thrombus or embolus. Brain cells are extremely sensitive to oxygen deficiency, so every minute of delay means the loss of some neurons and the functions they support. Correct recognition of the first signs and prompt patient transport to a specialized vascular center dramatically improves the chances of recovery. [1]

The scale of the problem is enormous: the World Stroke Organization estimates that by 2022, there will be approximately 12.2 million new cases of stroke, more than 6.5 million deaths, and 143 million disability-adjusted life years lost. Ischemic strokes account for the vast majority of strokes, with mounting social and economic consequences for families and healthcare systems worldwide.

Ischemic stroke differs from hemorrhagic stroke in that it is caused by a "blockage" rather than a "rupture" of a vessel. However, both forms can begin with similar symptoms, so the only reliable course of action is immediate hospitalization and neuroimaging to confirm the type of stroke and determine treatment. In everyday practice, the "FACE-HAND-SPEECH-TIME" rule should be used: facial distortion, arm weakness, or speech impairment are all reasons to immediately call an ambulance and record the time of symptom onset. [2]

The key to successful treatment is "time equals brain." Modern methods of restoring blood flow work best in the first few hours: the sooner thrombolytic therapy or mechanical clot removal is performed, the higher the chance of survival without severe cardiac arrest. Therefore, until the emergency medical team arrives, avoid giving food, water, blood thinners, or attempts to "tough it out"—rest and air are essential.

ICD-10 and ICD-11 codes

The International Statistical Classification of Diseases, Tenth Revision, classifies ischemic stroke under the heading I63 "Cerebral Infarction," with additional subsections for cause and vascular bed. These codes are used for diagnosis, reporting, and patient routing, as well as for prescribing rehabilitation and subsidized drug provision. [3]

The eleventh revision of the International Classification of Diseases introduced the category 8B11 "Ischemic stroke," to which expanded codes can be added for the mechanism of injury, location, and risk factors. The transition to the eleventh revision provides a more precise description of stroke subtypes, which helps in choosing optimal recurrence prevention strategies. [4]

Table 1. Codes for ischemic stroke

Classifier	Code	Name
ICD-10	I63	Cerebral infarction
ICD-10 (examples of clarifications)	I63.0, I63.3, I63.8	Cerebral infarction due to thrombosis of cerebral arteries, due to embolism, other forms
ICD-11	8B11	Ischemic stroke
ICD-11 (expanders)	8B11.0-8B11.Z	Clarification of the mechanism, localization, and circumstances (based on the clinical situation)
[5]

Epidemiology

Ischemic stroke accounts for the majority of all strokes and remains the leading cause of long-term disability in the adult population. The cumulative lifetime probability of stroke in some high-income countries approaches one in five, and in low-income countries, one in two. This reflects both population aging and inequalities in risk factor control. [6]

Global reviews show that over recent decades, the burden of stroke has shifted toward younger ages in regions with inadequate prevention of hypertension, diabetes, and tobacco use. This leads to an increase in cases among people of working age, increasing economic losses.

Despite the expansion of the stroke center network and improvements in door-to-needle and door-to-recanalization routing, significant disparities in access to reperfusion therapy persist, especially outside major cities. Optimization of regional care systems, mobile stroke teams, and telemedicine are helping to reduce delays and increase the proportion of patients reaching their treatment windows.

The risk of recurrent stroke remains significant: without targeted secondary prevention, it reaches several percent per year. Current guidelines emphasize the need for systematic monitoring of blood pressure, lipids, and glycemia, smoking cessation, and targeted antithrombotic prophylaxis based on the stroke subtype.

Reasons

More than half of ischemic strokes are caused by atherothrombosis of the large arteries of the head and neck or cardioembolism, most often associated with atrial fibrillation. Atherosclerosis causes an unstable plaque to form, on which a thrombus develops and subsequently migrates to the cerebral arteries. In atrial fibrillation, thrombi most often form in the left atrial appendage and embolize to the brain.

Some strokes are associated with damage to small perforating arteries of the brain due to long-term hypertension and diabetes. These "lacunar" infarctions often present with isolated motor or sensory symptoms, but when multiple lesions occur, they can lead to cognitive and gait impairment.

Other causes include carotid or vertebral artery dissection, paradoxical embolism through a patent foramen ovale, vasculitis, thrombophilia, and malignant tumors with hypercoagulability. Identifying the underlying mechanism is critical: secondary prevention strategies for cardioembolism, atherosclerosis, and small vessel disease differ fundamentally.

To standardize causes, the TOAST classification is used, which distinguishes between the atherothrombotic subtype, the cardioembolic subtype, small artery disease, other established causes, and an unspecified mechanism. This scheme helps standardize assessments and maintain quality-of-care registries. [7]

Risk factors

Modifiable risk factors include hypertension, smoking, dyslipidemia, diabetes mellitus, obesity, physical inactivity, poor diet, alcohol abuse, as well as atrial fibrillation and other sources of cardiogenic embolism. According to an international study, the combined contribution of these key factors explains the overwhelming majority of the population risk of stroke. [8]

Arterial hypertension is the leading and most modifiable risk factor. Recent European and American guidelines recommend aiming for blood pressure levels below 130/80 mmHg in most high-risk patients, provided treatment is well tolerated. Controlling blood pressure reduces the likelihood of both a first stroke and a recurrence after an episode. [9]

Atrial fibrillation significantly increases the risk of ischemic stroke, especially in older adults. Direct oral anticoagulants are preferred for most patients without mechanical valves and those with rheumatic mitral stenosis, as reflected in current secondary prevention guidelines.

Behavioral factors are also important: quitting smoking, losing weight, regular aerobic activity, a Mediterranean diet, and limiting salt intake significantly reduce the likelihood of stroke and other cardiovascular events, which has been confirmed by meta-analyses and included in prevention recommendations. [10]

Table 2. Key risk factors and indicative value for risk reduction during correction

Factor	Why is it dangerous?	What to do	Expected contribution to risk reduction under control
Arterial hypertension	Damages the vascular wall, causing thrombosis	Titrate antihypertensive drugs to <130/80 mmHg if well tolerated	Significant reduction in the risk of first and recurrent stroke
Atrial fibrillation	Cardiogenic embolism	Direct oral anticoagulants in the absence of contraindications	Multiple reduction in the risk of stroke
Dyslipidemia	Atherosclerosis of large arteries	Intensive statins, ezetimibe if necessary, proprotein convertase inhibitors	Marked reduction in the risk of vascular events
Smoking	Atherothrombosis, endothelial dysfunction	Complete withdrawal, behavioral and medication support	Significant risk reduction within 1-5 years
Diabetes mellitus	Microangiopathy, atherogenesis	Control of glycemia, blood pressure, lipids, weight loss	Overall risk reduction with an integrated approach
[11]

Pathogenesis

After arterial occlusion, a central "necrotic zone" forms, where neurons rapidly die, and a "penumbra," where blood flow is reduced but cells are still potentially reversible. Here, an "ischemic cascade" unfolds: excitatory toxicity, calcium imbalance, oxidative stress, an inflammatory response, and microvascular "unrestored blood flow." Reperfusion can salvage the penumbra if performed promptly. [12]

Disruption of the blood-brain barrier increases the risk of hemorrhagic transformation of infarction, especially with a large initial volume of necrosis, uncontrolled pressure, and late reperfusion. This explains the need for strict selection for thrombolytic therapy and mechanical thrombectomy, as well as subsequent pressure monitoring and repeat CT imaging.

Despite decades of research into neuroprotective agents, no drug has yet demonstrated a convincing clinical effect. Promise is associated with a combination of reperfusion and "cerebroprotection," but large randomized trials remain negative or inconclusive. [13]

Experimental agents such as the peptide nerinetide have shown signs of efficacy in subgroups without concomitant thrombolytic therapy, suggesting potential drug interactions when co-administered with alteplase. However, blood flow restoration and proven secondary prevention strategies remain the standard treatment for ischemic stroke today. [14]

Symptoms

Typical signs include sudden weakness or numbness on half the body, facial distortion, speech or understanding difficulties, sudden blindness in one eye, severe loss of coordination, and a severe headache of an unusual nature. These symptoms appear suddenly and peak within minutes. Their detection requires an immediate call for emergency medical assistance. [15]

Damage to the anterior circulation most often results in unilateral paresis, aphasia, and visual disturbances. Damage to the posterior circulation can manifest as double vision, dizziness, unsteadiness, difficulty swallowing, and speech and breathing disturbances. Silent cognitive and visual deficits are also observed with small infarcts in strategic areas.

Brief focal symptoms without signs of acute infarction on neuroimaging are consistent with a transient ischemic attack. This is a "red flag" for a high risk of imminent stroke, requiring the same urgent evaluation and preventive measures as for a full-blown stroke. [16]

Early recognition at the prehospital stage using simple scales and referral to a stroke center reduces the time to reperfusion. Education of the public and healthcare workers on the "FACE-HAND-SPEECH-TIME" rule remains a fundamental measure for improving survival. [17]

Classification, forms and stages

Based on the mechanism of injury, the "TOAST" scheme is used: atherothrombosis of large arteries, cardioembolism, small perforating artery disease, other established causes, and an unspecified mechanism. This classification guides the scope of the examination and the choice of secondary prevention. [18]

Based on location, infarctions are classified into those occurring in the internal carotid artery and its branches, vertebral arteries, and basilar arteries, as well as multifocal lesions due to embolism. A simple distinction between "anterior" and "posterior" blood supply helps correlate symptoms with the likely occluded vessel and plan targeted angiography.

Expert consensus suggests using the following time intervals for the phases: the first 24 hours—the hyperacute phase; 1–7 days—the acute phase; 7 days–3 months—the early subacute phase; 3–6 months—the late subacute phase; and more than 6 months—the chronic phase. This division helps plan the reperfusion window, early prevention of complications, and staged rehabilitation. [19]

Validated scales, such as the National Institutes of Health Stroke Scale, are used to assess the severity of neurological deficits and guide decisions on reperfusion methods. Standardized assessment facilitates comparison of treatment outcomes between centers.

Table 3. Time phases of stroke and key tasks

Phase	Interval	Main objectives
Hypercutaneous	0-24 hours	Confirmation of diagnosis, reperfusion, monitoring of pressure, glucose and temperature
Acute	1-7 days	Prevention of pneumonia and venous thrombosis, early rehabilitation, selection of antithrombotics
Early subacute	7 days - 3 months	Intensification of rehabilitation, secondary prevention, control of risk factors
Late subacute	3-6 months	Sustainable restoration of functions, correction of therapy according to response
Chronic	More than 6 months	Long-term prevention of relapse and complications, maintenance of quality of life
[20]

Complications and consequences

In the first few days, cerebral edema and midline displacement are dangerous, especially in cases of extensive middle cerebral artery infarction. In such cases, early decompressive hemicraniectomy is considered in selected patients, which reduces mortality and improves functional outcomes. The decision is made by a multidisciplinary team and depends on age, infarction volume, and clinical dynamics. [21]

Hemorrhagic transformation of the lesion is associated with disruption of the vascular wall and reperfusion. The risk is increased with large infarct volumes, high blood pressure, and delayed thrombolytic therapy. Therefore, after thrombolysis, control neuroimaging is performed before initiating antiplatelet or anticoagulant therapy. [22]

Aspiration pneumonia is a common and preventable complication. All patients undergo swallowing screening according to an established protocol before the first meal or medication, and if dysphagia is suspected, an in-depth assessment by a swallowing specialist is performed. Regular oral hygiene reduces the risk of respiratory tract infections. [23]

In the long-term period, post-stroke depression, cognitive impairment, epileptic seizures, chronic pain, and spasticity are significant. Systematic rehabilitation, psychosocial support, and early correction of complications improve independence and quality of life. [24]

When to see a doctor

Call emergency medical help immediately if you experience sudden facial contortions, weakness or numbness in an arm or leg, slurred speech, double vision, sudden severe headache, or severe dizziness. It is important to remember the exact time of onset of symptoms—this determines the possibility of reperfusion treatment. [25]

Brief focal symptoms that resolve completely within a short time are no small matter: they constitute a transient ischemic attack and a direct path to an imminent stroke, requiring urgent evaluation at a stroke center within a few hours. Self-administration of painkillers or blood thinners without diagnosis is dangerous. [26]

Patients with known atrial fibrillation, severe hypertension, diabetes, high cholesterol, smokers, and obese individuals should routinely discuss individualized stroke and cardiovascular event prevention strategies with their physician. Regular monitoring of blood pressure and lipids is an essential part of self-care.

If a stroke has occurred previously, any new neurological symptoms require the same urgent evaluation: they could indicate a relapse or a complication. Monitoring by a neurologist, cardiologist, and general practitioner in your community reduces the risk of recurrence.

Diagnostics

The first line of treatment is a non-contrast computed tomography scan to rule out intracranial hemorrhage and confirm an ischemic mechanism. Subsequently, if indicated, computed tomography angiography or magnetic resonance angiography is performed to detect occlusion of large arteries, and, with extended time windows, perfusion assessment of viable tissue.

The minimum laboratory workup includes determination of blood glucose, electrolytes, coagulation parameters, complete blood count, and creatinine. Glucose levels are essential before thrombolytic therapy, and coagulation parameters are required if coagulopathy or warfarin use is suspected. An electrocardiogram is recorded simultaneously, and rhythm monitoring is initiated. [27]

All patients undergo swallowing screening using a standardized protocol before meals and medications, as dysphagia is often detected within the first few hours and increases the risk of pneumonia. If indicated, ultrasound examination of the brachiocephalic arteries, transcranial Doppler sonography, and echocardiography are performed to identify the source of embolism. [28]

In extended time windows of 6 to 24 hours, when a large artery occlusion is suspected, perfusion computed tomography or diffusion-perfusion magnetic resonance imaging maps are used to select thrombi for mechanical removal based on extended-window criteria. This approach allows for the salvage of viable tissue beyond the classic thrombolysis window. [29]

Table 4. Diagnostic algorithm by time

Stage	What is being done?	For what
Pre-hospital	Recognition using the "FACE-HAND-SPEECH-TIME" scheme, calling an ambulance	Reduce delay to treatment
Admission	Non-contrast computed tomography, blood glucose, electrocardiogram	Exclude hemorrhage, assess indications for reperfusion
Extension	Computed tomography angiography, magnetic resonance angiography, perfusion	Find the occlusion and penumbra for mechanical removal of the thrombus
Etiology	Echocardiography, ultrasound examination of the carotid arteries, rhythm monitoring	Determine the cause for secondary prevention
[30]

Differential diagnosis

"Stroke mimics" are common and require attention, as misinterpretation of symptoms can waste the patient's time. Common mimics include hypoglycemia, postictal paralysis after an epileptic seizure, migraine with aura, vestibular paroxysms, and functional neurological disorders. The presence of focal deficits with acute onset always requires neuroimaging. [31]

Weakness on one side of the face without arm weakness, gradual onset of symptoms, the presence of a typical migraine aura, or obvious precursors of an epileptic seizure increase the likelihood of a "mock attack" but do not preclude urgent investigation. Blood glucose testing and a non-contrast CT scan are mandatory at any suspicion. [32]

Tumors, demyelinating diseases, infectious lesions, subdural hematomas, and metabolic encephalopathies can also mimic stroke. The decision to initiate thrombolytic therapy is made only after excluding hemorrhage and assessing the time window, as delay is more dangerous than false-positive suspicions. [33]

Systematic approaches—standardized scales, telemedicine support, routing protocols—reduce the proportion of missed strokes and speed up the initiation of treatment, especially in resource-limited areas.

Table 5. Stroke and common “imitators”: what is alarming

State	Signs of a stroke	Signs of imitation	First steps
Ischemic stroke	Suddenness, focality, asymmetry	No	Urgent CT scan, assessment of onset time
Hypoglycemia	Sweating, tremors, confusion	Focality is possible	Immediate glucose check, correction
Epileptic seizure	Todd's post-ictal paralysis	Convulsions, tongue biting	CT scan, glucose, neurological examination
Migraine with aura	History of migraine, symptom spread	Visual phenomena	Neuroimaging in first episode or unusual course
[34]

Treatment

General measures in the first hours. Ensure airway patency, oxygenation, and hemodynamic stability. Maintain body temperature within the normal range, avoid hyperglycemia and hypoglycemia. Blood pressure is reduced gradually, focusing on guideline-recommended targets, taking into account the planned reperfusion. Before thrombolytic therapy, blood pressure usually needs to be reduced below 185 over 110 mmHg, and afterward, maintained below 180 over 105 mmHg. [35]

Intravenous thrombolytic therapy with alteplase. If the ischemic mechanism is confirmed and there are no contraindications, recombinant tissue plasminogen activator is administered at a dose of 0.9 mg/kg (maximum 90 mg) with an initial bolus followed by infusion. The greatest benefit is observed within the first 3 hours, with an acceptable benefit of up to 4.5 hours in selected patients. There is a risk of symptomatic intracranial hemorrhage, but its likelihood is comparable to the benefit if the selection criteria are strictly followed. [36]

Intravenous thrombolytic therapy with tenecteplase. Current European guidelines allow the use of tenecteplase at a dose of 0.25 mg/kg as an alternative to alteplase in eligible patients, including those with planned mechanical thrombolysis. Meta-analyses demonstrate similar safety to alteplase and signals of superior recovery in terms of the proportion of "excellent" outcomes. [37]

Mechanical thrombus removal from large arteries. In selected patients with occlusion of the internal carotid artery or proximal middle cerebral artery, mechanical thrombectomy within the first 6 hours dramatically increases the chance of successful recovery. In extended windows of up to 16 hours and up to 24 hours from symptom onset, selection is based on perfusion-diffusion criteria, as demonstrated in large extended-window studies. [38]

Thrombectomy for basilar artery occlusion. For the posterior circulation, the evidence base is evolving: the 2024 multidisciplinary European guidelines support endovascular treatment in patients with moderate-to-severe basilar artery occlusion, taking into account data from recent randomized and observational studies. The decision is strictly individualized, taking into account clinical presentation, imaging, and time factors. [39]

Antiplatelet therapy. In the absence of thrombolytic therapy, it is recommended to initiate aspirin within the first 24 hours. After thrombolysis, antiplatelet agents are administered no earlier than 24 hours later and only after control neuroimaging shows no signs of hemorrhage. In patients with "minor" stroke or high-risk transient ischemic attack, short-term dual antiplatelet therapy for 21-30 days reduces the risk of early recurrence. [40]

Anticoagulants for the cardioembolic subtype. For strokes associated with atrial fibrillation, direct oral anticoagulants are recommended unless there are mechanical valves or severe rheumatic mitral stenosis. The initiation and timing of anticoagulation depend on the infarct size and the risk of hemorrhage; the decision is made on an individual basis after repeated imaging.

Carotid artery revascularization. For symptomatic, high-grade internal carotid artery stenosis in suitable patients, carotid endarterectomy is preferred within 14 days of symptoms with acceptable surgical risk. Carotid stenting is considered in patients with high surgical risk or complex anatomy; the decision is made by the vascular team. [41]

Prevention of deep vein thrombosis and pneumonia. In the first few hours, pneumatic compression of the lower legs is prescribed for immobile patients, swallowing screening is provided, early verticalization in safe doses, and oral hygiene is maintained. Very early and excessively intensive mobilization in the first 24 hours can worsen outcomes, so the rehabilitation regimen is selected gradually. [42]

Rehabilitation begins as soon as possible after stabilization, with the participation of a multidisciplinary team: a physical therapist, occupational therapist, speech therapist, and neuropsychologist. Targeted, regular exercises focused on functional goals increase the likelihood of restoration of walking, speech, and self-care. [43]

Table 6. Reperfusion strategies and time windows

Method	Who is it indicated for?	Time window	The key to selection
Alteplase 0.9 mg per kg	Most of the selected patients have no contraindications	Up to 4.5 hours	Non-contrast CT scan rules out hemorrhage
Tenecteplase 0.25 mg/kg	An alternative when indicated, including before thrombectomy	Up to 4.5 hours	Compliance with clinical and radiological criteria, single bolus
Mechanical thrombectomy	Occlusion of a large artery	Up to 6 hours standard, up to 16-24 hours for selected ones	Perfusion or diffusion-perfusion sampling
[44]

Table 7. Antithrombotic tactics according to clinical scenarios

Scenario	Tactics
Without thrombolysis, mild stroke	Acetylsalicylic acid in the first 24 hours
"Minor" stroke or high-risk transient attack	Short-term dual antiplatelet therapy 21-30 days
After thrombolysis	Withhold antiplatelet agents for at least 24 hours and based on follow-up imaging
Cardioembolic subtype	Direct oral anticoagulant in the absence of contraindications, start time is individual
[45]

Prevention

The basic strategy for secondary prevention includes target blood pressure levels below 130/80 mmHg if well tolerated, intensive lipid-lowering therapy with a target low-density lipoprotein cholesterol below 70 milligrams per deciliter or below 1.8 millimoles per liter, smoking cessation, weight management, regular aerobic activity, and a Mediterranean-type diet.[46]

In atrial fibrillation, direct oral anticoagulants are the most effective measure for reducing the risk of recurrent stroke. In cases of intolerance or contraindications, alternative interventions are discussed with the cardiology team. Continuous rhythm monitoring in the subacute period helps identify hidden arrhythmia.

With regard to primary prevention with acetylsalicylic acid, the approach has become more cautious: routine initiation in people 60 years and older without established cardiovascular disease is not recommended due to the risk of bleeding; in those aged 40–59 years, the decision is made on a personalized basis with a high ten-year risk. [47]

Control of glycemia, blood pressure, and lipids in people with diabetes, the use of drugs with proven cardiovascular benefit, and systemic management of associated risk factors are most effective when implemented simultaneously. [48]

Table 8. Goals of secondary prevention after ischemic stroke

Direction	Target setting
Blood pressure	Below 130 to 80 millimeters of mercury with good tolerance
Low-density lipoprotein cholesterol	Below 70 milligrams per deciliter or below 1.8 millimoles per liter
Smoking	Complete refusal
Physical activity	Regular aerobic activity of at least 150 minutes per week at moderate intensity
Atrial fibrillation	Direct oral anticoagulant in the absence of contraindications
[49]

Forecast

The sooner blood flow is restored and supportive therapy is initiated, the higher the likelihood of independence within 3 months. Extended window studies have shown that proper selection based on perfusion criteria allows for the salvage of viable tissue even after 16-24 hours, although maximum benefit is still achieved in the first few hours. [50]

Globally, stroke remains a leading cause of death and disability, but mortality is declining in areas where stroke care systems are developed and prevention programs are implemented. The contribution of the family and rehabilitation team is critical to restoring function and preventing complications.

The risk of relapse is highest in the first weeks and months, then stabilizes but persists despite uncontrolled risk factors. Individualized secondary prevention and specialist monitoring can significantly reduce the likelihood of a recurrence.

Psychological and cognitive consequences often determine quality of life as much as motor deficits. Timely assessment of memory, attention, mood, and speech, targeted rehabilitation, and support from loved ones help return to school, work, and normal activities. [51]

FAQ

Can you "wait and see if it goes away"? No. Every minute of delay increases irreversible necrosis. Call an ambulance immediately at the first sign of trouble. [52]

Why are the first hours so important? Reperfusion techniques are most effective early; some patients are suitable for extended windows if viable tissue is present, but waiting reduces the chances. [53]

What is the difference between alteplase and tenecteplase? Both are plasminogen activators. Tenecteplase is administered as a bolus dose of 0.25 mg/kg and is considered an alternative to alteplase with comparable safety profiles in European guidelines. [54]

When is dual antiplatelet therapy prescribed? For a short course during the first 21-30 days of a "minor" stroke or high-risk transient attack to reduce early relapses. [55]

Should you take aspirin "just in case" if you haven't had a stroke? For people 60 years and older without established cardiovascular disease, starting it is not recommended due to the risk of bleeding; for those aged 40-59, the decision is individualized. [56]

Are there "neuroprotective pills" that save the brain after a stroke? Currently, there is no convincing evidence of the effectiveness of individual neuroprotectors; the basis for success is rapid reperfusion and modern prevention. [57]

Is it possible to begin rehabilitation in the first few hours? Very early and excessive mobilization in the first 24 hours can worsen the outcome; rehabilitation should be started early, but in a measured and safe manner. [58]

Useful summary tables for doctors and patients

Table 9. Minimum set of examinations in the first day

Direction	What's included	Comment
Neuroimaging	Non-contrast computed tomography, if indicated, computed tomography angiography and perfusion	Confirmation of the mechanism, search for occlusion
Laboratory	Glucose, electrolytes, creatinine, complete blood count, coagulation parameters	Before thrombolysis, it is necessary to know the glucose level.
Cardiology	Electrocardiogram, rhythm monitoring, echocardiography	Search for the source of embolism
Screenings	Swallowing screening, venous thrombosis risk assessment, pneumonia risk	Prevention of complications
[59]

Table 10. What is important for the family to do before the ambulance arrives

Action	For what
Remember the exact time of onset of symptoms	Determines availability of reperfusion
Provide rest and air access	Stabilization of the condition
Do not give food, water, or pills	Reduce the risk of aspiration and bleeding
Prepare a list of medications and illnesses	Speed up decision-making in hospitals
[60]