Cerebral Infarction (Ischaemic Stroke)

Essentials

• The treatment of cerebral infarction has been intensified during the recent years. Most patients nowadays regain independence and an ever greater proportion have no residual symptoms. This is mainly a result of thrombolytic therapy in the acute phase and/or thrombectomy and of treatment in stroke units, as well as of effective rehabilitation commenced in the initial phase already.
  • A previously self-sufficient patient with acute cerebral infarction is investigated at the hospital emergency department where the treatment is also provided and from where a consultation regarding thrombectomy can be made through remote connection.
  • The patient is transported by ambulance to an adequately equipped hospital where the thrombolytic therapy is administered and where a CT angiography is carried out in order to identify patients suitable for thrombectomy to be further referred to an appropriate tertiary level hospital.
  • Time windows
    • Thrombolytic therapy http://www.dynamed.com/management/stroke-acute-management-1#THROMBOLYTICS is administered within 4.5 hours from the onset of symptoms (or, when the exact starting time is not known, within less than 9 hours if infarction is excluded by imaging)
    • In basilar artery thrombosis, in accordance with its clinical picture, the time window of thrombolytic therapy is longer, even up to 12-48 hours.
    • Thrombectomy http://www.dynamed.com/management/stroke-acute-management-1#ENDOVASCULAR_THERAPY is performed mainly within 6 hours and at discretion within 6-24 hours from the onset of symptoms.
• According to the current knowledge, 4 out of 5 cerebral reinfarctions can be prevented by effective secondary prevention.
• A healthy lifestyle is the most important factor in the primary prevention of cerebral infarction. Prevention directed at the risk factors of vascular diseases is the best possible treatment.

Epidemiology Hormone Replacement Therapy and the Risk of Stroke, Ischaemic Stroke and Myocardial Infarction Risk with Combined Oral Contraceptives

• One in five patients are adults in working age.
• In many countries, like in Finland, the incidence of cerebral infarction has decreased in recent decades, but increased in the younger age groups (less than 50 years olds), causing concern.
• How well secondary prevention is implemented determines the future increase in the number of patients with cerebral infarction, due to the increase in the proportion of aged people in the population.
• The most common risk factors for cerebral infarction are advanged age, hypertension, atrial fibrillation, diabetes, hypercholesterolaemia, truncal obesity, and of the living habits unhealthy diet, low level of physical activity, excessive alcohol use and smoking.
• Triggering factors include dehydration, surgery, pregnancy, immobilization, the instigation and cessation of anticoagulant therapy, acute excessive alcohol intake and acute infection.

Aetiology

• Atherosclerosis of the large vessels, microangiopathy and cardiogenic embolism each account for approximately one third of infarctions with an identified cause. In every third cerebral infarction the cause cannot be found even in thorough investigations.
  • The aetiology of cerebral infarction is highly dependent on age.
    • In the younger age groups the underlying cause is more often carotid artery dissection, vasculitis, cerebral vasospasm, hereditary or acquired coagulation disorder, or paradoxical embolism associated with a prothrombotic state, especially in patients with patent foramen ovale or some other rare cause.
    • In patients aged over 80 years, atrial fibrillation is the causative factor in one out of four cases.
    • If the cause remains unknown or the only finding is a source of embolism that entails a minor or uknown risk, and imaging findings match an embolic infarction, the condition may be regarded as ESUS (Embolic Stroke of Undetermined Source, about 17% of all cerebral infarctions).
• The most common cause of cardiogenic embolism is atrial fibrillation. Other high-risk causes include new or earlier myocardial infarction, sick sinus syndrome, atrial flutter, akinesia/aneurysm of the left ventricle, thrombosis in the left ventricle or atrium or atrial auricle, dilated cardiomyopathy, mechanic valve prosthesis, mitral valve stenosis and endocarditis, as well as atheroma in the ascending aorta or aortic arch.
• Microangiopathic infarcts result from thrombosis of the small distal arteries and are located either subcortically or in the basal ganglions or the brain stem. They are most commonly caused by hypertension. Other causes include type 2 diabetes and hypercholesterolemia.

Symptoms Symptoms in the Diagnosis of Stroke, Magnetic Resonance Imaging Versus Computed Tomography for Detection of Acute Vascular Lesions in Patients Presenting with Stroke Symptoms

• Location of the infarction affects essentially the symptom picture. In 80-90% of the cases the infarction is located in the carotid region (anterior circulation) and in 10-20% to the vertebrobasilar region (posterior circulation).
• Cerebral infarction will generally lead to acute hemiplegia and/or sensory disturbance and expressive language impairment. The patient may also present with hemiparesis, a drooping mouth, visual disturbances and disturbed eye movements, dysphagia, vertigo, balance problems, or tetraplegia. An acute neuropsychological deficit, e.g. dyspraxia, memory loss or confusion, may also be indicative, of cerebral infarction.
  • Vertigo, binocular visual disturbance or swallowing or speech difficulties, when occurring alone, usually do not indicate a disturbance of the cerebral circulation.
• Carotid (hemispheral) infarction typically presents with hemiparesis and/or sensory disturbance, often accompanied by weakness in the lower branch of the facial nerve.
  • Occlusion of the middle cerebral artery is the most common site; paralysis is more pronounced in the upper extremity.
  • Occlusion of the anterior cerebral artery, which is a rare condition, leads to paralysis most often involving the lower extremity and to urinary incontinence.
  • An infarction in the dominant hemisphere often involves expressive and receptive language impairment as well as reading and writing difficulties.
  • An infarction in the non-dominant hemisphere may include impairment in the sense of direction and spatial orientation as well as anosognosia (lack of a sensation of illness) and sensory neglect (ignoring the affected side of the body).
• Vertebrobasilar (brainstem) infarction typically presents as acute and severe vertigo, nausea, diplopia, dysphagia, dysarthria and sensory disturbance, weakness or paresis in the contralateral extremities. The symptoms are caused by the progressive (often lasting for several days) occlusion of vertebral artery, basilar artery and cerebellar arteries. Homonymous hemianopia without paralysis is most often caused by the occlusion of the posterior cerebral artery.
• The symptom picture of lacunar (microangiopathic) infarctions may involve pure motor or sensory hemiparesis which often fluctuates, as well as ataxia and hemiparesis or dysarthria- clumsy hand syndrome. See also Vascular dementia Vascular Cognitive Impairment (Vci).
• Cerebral infarctions rarely involve a headache, particularly at the initial stage. A large infarction may cause increased intracranial pressure, headache, nausea and lowered consciousness, but usually with a delay. The symptoms of a severe cerebral infarction may progress in up to 3 days after the incident.
• Sinus thrombosis (cerebral venous thrombosis) may occur during pregnancy or puerperium, or in association with hormone therapy, dehydration, coagulopathies, or malignancy. Sinus thrombosis causes symptoms of increased intracranial pressure: headache, lowered consciousness, or seizures with associated unconsciousness as well as paralysis inconsistent with the arterial distribution areas.

Diagnostic work-up at the emergency department

1. Is the condition caused by disturbed cerebral circulation or some other illness (migraine, epilepsy, encephalitis, brain tumour, or MS)?
2. Does the patient suffer from an ischaemic disturbance of cerebral circulation or haemorrhage? The two conditions need to be differentiated with the use of a CT scan, which still is the primary investigation in an emergency setting.
3. Is the patient's condition during examination stable, progressive or recurring?
   • An unstable phase usually persists until the occluded vessel is opened either spontaneously or through thrombolysis. Improved symptoms do not always translate to reduced risk.
4. Start aetiological investigations.
   • Cardiogenic?
     • An acute onset (e.g. whilst getting out of bed or during straining), loss of consciousness, seizures, and a history of a potentially embolic cardiac disorder suggest cardiogenic embolism. The symptom may also be isolated aphasia, visual field defect or tetraparesis, even as a transient symptom. A CT scan may show, for instance, a haemorrhagic infarction or multiple infarctions. Anticoagulant therapy is indicated.
   • Find stenoses of the carotid arteries.
   • Other, more rare causes
     • Neck pain, Horner's syndrome Neurological Eye Symptoms, and neck trauma prior to the stroke are suggestive of carotid dissection.

Treatment Fibrinogen-Depleting Agents for Acute Ischaemic Stroke, Calcium Antagonists for Stroke, Corticosteroids for Acute Ischaemic Stroke, Gamma Aminobutyric Acid (Gaba) Receptor Agonists for Acute Stroke, Naftidrofuryl for Acute Stroke, Sonothrombolysis for Acute Ischaemic Stroke, Piracetam for Acute Stroke, Antibiotic Therapy for Preventing Infections in Patients with Acute Stroke, Atenolol for Preventing Stroke Recurrence, Continuous Vs. Intermittent Physiological Monitoring for Acute Stroke, Colony Stimulating Factors Including Erythropoietin (EPO), Granulocyte Colony Stimulating Factor (G-CSF) and Analogues for Stroke, Acupuncture for Acute Stroke, Physical Methods for Preventing Deep Vein Thrombosis in Stroke, Information Provision for Stroke Patients and Their Caregivers, Interventions for Preventing Depression after Stroke