Acute brain ischaemia

• Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
• Bilateral motor and/or sensory deficit
• Disorder or conjugate eye movement (vertical=midbrain, horizontal=pons)
• Cerebellar dysfunction without ipsilateral long-tract deficit
• Altered consciousness
• Dysarthrophonia, dysphagia
• Horner syndrome (also in carotid artery dissection)
• Isolated homonymous visual field defect

ähnlich wie bei thrombembolischen Ereignissen bis auf:

• Typical atherogenic risk factors
• Frequent TIAs, e.g. amaurosis fugax (internal carotid artery stenosis), in the same arterial territory
• Onset often during sleep or atherothrombotic stroke during activity, a gradual progression or stepwise course over minutes to hours is characteristic (attributable to gradual accumulation of thrombus or to lowering of blood pressure, e.g. following antihypertensive therapy).

• Recent trauma
• Previous infection
• Signs of connective tissue abnormalities (hyperextensible joints, Marfan syndrome, known mitral valve prolapse)
• Younger Patients!

is a focal neurological syndrome

• + unilateral headache or neck pain
• + pulsatile tinnitus
• 1 ipsilateral Horner syndrome in the case of internal carotid artery dissection

Hypoattenuation involving one-third or more of the middle cerebral artery (MCA) territory

●Obscuration of the lentiform nucleus

●Cortical sulcal effacement

●Focal parenchymal hypoattenuation

●Loss of the insular ribbon or obscuration of the Sylvian fissure

●Hyperattenuation of large vessel (eg, "hyperdense MCA sign")

●Loss of gray-white matter differentiation in the basal ganglia

Early signs of ischaemia + Ischaemieareal >1/3 des cerebri media -Territoriums

hypodensity of the white matter with emphasis on periventricular regions

Hämorrhagischer Infarkt: petechial or confluent petechial haemorrhage within the infarcted region and normally has few clinical consequences

Parenchymales Hämatom: the region is filled with a mass of blood which may encroach on surrounding structures, resulting in midline shift and clinical deterioration

• Aggravation of cerebral oedema related to migration through a permeable blood-brain barrier, reversing the osmotic gradient and exacerbating swelling
• Dehydration and shrinkage of normal brain tissue, facilitating displacement of brain tissue thereby increasing the risk of herniation
• Electrolyte imbalances
• Raised serum osmolarity
• Hypervolaemia with cardiac failure
• Renal dysfunction.

1.Massnahme ist Dekompression durch NCH

2. Drainage:

• The management of these drainage devices needs special expertise, because it may lead to further brain shifts. 
• relatively high infection rate of 2-10%, which increases when drainage is maintained beyond ten days.

• Ischaemic infarct with relevant neurologic deficit (2< NIHSS <25)
• Symptoms not regressing spontaneously
• Symptoms not minimal (however no NIHSS limit)

• *Time window >3h
• *Age >80 years
• *Very severe neurological deficit (i.e. hemiplegia, gaze deviation, coma)
• Suspicion of subarachnoid haemorrhage**
• Traumatic head and brain injury within last 3 months
• Myocardial infarct within last 3 months
• Gastrointestinal or urogenital bleeding within last 3 weeks
• Arterial puncture at an incompressible site within last week
• *Operation within last 2 weeks (NOTE: contact respective surgeons re risk of bleeding)
• *Seizures at symptom onset
• *History of intracerebral haemorrhage
• *Ischaemic stroke within last 3 months
• Blood pressure >185/100 mmHg despite antihypertensive therapy (In the US, a diastolic BP of >110 is used)
• Signs of acute bleeding or acute trauma
• Oral anticoagulant medication and INR >1.5 (in the US: INR=1.7)
• Heparin for last 48h with aPTT within normal range
• Platelets <100 000/µl
• *Diabetics with history of stroke
• *Large infarct in CT (early signs >1/3 of hemisphere)
• *Serum glucose <50 mg/dl (2.7 mmol/l) or >400 mg/dl (22.2 mmol/l)
• Tumour with increased bleeding risk
• Acute pancreatitis
• Endocarditis

• Calculate the total dose of rtPA: 0.9 mg/kg; maximum of 90 mg
• Administer 10% of the total dose given as a bolus
• Give the remaining 90% over 60 minutes via an infusion pump

3h (-4.5h, noch nicht freigegeben)

Je früher um so besser

In the case of basilar artery occlusion:

in specialised centres, intra-arterial therapy using urokinase up to 1.5 million IU or rtPA up to 50 mg may be the treatment of choice.

If cranial CT does not show any demarcated infarction, the time window for thrombolysis may be extended up to 12h

Individuelle Enscheidung:

demarkiertes Areal im CT?

Abschätzen des Ischämiealters mittels MRI?

Jounger Patient?

1. ASS 150-300mg/d

2. Emboliequelle suchen

3. Behandlung der vaskulären Risikofaktoren

bisher kein Benefit.

Evtl. erwägen nach thrombembolischen Ereignissen bei Carotisdissektion, VHFli, Sinusvenenthrombose...

• large infarcts (e.g. more than 50% of middle cerebral artery territory)
• uncontrollable arterial hypertension
• advanced microvascular changes in the brain.

Neigen zu zerebralen Hämorrhagien!

• VhFi, rheumatische Endokarditis, mechanische Klappen, ventrikelaneurysma
• PFO

bei TIA/minor Stroke sofort, bei grösseren Infarkten nach 4 Wochen(meistens)