Stroke Guidelines

of the Bern Stroke Center

04/2016

www.strokecenter.ch

S. Jung, R. Lüdi, M. Bühlmann, H. Mattle, C. Bassetti, M. Schlager, T. Horvath, M.L. Mono, A. Angelillo-Scherrer

J. Gralla, G. Schroth, M. El-Koussy, A. Raabe, J. Beck, W. Z`Graggen, U. Fischer, M. Arnold, Stroke-Team Bern

Physicians on duty Phone numbers Miscellaneous Phone numbers

Neurology Resuscitation (CPR)

Neuroradiology Laboratory results

Neurosurgery Bed scheduling

Radiology Stroke Unit

Anesthesia

Intenive Care Unit

Cardiology

Internal Medicine

Infectiology

2

Contents Contact information ………………………………………...………………………...……. 3

Treatment plan……..……………………………………...…………………………………… 4-5

Indications and choice of therapy………………………………………………………. 6

Contraindications ………………..…………………………………………………………….7

IVT alteplase dosage…….…………………………………………………………………... 8

IVT in patients treated with DOAC..…………………………………………………….8

Monitoring during IVT……………………………………………………………………….. 9

Antihypertensive medication.…...………………………………………………………. 9

Vasopressor therapy…………………………………………………………………………..9

Prescription of medication.………………………………………………………………...10

Agitation/delirium………….…………………………………………………………………. 10

Mobilization………………………………………………………………………………………. 10

Stroke Unit treatment………………...…………………………………………………..... 11

Management of hemorrhages..………………………………………………………... 12

Malignant infarcts…………….....……………………………………………………………. 13

Daily checklist…...…………….....……………………………………………………………. 14

DD neurological deterioration…………………………………………………………. 14

DD myocardial infarction DD stress cardiomyopathy……………………...…. 14

TIA and minor stroke…………………………………………………………………………. 15

Pathway for patients with TIA..………………………………………………………….. 15

ABCD2 score..……………………………………………………………………………………..15

Risk factors and causes of stroke…..…………………………………………………... 16

Diagnostic workup.……………………………………………………………………………. 17

Secondary prevention……………………………………………………………………….. 18

Prevention of deep vein thrombosis….………………………………………………. 18

Direct oral anticoagulants (DOAC)…..…………………………………………………. 19

Dissections…….………………………………………………………………………………….. 20

Symptomatic artery stenosis…….………………………………………………………...20

PFO………….…….………………………………………………………………………………….. 21

Secondary prevention in special situations……………………………………….. 21

Risk factor treatment……………………………………………………………………….. 22

Vasculitis examinations….………………………………………………………………….. 22

Fig. Scheme of functional systems….…………………………………………….….. 23

Fig. Brain supplying arteries…………………………………………………………………24-25

Fig. Distribution of vascular territories…………………………………………………26-27

Cerebral venous and sinus thrombosis….…………………………………………... 28

Therapeutic heparinization………………….…………………………………………... 28

Fig. Cerebral Vein and Sinus.…………………………………………………….…………29

Pictures for assessment of naming and spatial recognition..……………….30-31

Reading sample..………………………………………………………………………………...32

GCS, CHA2DS2-VASc score, modified Rankin Scale…...………………………..33

NIHSS………………………………..………………………………………………………………..34-35

Table for vision assessment...……………………………………………………………..36

Contact information PD Dr. med. S. Jung, Co-Leader Stroke Unit, Tel. +41 (0)31 632 78 32, email: simon.jung@insel.ch

Prof. Dr. med. M. Arnold, Leader Stroke Center, Tel. +41 (0)31 632 78 32, email: marcel.arnold@insel.ch

Prof. Dr. med. U. Fischer, Leader Emergency, +41 (0)31 632 78 32, email: urs.fischer@insel.ch

Administration Stroke Center: Pia Kupferschmid, Tel. +41 (0)31 632 78 32, email: stroke@insel.ch

The guidelines are also available free of charge as an app for android and Apple smartphones.

Links to further documents including pediatric stroke guidelines under

www.strokecenter.ch

Drawings from Anja Giger, may be freely distributed with appropriate source citation.

Eye chart: PD M. Abegg, S. Küng

Translation corrections: S. Kaplan

All information is supplied without guarantee. This version replaces the guidelines from 09/14 and 08/15.

University of Bern, Department of Neurology

Prof. M. Arnold, Prof. H. Mattle, Prof. U. Fischer, PD S. Jung, PD M.-L. Mono, Dr. M. Schlager, Dr. M. Bühlmann,

Dr. M. Heldner, Dr. S. von Arx, Dr. A. Galimanis, Prof. R. Müri, Prof. M. Sturzenegger, Prof. C. Bassetti

University of Bern, Department of Diagnostic and Interventional Neuroradiology

Prof. J. Gralla, Prof. G. Schroth, PD P. Mordasini, PD M. El-Koussy, Dr. K. Hsieh, Prof. R. Wiest, M. Mordasini

University of Bern, Department of Neurosurgery

Prof. A. Raabe, Prof. J. Beck, PD P. Schucht, Prof. W. Z`Graggen

University Bern, Department of Anesthesia and Pain Therapy

Prof. F. Stüber, Dr. F. Neff

University Bern, Department of Intensive Care

Prof. J. Takala, Prof. S. Jakob, PD M. Hänggi

University of Bern, Department of Emergency Medicine

Prof. A. Exadaktylos

University of Bern, Department of Cardiology

Prof. B. Meier, Prof. C. Seiler, Prof. T. Pilgrim, Prof. M. Wilhelm, Prof. J.P. Pfammatter

University of Bern, Department of General Medicine

Prof. D. Aujeski, Dr. M. Perrig, Prof. N. Rodondi

University of Bern, Department of Hematology

Prof. A. Angelillo-Scherrer, Dr. M. Nagler 3

Stroke Guide

Prehospital phase - control of respiration, BP, heart rate, Biox, temperature - GCS and FAST or NIHSS (without losing time) - ask about: symptom onset? Previous history/medication? Pacemaker/artificial heart valve? Phone number of GP/relatives - supine position—max. 30°, venous catheter - aim Biox > 92%; aim BB 120-220 sys, < 120 diast. - BP > 220mmHg syst. or >120mmHg diast.: lower carefully - BP < 120mmHg sys: 500ml NaCl - early information transmitted to stroke center to decide triage, fastest transportation

Patient selection for acute therapy (IVT/EVT) - emergency diagnosis with fastest transportation of patients with o neurological deficits with symptom onset within 24h o wake-up stroke and unclear symptom onset - fast diagnosis also in case of rapid symptom improvement (CAVE: persistent vessel occlusion with secondary clinical worsening possible) - Triage of patients Symptom onset < 4.5h: transport to the nearest hospital with possibility for IVT (if IVT can be initiated with 4.5h) => eventually IVT and transport to stroke center in case of occlusion of ICA, carotis T, M1, M2, BA, P1, A1 Symptom onset 4.5-24h: o direct transport to stroke center if transportation duration < 30min o otherwise CTA/MRA in the nearest hospital with capacity for CTA/MRA => transport to stroke center in case of occlusion of ICA, carotis T, M1, M2, BA, P1, A1

IVT: intravenous thrombolysis, EVT: endovascular treatment ICA: internal carotid artery, BA: basilar artery, M1-2: middle cerebral artery, A1: anterior cerebral artery, P1: posterior cerebral artery

Treatment plan

4

Hospital phase Prehospital information

Surname, first name, date of birth

ABCD

Main symptom

Time of symptom onset

Previous history/medication

(D)OAC/heparin?

Pacemaker/artificial heart valve?

Phone number GP/relatives

After registration

Inform:

Emergency room

Neuroradiology

Anesthesiology

Other specialists if necessary

Neuroradiography & Decision

MRI or CT with MRA/CTA

Immediate treatment decision

Patient information

Do not wait for laboratory results

Before IVT: BP target ≤185mmHg syst. + ≤105mmHg diast.

On arrival in the ER

Supine position

2 venous catheters; no bladder cathe-ter

Blood tests (including Troponin, BNP, differential BB)

ECG (chest pain?)

Fever (endocarditis?)

Foot-/inguinal pulse/-temperature; BP left/right (aortic dissection?)

Short (!) NIHSS score /neurological examination

Monitor stable patients only in CT/MRI/before IVT

Treatment plan

5

Sym

pto

ms

NIH

SS s

core

≥ 4

or

NIH

SS <

4 w

ith

re

le-

van

t d

efici

ts (

aph

asia

,

ano

psi

a, d

ista

l par

esis

,

etc.

)

or

con

sid

er in

cas

e o

f

min

or

defi

cits

an

d/o

r

rap

idly

imp

rovi

ng

sym

pto

ms

wit

h p

ersi

s-

ten

t ve

ssel

occ

lusi

on

+

Ve

sse

l occ

lusi

on

Ti

me

& im

agi

ng

resu

lts

< 4.

5h

In c

ase

of

no

mis

mat

ch

no

rmal

ly t

reat

an

yway

> 4

.5h

in c

ase

of

mis

mat

ch:

4

.5h

– a

t le

ast

12h

m

ech

anic

al a

pp

roa

ch

4

.5h

-6h

Uro

kin

ase

i.a.

In

ca

se o

f n

o m

ism

atch

an

d <

8h

: in

div

idu

al

dec

isio

n

up

to

24h

aft

er B

A

occ

lusi

on

Wak

e-u

p s

tro

ke/

Un

kno

wn

sym

pto

m

on

set

In c

ase

of

mis

mat

ch:

(co

nsi

der

T2/

FLA

IR d

emar

-

cati

on

bu

t d

o n

ot

ove

rsta

te

it*)

ICA

, car

oti

d-T

, M1,

BA

B

rid

gin

g EV

T

EVT

M2,

P1

, A

1, V

A

IVT

+ co

nsi

der

EV

T

con

sid

er E

VT

co

nsi

der

EV

T

M3/

4, P

2, A

2

IVT,

co

nsi

der

Uro

-

kin

ase

i.a.

/ /

No

ve

ssel

occ

lusi

on

IV

T /

/

Ind

icati

on

s an

d c

ho

ice

of

the

rap

y

* 40

% o

f p

atien

ts w

ith

sym

pto

m o

nse

t <

4.5h

sh

ow

a F

LAIR

dem

arca

tio

n in

MR

I .

D

iffu

sio

n r

estr

icti

on

wit

ho

ut

FLA

IR d

emar

cati

on

: 83

% P

PV

an

d 5

4%

NP

V f

or

tim

e fr

om

sym

pto

m t

o M

RI i

s w

ith

in 4

.5h

.

IVT:

intr

ave

no

us

thro

mb

oly

sis,

EV

T: e

nd

ova

scu

lar

trea

tmen

t, B

A: b

asila

r a.

, M1

-4: m

idd

le c

ereb

ral a

., A

1-2

: an

teri

or

cere

bra

l a.,

VA

: ver

teb

ral a

., P

1-2

: po

ster

ior

cere

bra

l a.

6

Contraindications IVT EVT

Ab

solu

te R

elati

ve

Septic embolization, endocarditis, encephalitis, pancreatitis

Intracranial hemorrhage

INR > 1.7

Thrombocytopenia < 100,000

Surgery at non-compressible sites within the last 10d

Severe trauma

Intraparenchymal hemorrhage within the last 3 months

Pregnancy (IVT may be considered as off-label treatment)

Delivery within the last 14d

Gastrointestinal hemorrhage within the last 21d

Blood pressure above 185 mmHg sys/105 mmHg dias after BP treatment

Re

lative

Coagulopathy, incl. tumor associated (e.g. in case of leukemia)

Ischemic stroke within the last 3 months

Septicaemia

Hypoglycemia < 2.7 mmol/l or hyperglycemia > 22.2 mmol/l

Sodium < 120 mmol/l or > 150 mmol/l

Severe underlying disease, short life expectancy

Notes - IVT in patients previously treated with antiplatelet aggregation therapy

- Monotherapy Aspirin/clopidogrel/Aspirin+dipyridamol/ticagrelor: no restrictions

- Dual therapy: Aspirin+clopidogrel: no restrictions; other combinations: consider IVT carefully

- Monotherapy or combination therapy with prasugrel: consider IVT carefully

- Triple therapies: no IVT

- Bridging (IVT + EVT):

- normally full dose Alteplase 0.9mg/kg KG

- normally no control-imaging before EVT except in case of clinical deterioration

- unknown symptom onset: consider EVT if DWI-PWI and DWI-FLAIR mismatch (max. only subtle FLAIR demar-

cation) is present; consider IVT exceptionally in case of very small DWI lesions without FLAIR demarcation

- no DWI-PWI/CBV-TTP mismatch: < 4.5h since symptom onset: normally IVT/EVT; otherwise individual

decision

- large infarction DWI/CBV (> 100mL): consider EVT in young patients (< 75 years, and especially if < 60 years)

- spinal ischemia: IVT may be considered

- A. ophthalmica/centralis retinae occlusions: IVT/EVT may be considered

7

IVT Alteplase dosage

Weight (kg) Total dose

0.9mg/kg body weight

Bolus

10% in 1min

Perfusor

90% within 60min

44-47 40mg = 40ml 4 ml 36 ml/h

48-51 44mg = 44ml 4 ml 40 ml/h

52-54 47mg = 47ml 5 ml 42 ml/h

55-57 50mg = 50ml 5 ml 45 ml/h

58-62 54mg = 54ml 5 ml 49 ml/h

63-67 59mg = 59ml 6 ml 53 ml/h

68-72 63mg = 63ml 6 ml 57 ml/h

73-77 68mg = 68ml 7 ml 61 ml/h

78-82 70mg = 70ml 7 ml 63 ml/h

83-88 77mg = 77ml 8 ml 69 ml/h

89-92 80mg = 80ml 8 ml 72 ml/h

93-97 86mg = 86ml 9 ml 77 ml/h

≥98 90mg = 90ml 9 ml 81 ml/h

Note: stop perfusor after 40min for 2/3 dosage

IVT in patients treated with DOAC Dabigatran

(Pradaxa®) Rivaroxaban (Xarelto®)

Apixaban (Eliquis®)

Edoxaban (Lixiana®)

Emergency measu-rement of:

- anti-IIa activity

- Thrombin time

- aPTT

- Anti-Xa activity for Rivaroxaban

- Quick

- aPTT

- Anti-Xa activity for Apixaban

- Quick

- aPTT

- Anti-Xa activity for Edoxaban

- Quick

- aPTT

IVT without restric-tions possible when last dose was taken more than 48h ago, or if:

Thrombin time normal

or anti-IIa activity not detectable

Anti-Xa activity not detectable

Anti-Xa activity not detectable

Measurement of - Anti-Xa activity for Edoxaban not available yet

Consider IVT in individual situation with possibly higher bleeding risk if:

Anti-IIa < 50 ng/ml + aPTT normal

_________________

If Anti-IIa > 50 ng/ml a./o. aPTT prolon-ged: consider antagonism with Idarucizumab (s.p. 12) and then start IVT

Anti-Xa activity < 100 ng/ml + Quick normal + aPTT normal

Anti-Xa activity < 10 ng/ml + Quick normal + aPTT normal

Measurement of - Anti-Xa activity for Edoxaban not available yet

Note: these recommendations require normal renal function (Clearance > 30 ml/min)

Monitoring during IVT 1. Measure BP every 5 minutes: target sys ≤ 185 mmHg, diast ≤ 105 mmHg - in case of > 185/105: re-check after 5 minutes - if BP persists > 185/105: BP lowering (see Antihypertensive medications below) 2. Respiration: Control of oxygen saturation: target Biox > 92% 3. Evaluation of pupils: 3 x per hour - in case of clinical deterioration: stop Alteplase; CT: hemorrhage? - in case of allergic reaction: stop Alteplase administer Clemastin 2mg, methylprednisolone 250mg i.v. for extreme anaphylaxis: adrenalin 0.3.-0.5 mg s.c. for very extreme anaphylaxis: adrenalin 0.05-0.1 mg i.v. - in case of plasma glucose > 11 mmol/l: reduce with insulin carefully

Antihypertensive medication (iv) Use (standard values) Medication Dosage Maximum

effect CAVE/Side effects

Urapidil 50mg/vial

2.5-10mg (1ml=5mg) max 50mg/d

10 min Vertigo, headache, dyspnea, arrhythmia (tachycardia or bradycardia)

bolus administ-ration for HR > 70

Labetolol 100mg/vial

5-10mg (1ml=5mg) max 200mg/d

15 min Bradycardia, AV-block, hypotensi-on, vertigo, nausea, paresthesia, bronchial spasm

bolus administ-ration for HR > 70

Metoprolol 5mg/vial

1-2.5mg (1ml=1mg) max 15mg/d

5 min Bradycardia, AV-block, low output syndrome, bronchial spasm

bolus administ-ration for HR < 70

Dihydralazin 25mg/vial

6.25mg slowly over 2 minutes (1ml=12.5mg) max 100mg/d

20 min

Edema, tachycardia, angina pectoris, excercice caution in case of liver or renal failure

KI: Coronary insufficiency

Perfusion therapy

Urapidil 50mg/vial

5-10 mg/h max. 40mg/h - Restricted to 48h therapy.

Perfusion therapy Labetolol

10-40 mg/h max 100 mg/h (1ml = 1mg)

- see above

Vasopressor therapy (iv) Use (standard values) Medication Dosage Start CAVE/Side effects

Perfusor

Noradrenalin®

Noradrenalin

10 mg/vial

20-400 g/h

Start with 20 g/h

then titrate

CI: Hyperthyreosis, tachycarde arrhythmias, angle-closure glau-coma, pheochromocytoma, cardiomyopathy (esp. hypertro-phic)

Compensate hypovolemia first

Prescription of medication - Do not prescribe antiplatelet aggregation therapy after IVT/i.a Urokinase before exclusion of hemorrhage in control CT/MRI after 24h - regular cardiac premedication should be continued, with eventual reduction of dose (CAVE cardiac failure/rebound tachycardia after stop) - stop any antihypertensive medication in case of hemodynamic stroke - antacids only if unequivocally indicated (stroke is not an indication)

Agitation/delirium Screening: CAM (Confusion Assessment Method), Asssessment parameter: RASS (Richmond Agitation Sedation Scale)

Start with low doses (CAVE transient neurological worsening may occur with higher dosages) In case of alcohol withdrawal delirium 1st choice benzodiazepines, otherwise following scheme:

Level 1: Pipamperon 20mg stepwise (maximal dose 360mg/d) or Quetiapin 12.5mg stepwise (maximal dose 800mg/d) or Risperidon 2x0.5mg/d (maximal dose 16mg/d) Level 2: Diazepam 5mg stepwise i.v. (increase up to 10mg stepwise is possible) in single cases: Midazolam Level 3: Clonidine with perfusor

Mobilization No restriction in mobilization of TIA patients or asymptomatic patients with small infarcts and open vessels

Mobilization delayed (possiby adapt) in case of:

Level 1: supine position (strictly/not strictly) Level 2: 30° (strictly/not strictly) Level 3: 60° Level 4: sitting Level 5: walking with assistance, if patient is steady then free mobilization possible

- hemodynamic strokes - persistent vessel occlusion - persistent penumbra in CT/MRI - strokes posing high risk for deterioration (esp. pontine and anterior choroidal artery strokes) - fluctuating neurological deficits

Mobilization fast (possiby adapt) in case of:

Level 1: supine position (strictly/not strictly) Level 2: sitting Level 3: walking with assistance, if patient is steady then free mobilization possible

Any other types of stroke not described above

!

10

Stroke Unit treatment First neurological examination at once after arrival Cardiovascular monitoring: - BP upper limits during the early phase: ≤ 185/105 mmHg after IVT/EVT ≤ 220/110 mmHg in conservatively treated patients - BP lower limit: only in selected cases in case of hypoperfusion/symptom worsening with drop of BP => to increase BP: only temporary administration of a limited volume of infusion solution (max. 500ml); in other cases use vasopressors (e.g. Noradrealine) - Tachycardia > 100 bpm => usually beta blockers; in case of tachycardic atrial fibrillation consi-der digoxin in addition - frequent ventricular extrasystole => magnesium 2g i.v. - bursts of ventricular extrasystole (more than 3 beats): usually beta blocker + magnesium; ≥10 beats or polymorph or >120/min or clinically symptomatic => consultation with cardiologist - Bradycardia: during sleep in asymptomatic patients, usually up to 35 bpm is tolerable - pause > 3 seconds => consultation with cardiologist Respiration: target Biox ≥ 92; screening for sleep apnea - if > 4l O2/min is necessary or respiration frequency > 20 => clinical examination, arterial blood gas analysis, chest X-ray (pulmonary embolism? cardiac failure? pneumonia?) - if respiration frequency > 25-30 there may be danger of respiratory exhaustion Body temperature: ≥ 38° -> antipyretics (1st choice paracetamol) + 2x2 blood culture, empiric/causal treatment Neurological evaluation: every 2h during the first 24h Clinical internal medical evaluations: cardiac compensation, lung, abdomen to be checked daily

Laboratory controls: (24h after IVT/EVT) - Hb, Lc, Tc, CRP, glucose, Na, K, creatinin, INR - hs-Troponin T and ECG after 1 h if initially abnormal - anemia: transfusion if Hb < 90 g/l - Tc daily under heparin therapy; further laboratory examinations individually determined

Neuroradiological control: - 24h after IVT/EVT, MRI (or CT), including MRA (CTA) except in cases with severe renal insuffi-ciency - in case of neurological deterioration immediately

Swallowing: in case of dysphagia, reduced consciousness , facial palsy or relevant neuropsy-chological deficits: swallowing test (GUSS: Gugging Swallowing Screen)

Nutrition and fluid balance: - Fluid intake requirement: 30-35 ml/kg body weight - daily energy demand: 35kcal x body weight - if sufficient oral energy supply cannot be achieved within 3 days after stroke: enteral feeding via nasogastric tube with high caloric fibrous enteral feeding as bolus application 3-4x/d; control of electrolytes (incl. magnesium and phosphate) - if fasting period > 7 days: delayed feeding (CAVE refeeding syndrome)

11

Management of spontaneous intracerebral hemorrhage and hemorrhage under heparin, IVT, or (D)OAC treatment

Non-traumatic hemorr-hages

General suggestions for all hemorrhages

- BP target < 140/90 mmHg - treatment of elevated ICP - elevate upper body ≥ 45% - event. treatment of source of hemorrhage surgically or with EVT - ventricle drainage in cases of intraventricular hemorrhages or impaired CSF drainage

stop administration of (D)OAC, heparin or thrombolytics in case of thrombocytopenia or platelet dysfunction: platelet infusion in case of hemophilia: substituti-on of coagulation factors

Alteplase stop Alteplase individual measures depending on coagulation status

Phenprocoumon

(INR aim <1.5)

Prothrombin complex concentra-te

+ vitamin K

Prothrombin dosage: 2400 U (if <50 kg bw: 30 U/kg bw)

Vitamin K dosage: if INR ≥ 1.5 → 10 mg i.v., then dosing depends on INR development; onset of drug effect after approx. 4-6 h

Heparin

(UFH/LMH) Protaminesulfate

1000 U protamine i.v. (1ml) to inactivate 1000 U of the heparin given within the previous 4 hours

beware of contraindications!

DOAC: Xa-inhibitors Prothrombin complex concentra-te

2400 IU

(if <50 kg bw: 30 U/kg bw)

Measure anti-Xa activity of DOAC before and afterwards

Idarucizumab 2 x 2.5 g idarucizumab bw as fast as possible; measure anti-IIa activity before and afterwards

DOAC: Dabigatran If Idarucizumab not available:

activated prothrombin complex concentrate

if anti-IIa activity is very high => consider hemodialysis

30-50 U/kg bw

12

Malignant infarcts General - usually 30° supine position - BD aim: MAP > 85 mmHg, sys < 220 mmHg - in case of imminent craniectomy: stop antiplatelet therapy - pneumatic compression stockings for prevention of deep vein thrombosis - as emergency medication until craniectomy considerable: - mannitol/hypertonic saline solution (dosage control mannitol via osmotic gap, hypertonic saline solution via Na and osmolality) - Hyperventilation Decompressive craniectomy - craniectomy if possible within 24-48h and before relevant neurological deterioration - critical phase with risk for neurological deterioration: 72-96h (rarely up to as late as 10d) - signs of rising ICP: decreasing consciousness, disturbance of pupillomotoric usually with dilatation in case of supratentorial swelling and miosis in case of infratentorial swelling, increasing paresis, new paresis ipsilateral, pathological breathing pattern, rhythmic disorders - possible practical approach: o general actions see above o strict clinical control and CT control o in case of beginning consciousness decrease or other signs of rising ICP with corresponding increase of edema, craniectomy as early as possible o in very young patients and predictable course (very large infarcts) prophylactic craniectomy

Malignant infarctions of the middle cerebral artery territory

Predictors for malignant infarction: young patient, persistent vessel occlusion, early midline shift ≥ 4mm, critical infarct volume dependent upon age/atrophy but >>80ml or >1/2 media territory, additional infarction in anterior– or posterior territory

Indications for craniectomy: 1. usually < 60 years, in rare cases up to 70 years 2. symptom onset within the last 24 h (in exceptional cases this may be longer) 3. infarction of at least half of the middle cerebral artery territory 4. consent of patient or family 5. no contraindication for intervention Contraindications 1. Bilateral fixed pupils and coma 2. More than 3 of the following unfavorable prognostic factors: a. age >50 years b. infarction extends beyond the middle cerebral artery territory c. unilateral dilated pupil d. GCS <8 3. severe comorbidity; severe preexisting disability

Malignant cerebellar infarctions

Predictors for malignant infarction: young patient, persistent vessel occlusion, bilateral infarction, the size has less predictive value because small infarcts may induce large edema Indications for craniectomy 1. neurological signs of progressive increasing pressure in the brainstem 2. imaging shows space occupying infarction 3. consent of patient or relatives Contraindications 1. clinical or imaging signs of severe irreversible brainstem damage 2. severe comorbidity, severe preexisting disability

Daily checklist—visiting stroke patients 1 Neurological evaluation

NIHSS and symptom-orientated functional examination (results of physio-, ergotherapy, speech therapy)

2 Clinical internal evaluation Cardiac compensation Lung Abdomen Fever?

3 Monitoring Relevant rhythmic disorders (regarding reason, hemodynamic, cardiac pathology) BP target value? BP actual value?

4 Mobilization?

5 Nutrition, Dysphagia?

6 Laboratory controls ? (especially electrolytes, inflammation parameters, kidney, hemostasis)

7 Medication Antithrombotic therapy? Deep vein thrombosis prophylaxis? BP therapy?

DD Neurological deterioration ? Reinfarction ? Infarct localization: e.g. secondary deterioration more frequent in capsula interna or pontine infarctions ? Hemodynamic: BP associated? Associated with mobilization? ? Bleeding ? Rising ICP ? Epileptic seizure ? Infection ? Sedation and other less frequent causes

DD Myocardial inf. DD stress cardiomyopathy hsTnT-elevation in approx. 20% of ischemic stroke patients, DD: MI, stress cardiomyopathy (SCM), renal insuffi-ciency, hypertensive crisis, tachycardia, aortic dissection

Variable manifestation of SCM: hsTnT ↑ < regional hypokinesia < transient apical ballooning

- the extent of hsTnT-elevation does not discriminate between MI and SCM - SCM is an exclusion diagnosis - in case of doubt consider cardiac MRI (best discrimination) or ergometry

Possible practical approach in case of hsTnT-elevation: - clinical correlate for MI (repolarization disturbance a./o. angina pectoris) → coronary angiography - no clinical correlate: repeat ECG and hsTnT after 1-4h, if no ECG changes and few risk factors → more likely SCM; otherwise → cardiac MRI recommendable - in case of renal insufficiency: 3 measurements, if stable → hsTnT elevation due to renal insufficiency

14

TIA and minor stroke Perform MRI in clinical TIA patients whenever possible Pathologic definition of TIA: transient neurological deficit without diffusion restriction in MRI Time- dependent definition of TIA: transient neurological deficits of < 24h duration Definition of minor stroke: NIHSS < 4, symptoms stable or improving

ABCD2 score (stroke risk after TIA) Risk factor Points

Age ≥ 60 years 1

Systolic BP ≥ 140 or diastolic ≥ 90 1

Unilateral weakness with/without speech disturbance Speech disturbance without weakness

2 1

TIA duration ≥ 60 min TIA duration 10-59 min

2 1

Diabetes mellitus 1

6-7 points: high 2-days risk (8%) 4-5 points: intermediate 2-days risk (4%) 0-3 points: low 2-days risk (1%)

Treatment plan for patients with TIA

Frequent risk factors and causes

Ris

k fa

cto

rs (n

ot

dir

ectl

y ca

usa

l)

Spe

cifi

c ca

use

s (p

ote

nti

al c

ausa

tive

ris

k fa

cto

rs)

Hyp

erte

nsi

on

(>

140

/90

mm

Hg)

C

ard

ioe

mb

olis

m/p

arad

oxi

cal e

mb

olis

m

Dia

bet

es m

ellit

us

(fas

tin

g b

loo

d s

uga

r ≥7

mm

ol/

l, H

bA

1c

≥

6.5%

); im

pai

red

fas

tin

g gl

uco

se:

5.6

-6.9

mm

ol/

l

- A

tria

l fib

rilla

tio

n/fl

utt

er

Dys

lipid

emia

(LD

L ≥2

.5 m

mo

l/l,

TG >

5.2

mm

ol/

l, H

DL

<1.

0mm

ol/

l)

- M

yoca

rdia

l in

farc

tio

n

Fam

ily h

isto

ry (

m <

55

year

s, f

<65

yea

rs)

- O

ther

dys

rhyt

hm

ia (

e.g.

Sic

k-Si

nu

s, s

ilen

t at

riu

m)

Pre

-str

oke

/TIA

-

Val

vula

r d

isea

se

Smo

kin

g (i

ncl

. pip

e, c

igar

s)

- En

do

card

itis

Lack

of

ph

ysic

al a

ctivi

ty

(< 1

50m

in/w

eek

mo

der

ate

or

<75

min

inte

nsi

ve)

- P

FO/A

SD

Wei

ght

(BM

I >2

5, a

bd

om

inal

gir

th >

m:9

4cm

/f:8

8 cm

) La

rge

arte

ry d

ise

ase

Alc

oh

ol a

bu

se

(> 3

0 d

rin

ks/m

on

th; f

>15g

/d, m

>30

g/d

)

- A

rter

io-a

rter

ial e

mb

olis

m

Slee

p r

ela

ted

bre

ath

ing

dis

ord

ers

-

Ao

rtic

arch

em

bo

lism

Dep

ress

ion

-

No

n a

ther

oth

rom

bo

tic

vasc

ulo

pat

hy

(e.g

. FM

D)

Mig

rain

e w

ith

au

ra (

at le

ast

2 au

ras

in a

life

tim

e)

Oth

er c

au

ses

Pre

gnan

cy

- D

isse

ctio

n (

incl

. ao

rta)

Atr

ial t

ach

ycar

dia

-

Smal

l art

ery

dis

ease

(la

cun

ar <

1.5c

m +

BG

)

Tach

ycar

dia

at

rest

-

Vas

culiti

s

Incr

ease

d v

aria

bili

ty in

blo

od

pre

ssu

re

- C

hro

nic

infe

ctio

n (

in p

arti

cula

r H

IV, H

ep B

/C, s

yph

ilis)

Co

ntr

acep

tio

n

- Fa

cto

r V

Le

iden

/Th

rom

bo

ph

ilia/

anti

Car

dio

lipin

/Lu

pu

s an

tico

agu

lan

t

Ho

rmo

ne

rep

lace

men

t th

erap

y -

Acu

te c

oag

ula

tio

n d

iso

rder

s (e

sp. D

IC)

Acu

te in

fecti

on

(es

p. i

nfl

ue

nza

) -

Co

agu

lati

on

dis

ord

ers

asso

ciat

ed w

ith

tu

mo

r

Ch

ron

ic r

en

al in

suffi

cien

cy

- Fa

bry

dis

ease

-

Sick

le c

ell d

isea

se/o

ther

hae

mo

lyti

c cr

ises

-

Po

lygl

ob

ulia

/th

rom

bo

cyto

sis

-

Dru

gs

-

Iatr

oge

nic

(e.

g. p

eriin

terv

enti

on

al)

16

17

Diagnostic work-up MRI incl. MRA (for a reliable evaluation of the distribution pattern of acute/chronic infarction and deter-

mination of the etiology, esp. in view of a CEA!), if not possible, CT incl. CTA

consider neurovascular ultrasound

12-lead ECG

3x 7-day-ECG (minimum)

TEE (or poss. TTE)

Routine laboratory testing: Na, K, CRP, ESR, glucose, HbA1c, creatine, Urea, hs-Troponin T, CK, CK-MB, AST, ALT, GGT, TSH, pro-BNP, D-Dimer, complete blood count, coagulation state, blood lipids

DD according to medical history and physical examination ? Circumstance at onset (e.g.. Valsalva?) ? Positive familial history with onset < 40 years (Fabry, Coagulopathy) ? < 50 years, previous art/ven thrombosis, abortion (anti-Phospholipid syndrome) ? Throat/neck/eye pain, Trauma (Dissection ICA/VA) ? Headache (vasculitis), thunderclap headache (reversible vasoconstriction syndrome) ? Heart murmurs (endocarditis, valvular calcification) ? Angina pectoris (acute or in the past) ? Acute chest/back pain (aortic dissection!, coronary syndrome) ? Peripheral vascular examination incl. BP-difference left-right (aortic dissection) ? Skin lesions (septic emboli, Fabry: angiokeratoma, Sneddon: Livedo racemosa)) ? Vision disturbance + hearing disturbance (Susac`s syndrome => corpus callosum affected?) ? Signs for systemic rheumatic disease ? B symptoms ? Acute or chronic infection

Embolic stroke of

unknown origin

Known cause

Distribution on MRI:

1 vascular territory

Distribution on MRI:

Multiple vascular

territories

Small, multiple/recurring

ischemic lesions

Large/cortical lesions

Arteriogenic

embolism ?

Cardiogenic embo-

lism? D-Dimer ↑

frequent

Paraneoplastic

coaguloathy?

D-Dimer frequently ↑↑

Coagulopathy ?

Aortic arch embolism?

Prolonged

ECG monitoring

Cardiac MRI?

Laboratory tests (phospholipid: repeat after 3 months)

Lupus-anticoagulant, anti-cardiolipin, anti-2GPI

APC resistence (Factor V), protein C/S

< 50 years

Embolic stroke of

undetermined source Cause still unknown:

Tumor screening

CTA/MRA

Plaque-MRI/-CT

Secondary prevention Antiplatelet agents/(D)OAC

IVT, bridging, Urokinase i.a. Mechanical thrombectomy

First 24hr

For 24 hours no antiplatelet aggregation agents, no LMWH/no heparin

usually 500mg aspirin during angiography usually prophylactic LMWH immediately

After 24hr

After 24 hours and exclusion of cerebral haemorrhage (CT/MRI) Depending on the indication: - aspirin or clopidogrel (possibly as loading-dose) - aspirin+dipyridamole (Asasantin®) in high risk patients - aspirin + clopidogrel in case of symptomatic intracranial stenosis for 3 months - (D)OAC in case of: — atrial fibrillation (primarily DOAC) — cardiac thrombi (consider DOAC) — extracranial dissection (no DOAC) — consider in case of recurrent TIA despite antiplate-let treatment

Depending on the indication: - aspirin or clopidogrel - aspirin+dipyridamole (Asasantin®) as an alternative to clopidogrel in high risk patients - aspirin + clopidogrel in case of symptoma-tic intracranial stenosis for 3 months - (D)OAC in case of AF (time to start see below)

In case of imminent space-occupying brain edema neurosurgeons should be immediately involved. If a craniec-tomy is considered possible, no administration of antiplatelets (see separate guidelines).

Instructions for the earliest initiation of (D)NOAC after stroke - possibly higher bleeding risk in case of basal ganglia (BG) infarction -the instructions assume the exclusion of hemorrhagic transformation and endocarditis and might have to be adapted TIA/smallest infarctions: immediate initiation or continuation of previously established (D)OAC Small infarction (≈ <40ml): initiation after 3d (with BG involvement 6d) or continue previously established (D)OAC Middle-sized infarction (≈ 40-100ml): initiation after 6d (with BG involvement 9d) after exclusion of hemorrhage in control-imaging. In case of occurrence of stroke under OAC with INR 2-3 or DOAC: normally change (see below) + begin immediately Large infarction (≈ >100ml): initiation after 12d (with BG involvement 15d) after exclusion of hemorrhage in control-imaging. Occurrence under (D)OAC: interruption for 10d, then change (s.u.) - highly embolic source of embolism (e.g. mechanical heart valve) immediate initiation of a therapeutic hepa-rinization except if infarction is very large (therapeutic heparinization for better control) - in case of hemorrhagic transformation, initiation usually after 2 weeks (following CT scan)

Stroke occurring under antiplatelet agents/N(OAC)

- occurence under aspirin: normally change to clopidogrel or aspirin+dipyridamole - occurence under clopidogrel: continue or consider asprin+dypirdiamol or aspirin + clopidogrel for 3 months - occurence under sufficient or insufficient OAC: change to DOAC - occurence under DOAC: substance class change (factor X-inhibitor <=> factor II-inhibitor)

Prevention of deep vein thrombosis - in case of IVT, bridging, Urokinase initiation: after exclusion of cerebral haemorrhage in the follow-up-imaging - after mechanical thrombectomy without IVT: as early as possible - under heparin Tc control at day 1, then every 3 days (HIT?, 4Ts Score) - pneumatic compression stockings may be an alternative to LMWH in case of contraindications for LMWH

≈40ml

≈100ml

Direct oral anticoagulants (DOAC) - indicated in strokes with evidence of non-valvular AF - - in cerebral venous thrombosis and dissection: phenprocoumon/acenocoumarol, no DOAC (only off label exceptionally possible) - not recommended in anti-phospholipid-antibody syndrome, paraneoplastic coagulopathy or non-valvular AF (valvular: rheumatic mitral stenosis/-regurgitation) - in case of known elevated GIT bleeding risk: preferable lower doses of DOAK especially in patients > 75 years

Factor II-inhibitor Factor X-inhibitors

Dabigatran (Pradaxa®)

Apixaban (Eliquis®)

Rivaroxaban (Xarelto®)

Edoxaban (Lixiana®)

General informa-tion

CI: Child-Pugh A-C

CI: Child-Pugh C CI: Child-Pugh B+C

CI: Child-Pugh C

Dose if CrCl ≥ 50 ml/min

2 x 150mg (≥ 80 years: 2x110mg)

2 x 5mg (2 x 2.5mg if two of the following criteria are fullfilled: ≥80 years, ≤60kg, crea-tinine ≥ 133 l/l)

1 x 20mg 1 x 60mg (1 x 30mg if bw < 60kg)

Dose if CrCl 30-49 ml/min

2 x 110mg 1 x 15mg 1 x 30mg

Dose if CrCl 15-29 ml/min

contraindicated not recommended not recommended

Dose if CrCl <15 ml/min

contraindicated not recommended contraindicated not recommended

Inductors (effect diminis-hed) (bold print: contraindication)

Rifampicin, St John's wort, carbamazepine

Rifampicin (edoxaban: dosage reduction not necessary), phenytoin, carbamazepine, phenobarbital, St John's wort

Inhibitors (effect enhanced) (bold print: contraindication)

Verampil, ketocona-zole, itraconazole, voriconazole, HIV-protease inhibitors, quinidine, droneda-rone, ciclosporin, tacrolimus, amioda-rone

Verapamil, ketoconazole, itraconazole, voriconazole, posaconazole HIV-protease inhibitors

T1/2 12-17h 9-14h 5-9h 10-14h

Set off time pre- operatively (in agreement with surgeon)

24h before 48h in case of large operations 4d with CrCl < 50ml/min

24h before 48h in case of large operations

24 h before 24h before

19

(A)symptomatic artery stenosis Criteria for the classification of a symptomatic carotid artery stenosis: - confirmation by a neurologist - very likely: proof of a plaque rupture with apposition thrombus in CT/MR-angiography - probable: internal carotid artery stenosis of at least 50% + typical stroke distribution pattern in MRI, with no other cause of the stroke (TEE/TTE and at least 24-hour ECG monitoring test) In general: CEA/stenting normally within the first two weeks after first symptoms but consider early treat-ment within 2-3 days - always high-dose statin therapy, for antiplatelet aggregation therapy see below - in case of large apposition thrombus therapeutic heparinization prior to CEA/stenting - in case of additional atrial fibrillation as long as anticoagulation is possible (depending upon infarct size): o CEA: begin aspirin 100mg 1d preoperatively, therapeutic heparinization until surgery after surgery: 14d aspirin 100mg + prophylactic heparin, then stop aspirin/heparin + begin (D)OAC o Stenting: normally N(OAC) + aspirin 100mg; start aspirin at least 1 day before intervention

ICA stenosis extracranial

in case of CEA: normally pre- and postoperative aspirin 100mg or clopidogrel 75mg monotherapy (stroke occurrence under aspirin or clopidogrel: consider aspirin 100mg + clopidogrel 75mg perioperatively) in case of stenting: preinterventional aspirin 100mg + clopidogrel 75mg (eventually loading dose); postinterventional aspirin 100mg + clopidogrel 75mg for at least 6 months

Stenosis of verteb-ral artery origin

Stenting normally only in case of failure of best medical treatment (including transient therapy with aspirin + clopidogrel) preinterventional aspirin 100mg + clopidogrel 75mg (possibly as loading dose) postinterventional aspirin 100mg + clopidogrel 75mg for at least 12 months

Intracranial artery stenosis

aspirin 100mg + clopidogrel 75mg for 3 months, then de-escalate to monotherapy + statin at a high dose (for example atorvastatin 80mg) Stenting should be performed only in exceptional cases and after failure of conservative therapy

Hyperperfusion syndrome: -after revascularization of hemodynamically relevant stenosis there is a danger of hyperperfusion syndrome - risk factors: high grade stenosis, bilateral stenosis, perioperative hypertension, diabetes, woman, > 75 years, reduced reserve capacity - clinically: headache, seizures, neurological deficits; risk: intracerebral hemorrhage - occurrence 12h-7d after revascularization → therefore BP should normally be kept < 140/100 mmHg postoperatively/postinterventionally - in case of pronounced edema poss. additional dexamathasone

Dissections - according to current data aspirin and OAC are propably comparable - in case of higher grade extracranial stenosis due to dissection or occlusions without large infarction or hemorr-hagic transformations consider OAC/therapeutic heparinizaton followed by OAC - OAC is generally contraindicated in case of intradural dissections or dissections extending intradurally (elevated risk for SAH) - in case of uncertain diagnosis with fat-suppressed T1 sequences in MRI: extend to regular diagnostic work-up after stroke - off-label use of DOAC can be considered in single cases if OAC is not adjustable

- duration of secondary prevention with aspirin/OAC: switch OAC to aspirin after 3-6 months, continue aspirin 100mg/d as long term prophylaxis

20

PFO If TEE/TTE and at least one 7d ECG is negative and RoPE score > 5, PFO occlusion can be considered. The decision should be made individually and RoPE score serves as orientation. Consider circumstances that may facilitate paradoxical embolsim (e. g. deep vein thrombosis, onset of neurological symptoms after valsalva maneuver, co-existence of atrial septal aneurysm or eustachian tube (increase possibly recurrent risk) and poss. psychological factors). Antiplatelet aggregation should be continued lifelong after occlusion of PFO.

RoPE score (risk of paradoxical embolism)

No hypertension 1 Age 18-29 5 Sum 0-3 0% PFO attributable risk

No diabetes mellitus 1 Age 30-39 4 Sum 4 38% PFO attributable risk

No stroke/TIA 1 Age 40-49 3 Sum 5 34% PFO attributable risk

Non-smoker 1 Age 50-59 2 Sum 6 62% PFO attributable risk

Cortical infarct localization 1 Age 60-69 1 Sum 7 72% PFO attributable risk

Age ≥ 70 0 Sum 8 84% PFO attributable risk

Sum 9 88% PFO attributable risk

Secondary prevention in special situations Myocardial infarction (sub)acute

- consider DOAC application for 3 months also without thrombus finding, esp. with embolic infarct distribution - stenting in patients with (D)OAC indication → (D)OAC + clopidogrel (preferable DOAC low dose), triple therapy in acute stroke only in exceptional cases (esp. in-stent-thrombosis, stent main stem) If AF is indication for (D)OAC: consider atrial appendage closure, afterwards only dual antiplatelet therapy STEMI: Coro immediately; NSTEMI: Coro as soon as clopidogrel or (D)OAC + clopidogrel is possible; Coro immediately in case of severe rhythmic disorders, hemodynamic instability, persistent pain

Detection of AF or atrial thrombus in patients taking aspirin + clopidogrel due to coronary stent

DOAC long-term therapy + month 1: clopidogrel, months 2-12: Aspirin; during month 1-12: low dose DOAC

Ventricular thrombus

(D)OAC for 3 months, then control TEE and consider change to antiplatelet therapy

Detection of AF in patients with previous intracerebral bleeding/other relevant bleedings

Atrial appendage closure

Severe heart failure with severe hypokinesia/akinesia

Consider DOAC, especially in case of embolic infarct distribution

Endocarditis

No antiplatelet therapy/heparin/(D)OAC; if valvular replacement is indicated, early operation seems to be beneficial

Pulmonary embolism

DOAC, beginn in dependence of infarct size; duration: 6 months in case of uniquely provocative factors (surgery, immobiliza-tion >48h, contraceptive use, pregnancy, long flight, plaster cast on leg), otherwise long-term therapy; PFO occlusion in case of long-term DOAC therapy not indicated, otherwise PFO closure also with low RoPE score

Paraneoplastic Coagulopathy

LMWH therapeutic dosage (2x/d, not 1x/d); OAC only if LMWH not tolerated; no DOAC

Risk factor treatment 5 important: hypertension, physical activity, nutrition, smoking, obesity Arterial hypertension

1st choice: combination ACE inhibitor + diuretics or sartan + diuretics; aim BP < 140/90 mmHg

Dyslipidemia

- no arteriosclerosis : target LDL-C levels: < 2.6 mmol/l - in case of symptomatic stenosis: high dose (e.g. Atorvastatin 80mg), target LDL-C levels: < 1.8 mmol/l - effective strength : fluvastatin < pravastatin < simvastatin < atorvastatin < rosuvastatin - alternatively in case of intolerance: ezetimib in case of only hypercholesterinemia, otherwise fibrate - combination therapy in case of missed target value with monotherapy: statin + ezetimib, fibrate + ezetemib

Sleep-apnea syndrome

- Treatment with CPAP/APAP/ASV indicated with 1. AHI ≥ 5/h in symptomatic SAS (preexisting sleepiness) 2. AHI ≥ 30/h also in asymptomatic SAS 3. AHI 5-29/h + relevant internal indications (e.g. severe heart failure, untreatable arterial hypertension)

22

Vasculitis examinations (most relevant clarifications, see DGN guidelines for complete list)

- history: thunderclap headache? B symptoms? other symptoms? stay abroad? impaired vision/hearing? - physical examination: internal, dermatological or rheumatic manifestations? - additional examinations: TEE, MRI with dark-blood-sequences, cerebral angiography, CT chest/abdomen - laboratory testing: blood culture, complete blood count, ESR, CRP, ANA, ANCA, dsDNS, rheumatoid factor, SS-A, SS-B, anti-phospholipid-ab, lupus-anticoagulant, drug screening, LDH, CK, creatinine, AST, ALT, TSH, coagula-tion state, C3, C4, protein electrophoresis - serology: hepatitis B, C, HIV, syphilis, Borrelia, VZV, HSV, Mycoplasma, Chlamydia, toxoplasmosis, cysticercosis - consider Quantiferon test, procalcitonin, cryoglobulins, ferritin, soluble Interleukin receptor, fluorescein angiography eyes - cerebrospinal fluid: microscopy, cytology, culture, VZV cerebrospinal fluid-serum-index, consensus-PCR fungus-bacteria/mycobacteria - biopsy brain (meninges+parenchyma)

23

Motor areas

Speech areas

Visual areas

Sensory areas

Functional systems

Subclavian artery

Common carotid artery

Internal carotid artery

Vertebral artery

V0

Basilar artery

V1

V2

V3

V4

Brachiocephalic trunk

Cervical segment

Petrous segment

Cavernous segment

lower

mid

upper

border: skull base

border: Entrance cavernous sinus

border: outlet cavernous sinus/

ramification ophthalmic artery

(from here on intradurally)

Ophthalmic artery

Supraophthalmic segment

24

External carotid artery

Anterior cerebral artery

Middle cerebral artery

Posterior cerebral artery

M1 M2 M3

Superior cerebellar artery

Lenticulostriatal branches

Posterior anterior cerebellar artery

Posterior inferior cerebellar artery

Anterior choroidal artery

Pontine arteries

Posterior communicating artery

Anterior communicating artery

Basilar artery

Vertrebral artery

Anterior spinal artery

A1

A2

P1 P2

25

Internal carotid artery

Medial pontine a. of basilar a.; branches of posterior cerebral artery

Lateral pontine a. of basilar a.

Lateral pontine a. of basilaris a. Anterior inferior cerebellar a.(Fig. 8: Superior cerebellar a.)

Collicular and choroidal posterior medial a. of posterior cerebral a., superior cerebellar a.

Superior cerebellar artery

Posterior inferior cerebellar a.

Anterior inferior cerebellar a.

Pons (Fig. 5-8)

10 9

8 7

6 5

4 3

2 1

Anterior spinal artery

Anterior spinal artery Vertebral artery Posterior inferior cerebellar a.

Posterior spinal artery

Vertebral artery

Medulla oblongata (Fig. 1-4)

Anterior inferior cerebellar a.

Superior cerebellar a.

Central posteromedial a. of posterior cerebral artery Collicular and choroidal posterior medial a. of posterior cerebral artery

Collicular and choroidal posterior medial a. of posterior cerebral a.

Mesencephalon (Fig. 9-10)

Posterior inferior cerebellar a.

Lateral pontine a. of basilaris a.

posterior medial a. of posterior cerebral a., superior cerebellar a.

Posterior inferior cerebellar a.

posterior medial a. of posterior

Middle cerebral a.

Middle cerebral a., lenticuolostriate branches

Anterior cerebral a.

Posterior cerebral a.

Anterior choroidal a.

Posterior communi-cating artery

Anterior communi- cating artery

Posterior choroidal a. (from P2)

Thalamogeniculata a. (from P2)

Thalamoperforating A. (from P1 or BA; if jointly main trunk: Percheron artery)

Internal carotid a.

27

Cerebral venous and sinus thrombosis - LMWH in therapeutic dosage: e.g. enoxaparin (1mg/kg bw, 2x/d) (a non-randomized study even showed superiority in respect to efficacy and hemorrhagic com-plications; especially in patients with congestion hemorrhage) - alternatively therapeutic heparinization (aPTT 1.5-2.5x baseline aPTT) particularly in patients with risk of craniectomy; switch to OAC in the course of time - off-label use of DOAC can be considered in single cases if OAC is not adjustable (a case series of dabigatran in SVT patients was positive)

- continue therapeutic heparinization/LMWH also after occurrence of congestion hemorrhages - IVT or mechanical recanalization in exceptional cases or in studies (e.g. TO-ACT) - in case of large hemorrhagic infarctions and threat of lateral restriction: decompressive cra-niectomy as early as possible without removal of hematoma or infarcted tissue

- duration of OAC 6 months (except in case of progredient thrombosis at follow -up MRI or known thrombophilia) - usually examination for coagulation disorders after stopping OAC

Therapeutic heparinization with unfractio-nated heparin - complete baseline coagulation status before start of therapeutic heparinization - if baseline aPTT is abnormal (normal: 26-37sec) or in case of extensive thrombosis, consult a hematologist and control anti-factor-Xa-activity (aim 0.3-0.6 U/ml) - usual aPTT aim: 1.5-2.5x baseline aPTT - strictly check thrombocytes every 2 days during the course of therapy (HIT? => 4Ts score) The following dosage scheme is for patients in the Inselspital with low bleeding risk. Depending on infarct size, the dosage should be reduced individually.

Therapy start

Bolus 60-70 U/kg (max. 5000U) i.v. continuously 12-15 U/kg/h (max. 1000 U/h)

Re-evaluation after 6h

aPTT Anti-Xa

< 35 sec < 0.2 U/ml Bolus 40 U/kg Increase infusion rate by 3 U/kg/h

Re-evaluation after 6h

36-45 sec 0.2-0.29 U/ml No bolus, increaase infusion rate by 1.5 U/kg/h

Re-evaluation after 6h

46-70 sec 0.3-0.7 U/ml No change Re-evaluation after 6h, then 1x/day

71-90 sec 0.71-1.0 U/ml Reduce infusion rate by 1.5 U/kg/h Re-evaluation after 6h

> 90 sec > 1.0 U/ml Pause infusion for 1 h then reduce by 2-3U/kg/h (if aPTT >200sec pause infusion for 2h)

Re-evaluation after 6h

Superior sagittal sinus Cortical vein

Inferior sagittal sinus

Superior anastomotic vein

(Vein of Trolard)

Transverse sinus

Sigmoid sinus

Jugular vein

Basal vein of

Rosenthal

Inferior anastomotic vein

(Labbe)

Middle superficial

cerebral vein

Superior petrosal sinus

Anterior & posterior

intercavernous sinus

Cavernosus sinus

Sinus sphenoparietalis

Ophthalmic V.

Vein of Galen

Internal cerebral vein

Straight sinus

29

31

Close your eyes

He‘s a chip off the old block.

Harm set, harm get.

HUCKLEBERRY

BASEBALL PLAYER

32

Glasgow Coma Scale Eye opening response 4 Spontaneously

3 To speech 2 To pain 1 No response

Best verbal response 5 Oriented to time, place, and person 4 Confused 3 Inappropriate words 2 Incomprehensible sounds 1 No response

Best motor response 6 Obeys commands 5 Moves to localized pain 4 Flexion withdrawal from pain 3 Abnormal flexion (decorticate) 2 Abnormal extension (decerebrate) 1 No response

Modified Rankin Scale (mRS) 0 No symptoms at all

1 No significant disability despite symptoms; able to carry out all usual duties and activities

2 Slight disability; unable to carry out all previous activities, but able to look after own affairs

3 Moderate disability, requiring some help, but able to walk without assistance

4 Moderately severe disability; unable to walk without assistance and unable to attend own bodily needs

5 Severe disability; bedridden, incontinent and requiring constant nursing care and attention

6 Dead

CHA2DS2-VASc-Score (stroke risk with atrial f.) Risk factor Points (N)

O A C I F >1 P O I N T

Sum Risk/year taking Aspirin

Congestive heart failure 1 0 0%

Hypertension 1 2 2.2%

Age > 75 2 3 3.2%

Diabetes mellitus 1 4 4.8%

Stroke/TIA/thromboembolism 2 5 7.2%

Vascular disease (heart, peripheral) 1 6 9.2%

Age 65-74 years 1 7 11.2%

Woman 1 9 12.2%

33

NIH Stroke Scale Points Category Explanation

Level of conscious-ness

0 Alert 1 Not alert, but arousable by minor stimulation 2 Not alert, requires repeated stimulation to attend. Or, ob-tunded and requires painful stimuli to make movements 3 Makes only reflexive posturing movements to repeated painful stimuli. Or, they are totally unresponsive

Orientation anarthria, intubation=1, coma=2

Ask the current month and the patient‘s age. 0 Answered both questions correctly 1 Answered one correctly 2 Answered neither question correctly or aphasia

Commands

Ask the patient to open/close the eyes and make a fist/relax the non-paretic hand. 0 Performed both correctly 1 Performed one correctly 2 Performed neither correctly

Best gaze uncooperative=1, coma=2

0 Normal 1 Partial gaze palsy = Conjugate gaze deviation that can be overcome with voluntary or reflexive activity 2 Forced deviation

Visual Fields not evaluable=0, neglect=1, coma=3, in case of aphasia, evaluate reaction

0 No visual loss 1 Partial hemianopia 2 Complete hemianopia 3 Bilateral hemianopia

Facial palsy coma=3

0 Normal 1 Minor paralysis (flattened nasolabial fold or mild asymmetry while smiling) 2 Partial paralysis (total or near total paralysis of lower face) 3 Complete paralysis of upper and lower face

Left: Motor arm coma=4

0 No drift, remains in position for 10 sec. after an initial dip 1 Jerks or drifts to an intermediate position without encoun-tering support before the full 10 sec. 2 Some effort against gravity. Drifts down before 10 sec. 3 No effort against gravity and the arm falls 4 No voluntary movement Right:

Left: Motor leg coma=4

0 No drift, remains in position for 5 sec. after an initial dip 1 Jerks or drifts to an intermediate position without encoun-tering support before the full 5 sec. 2 Some effort against gravity. Drifts down before 5 sec. 3 No effort against gravity and the leg falls 4 No voluntary movement Right:

34

NIH Stroke Scale (part 2) Points Category Explantion

Limb ataxia coma, aphasia, paralyzed=0

0 Absent 1 Present in one limb 2 Present in two limbs

Sensory bilateral loss=2, coma=2 aphasia=rather 1

0 Normal 1 Mild to moderate sensory loss, patient feels asymmetry between the two sides but is still aware of being touched 2 Severe or total sensory loss, patient is not aware of being touched on the face, arm, and leg

Best language Intubated patients should be asked to write, coma=3

0 No aphasia 1 Mild to moderate aphasia; some obvious loss of fluency or facility of comprehension without significant limitation on ideas expressed or form of expression 2 Severe aphasia; all communication is fragmentary; great need for inference, questioning, and guessing by the examiner 3 Mute or global aphasia; globally aphasic patients have no usable speech or auditory comprehension

Dysarthria coma=2

0 Normal 1 Mild to moderate dysarthria; patient can still be understood 2 Severe dysarthria; patients are either mute or speech is so slurred they cannot be understood out of proportion to any dysphasia that is present

Extinction and inattention coma=2

0 Absence of neglect 1 Inattention to one modality only (visual, tactile, auditory, spatial, or personal inattention) 2 Profound hemi-inattention or extinction to more than one modality; does not recognize own hand or orients only to one side of space

35