Delayed Cerebral Infarction Beyond Endoluminal Spasmolysis and Induced Hypertension
Conditions: Subarachnoid Aneurysm Hemorrhage, Cerebral Vasospasm After Subarachnoid Hemorrhage
Sponsor: Region Stockholm

“DElayed Cerebral Ischemia Beyond EndoluminaL 
spasmolysis and induced hypertension”  
(DECIBEL) 
 
NCT: Not assigned 
 
Date: 10/9/25 
 
 
 
 
 
 
 
 
 
 
 

1 Scientific Question  
By employing novel diagnostic strategies, can we establish better and individualized 
treatment goals and thereby improve outcomes in patients with severe cerebral vasospasm 
after subarachnoid hemorrhage?  
2 Background 
Subarachnoid hemorrhage (SAH) is the third most common cause of stroke. Survivors suffer 
from morbidity and reduced quality of life (1). With over 600 cases annually, SAH is the 
tenth most common intensive care diagnosis in Sweden (2). Despite adequate therapy, 
complications are common (3–5). Approximately 20-30% of patients suffer from cerebral 
vasospasm, a condition associated with "delayed cerebral ischemia" (DCI), which in turn is 
associated with poorer long-term outcomes (6). 
DCI is regarded as a neurological syndrome that arises between approximately day 4 and 14 
after SAH (7). The condition, which requires neurocritical care, leads to new cerebral 
infarctions (8). Underlying mechanisms are incompletely understood, but probable 
contributing factors include, among others, macro- and microvascular vasospasm, 
inflammation, and disturbances in cerebral autoregulation (9). 
DCI is the most important cause of morbidity after SAH (10,11). Its treatment is controversial 
as randomized studies are few and clear benefit has been difficult to demonstrate 
(1,12). Differences exist between centers regarding diagnostic strategies and treatment 
protocols, and there is a lack of established, evidence-based guidelines and consensus 
regarding which methods should be applied to evaluate treatment effect (13). 
In the intensive care patient, the clinical examination is often insufficient due to reduced 
consciousness caused by brain injury, sedation, or by a lack of patient cooperation. Therefore, 
multimodal neuromonitoring is warranted, employing biomarkers, invasive and non-invasive 
neuromonitoring, and serial radiological examinations. Individually or in combination, these 
can detect threatening or established injury such as DCI. 
Transcranial Doppler (TCD) is, in addition to clinical examination, a well-established, 
validated, and easily accessible screening method for detecting vasospasm in the brain's 
vessels, where changes in blood flow velocities can be measured with good reliability 
(14). With robotic TCD for continuous measurement, the procedure can be better 
standardized, and measurement errors and inter- as well as intra-rater variability minimized 
(15). 
Treatment methods for vasospasm/DCI are few and insufficiently studied. The most well-
established consist of pharmacological elevation of cerebral perfusion pressure and 
endovascular therapy with angioplasty or endoluminal spasmolysis (ES). ES often results in 
an angiographically demonstrable effect, but the duration of effect and outcome on both 
macro- and microvascular spasm as well as DCI and clinical outcome is 
unknown. Previously, improved flow velocities measured with TCD have been demonstrated, 
but without demonstrable clinical neurological improvement (16). 

Beyond oral nimodipine and neuroprotective intensive care, standardization and consensus 
are still lacking regarding which diagnostic and therapeutic methods should be 
applied. Guidelines for initiating, continuing, or terminating treatment vary both within and 
between centers, and subjective perceptions can become guiding factors. Long-term follow-up 
after endovascular treatment is lacking (17,18). 
In cases of vasospasm/DCI, elevation of cerebral perfusion pressure is often recommended, 
provided that baseline pressure is not elevated or heart disease hinders. Recommendations are 
based on convincing clinical results; however, larger positive or randomized studies are 
lacking (14). In a randomized study comparing induced hypertension against non-
hypertension, no difference in CBF between groups could be registered, as evaluated by CT-
perfusion (12). It has also been shown that there is no difference in ischemic burden when 
comparing direct versus incremental pressure elevation (21). Retrospectively, benefit from 
expanded invasive monitoring with improved clinical outcomes has been demonstrated for the 
patient group (19, 20). 
The degree of pressure elevation is up to the responsible physician to decide. Not 
infrequently, these patients carry cardiovascular comorbidities. Takotsubo cardiomyopathy or 
"cardiac stunning" is present in 5-10% of patients with SAH (22), which complicates the 
implementation of blood pressure elevation. 
It is unclear whether the favorable effects of pressure elevation in cerebral vasospasm can 
solely be attributed to increased flow or transmural pressure in the brain's vessels, or if the 
pharmacological treatment is wholly or partially affected by other variables such as increased 
stroke volume or cardiac output. Effect measures before, during, and after blood pressure 
elevation in severe cerebral vasospasm need to be studied with continuous TCD parallel to 
cardiac output monitoring and multimodal intracranial monitoring to better understand the 
link between regional blood pressure and blood flow as well as global circulation. 
For endovascular treatment in cerebral vasospasm/DCI, the support is even weaker, and it is 
recommended in cases where pressure elevation is considered insufficient (14). Randomized 
studies are lacking. Intervention consists of balloon dilation/angioplasty or endoluminal 
spasmolysis (ES), where consensus is lacking regarding drug choice and dosage as well as 
appropriate start time for treatment and treatment frequency. 
A limitation of this treatment is an expected short duration of effect, but currently, it is not 
known how long it is, nor how it should be monitored. Usually, ES is followed up with TCD 
the day after treatment, but such measurement lacks the conditions to provide information 
regarding how long the duration of effect existed, and therefore knowledge regarding the 
optimal frequency of treatment is lacking. 
At the transition from moderate to severe cerebral vasospasm, the flow velocity measured 
with TCD is a poor criterion for the degree of cerebral perfusion (23), and no specific 
threshold value for mean flow velocity (MFV) has been shown to accurately diagnose 
clinically significant angiographic vasospasm (24). Furthermore, TCD velocities quantify an 
associated phenomenon and possibly a surrogate marker (macrovascular vasospasm), which 
makes conclusions regarding the development of DCI in unconscious or sedated patients 
complex and likely requires expanded multimodal neuromonitoring to enable early diagnosis 
and treatment considerations. 

In a study by Albrecht et al., a majority (71%) of conscious patients with DCI improved after 
endovascular intervention (median number of interventions = 1, max = 14), while in the 
unconscious group, 83% of patients suffered deterioration with new ischemia, despite 
intervention. This discrepancy could possibly be due to a lack of sensitivity, or too long 
intervals between examinations with manual TCD, or alternatively depend on other causes 
such as microcirculatory dysfunction. Interestingly, TCD MFV increased in 37% of cases 
with new infarctions after intervention (25). The authors called for prospective studies 
specifically examining subgroups of patients, such as those with poor neurological 
status. Weiss et al. evaluated continuous intra-arterial nimodipine as a salvage endovascular 
procedure and were able to demonstrate an immediate increase in PBTO2 at the start of 
therapy, as well as an immediate decrease at the stop of treatment, and additionally clear 
reductions of manual TCD MFV values (pretreatment levels 139.0±46.3 cm/s) in a cohort of 
conscious and unconscious patients (26). 
In summary, diagnostic and therapeutic challenges in severe cerebral vasospasm and DCI 
after SAH are prevalent. A closer examination of the relationship between peri- and post 
interventional changes for continuous TCD MFV or derived indices, combined with oxygen 
saturation or oxygen tension, could provide a better understanding of the mechanism of action 
and duration of effect of pressure elevation and endoluminal spasmolysis in the most severely 
ill patients with cerebral vasospasm after SAH. Stronger evidence is necessary to standardize 
diagnostic and therapeutic strategies and to improve and individualize treatment for better 
outcomes in this patient group. 
3 Project Description  
3.1 Overall purpose and conditions 
The overall purpose of the research project is to characterize and better understand the disease 
course and treatment effects, including measurable duration of effect and potential link to 
outcome in severe cerebral vasospasm after subarachnoid hemorrhage. All clinical decisions 
and all treatment in the study patients occur entirely within the framework of ordinary care 
and practice. 
The patient group is usually very well-monitored. In addition to one or two ventricular drains, 
patients with a confirmed diagnosis of severe cerebral vasospasm often receive multiple 
catheters in the brain parenchyma's watershed areas, such as pressure monitors (with 
temperature measurement and monitors for partial pressure of oxygen or local saturation) and 
microdialysis catheters, often bilaterally. 
In attempts to answer the research questions, we intend to apply the following measurement 
methods: 
1. Continuous Transcranial Doppler (TCD) with Delica EMS 9D (CE-marked) (27). 
2. Capnodynamics, a non-invasive capnodynamic method for determining cardiac 
output via the patient's ventilator, Maquet Servo-I. The method is based on a 
periodically altered breathing cycle in the ventilator and is CE-marked for the purpose, 
validated, and shows good agreement with the golden standard (28,29). 

3. Continuous EEG with automated analysis (alpha power, alpha-variability, and 
alpha/delta-ratio). Automated detection algorithms and integration with other 
neuromonitoring appear promising (30). 
Otherwise, diagnostics and monitoring will occur within the framework of the department's 
clinical routine, as will the application of intraparenchymal cerebral catheters. No extra 
catheters or invasive procedures will take place within the framework of the study. The 
catheters Bowman® and Luciole® (both CE-marked) have the conditions to provide 
information on local blood flow and perfusion. Usually, two to three, sometimes more, MRI 
perfusion or CT-perfusion examinations are performed during the care period, which also 
gives a picture of local blood flow and perfusion in affected areas. 
Overall, the multimodal neuromonitoring is expanded and can provide us with new cerebral 
blood flow-related parameters and their relation to cardiac output. The project has the 
possibility to contribute to a better understanding of the condition's course and provide 
guidance for improved and individualized treatment of this patient group. 
3.2 Study Center  
The studies are conducted at the Neurontensive Care Unit, Karolinska University Hospital, 
Solna, Sweden. 
3.3 Study Period  
Patient inclusion is planned from December 2025, or as soon as the ethics application allows, 
and is planned to continue through December 2030.  
3.4 Study Registration  
The study will be registered on ClinicalTrials.gov or equivalent. 
3.5 Power Analysis  
The study consists of several prospective observational cohort studies intending to compare 
data from continuous monitoring with multiple resolutions against low-resolution 
information, where information regarding the natural variance is unknown. A guiding sample-
size calculation assuming a normal population with severe cerebral spasm has mean flow 
velocities in the middle cerebral artery of 200 cm/s +/- 20 cm/s and a detectable treatment 
effect of approximately 5% upon pressure elevation and endoluminal spasmolysis 
respectively, with alpha set to 0.05 and power 90%, yields a calculated sample size of 42 
individuals per treatment method. Given that some patients will be treated and studied 
regarding both methods, the study group does not necessarily need to be doubled. Given that 
many patients with risk for or established severe spasm will not develop a degree of spasm 
that according to clinical assessment requires endoluminal spasmolysis, over-recruitment will 
likely be necessary. We assess that, taking attrition into account, we need to recruit 
approximately 200 patients, or up to 42 completed patients per arm. This observational study 
with several sub-components is, however, fundamentally hypothesis-generating, as formal 
power analysis is problematic in a multifactorial environment. The study expects to be able to 
better inform future treatment RCTs. 

3.6 Specific Research Questions 
1. What does the flow profile in the brain's vessels look like measured with continuous 
TCD during ongoing endoluminal spasmolysis in patients with severe cerebral 
vasospasm? Is the flow profile dose-dependent or independent? Is it possible to 
demonstrate a correlation between changed blood flow velocities and radiological 
outcome regarding macrovascular and microvascular spasm (visual estimation, mean 
transit time (MTT), etc.)?  
2. Secondary questions: Are there correlations between radiologic treatment outcome 
and TCD flow velocities, intraparenchymal saturation and estimated cerebral blood 
flow (eCBF) or ischemic burden as determined by follow-up radiology, microdialysis 
or serial S100?  
3. What does the flow profile in the brain's vessels look like measured with continuous 
TCD before, during and after endoluminal spasmolysis in patients with severe 
cerebral vasospasm? How long is the duration of effect regarding changed flow 
velocities in the brain's vessels after intervention? Is it possible to demonstrate an 
attenuation of the treatment effect with TCD to inform about the appropriate time for 
further treatment?  
4. Secondary questions: Is there a correlation between duration of effect or effect 
attenuation measured with TCD with intraparenchymal saturation measurement, serial 
biomarkers like microdialysis or S100? Is there a correlation between duration of 
effect or effect attenuation measured with TCD with other neuromonitoring such as 
quantitative EEG (qEEG / Alpha/Delta-ratio)? 
5. What does the temporal/dynamic flow profile in the brain's vessels look like, 
measured with continuous TCD and intraparenchymal oxygenation/saturation 
measurement during and after elevation of the cerebral perfusion pressure in patients 
with severe cerebral vasospasm?  
6. Secondary questions: Is the effect of pressure elevation attenuated or improved over 
time measured with continuous TCD or intraparenchymal saturation? Is there a 
correlation between blood pressure level and flow profile measured with TCD and 
intraparenchymal saturation regarding the relationship to the brain's autoregulation 
window, determined with Pressure Reactivity Index (PRx)?  
7. What relative increase in cerebral perfusion pressure or what absolute cerebral 
perfusion pressures are necessary to optimize cerebral blood flow during pressure 
elevation in severe cerebral vasospasm, measured with continuous TCD and 
intraparenchymal saturation, microdialysis, and qEEG?  
8. Secondary questions: Can threshold levels regarding pressure/flow markers be 
identified? Does pressure elevation correlate to other desirable or undesirable systemic 
effects, such as impact on cardiac output, measured with capnodynamic method? At 
what pressure levels can the benefit/risk ratio be considered optimal based on an 
overall assessment?  
9. Can predictors be identified to provide guidance on individualized/optimal cerebral 
perfusion pressures or treatment strategies in severe cerebral vasospasm?  
10. In the early stage of cerebral vasospasm, can continuous TCD describe trends 
regarding the acceleration of flow velocities?  
11. Does the acceleration follow a linear course, and can a trend analysis be applied to 
guide when treatment such as pressure elevation or endoluminal spasmolysis should 
be considered/initiated?  

12. Secondary question: If the acceleration trend is non-linear, are there associations 
between acceleration measured with continuous TCD and other physiological, 
pharmacological, nursing, or patient-related factors?  
13. Are there correlations between dynamic flow profile in the brain's vessels, measured 
with continuous TCD and intraparenchymal oxygenation/saturation measurement after 
endoluminal spasmolysis and perfusion pressure elevation respectively?  
14. Do other clinically applied diagnostic modalities such as serum biomarkers, data from 
invasive brain monitoring (microdialysis, cerebral autoregulation (PRx), cerebral 
saturation, rCBF) and/or non-invasive such as continuous quantitative EEG, 
quantitative pupillometry, near infrared spectroscopy (NIRS), as well as infarction 
development on CT scan and blood flow velocities and transit time on MRI (4D-MR) 
provide associations with continuous TCD? 
3.7 Method 
In this research project, we intend to increase the state of knowledge in severe cerebral 
vasospasm/DCI to better diagnose and monitor onset and progress, and to study possible 
outcome measures during and after treatment. We will study time series of blood flow 
velocities and pulsatility index in the brain's vessels with continuous and manual TCD 
respectively to establish effect outcome and duration of effect in connection to the established 
treatment methods: elevation of cerebral perfusion pressure and ES. 
At pressure elevation, continuous TCD will be connected for measurement shortly before 
pressure elevation and measurement continues until the intended pressure level is reached and 
thereafter up to 12h after. If the patient has received intraparenchymal tissue saturation 
measurement or partial pressure measurement of oxygen, within the framework of clinical 
practice, these data will be included. The patient's cardiac output will be measured with a non-
invasive capnodynamic method through the ventilator. A corresponding study design is also 
planned for planned pressure reduction. 
At endoluminal spasmolysis, continuous TCD will be connected for measurement at the 
decision of treatment and continues during and up to 24h after treatment, to establish duration 
of effect regarding flow velocities according to the description in the questions 
above. Findings regarding blood flow velocities and duration of effect in cerebral vasospasm 
are primarily assessed as a proxy for the duration of effect regarding DCI. Additionally, we 
will link series of high and low-resolution information before, during, and after treatment with 
pressure elevation and endoluminal spasmolysis respectively, when such monitoring is 
established in the patient. 
We intend to seek correlation in time series from continuous TCD with outcome measures 
with other invasive and non-invasive modalities (see above), and infarction extent on CT and 
infarction extent, blood flow, transit times on MRI-perfusion, possibly 4D-MR. In this way, 
we can enable a differentiation between duration of effect on flow velocities in vasospasm 
measured with TCD and possible duration of effect regarding ischemic burden, i.e., 
DCI. Overall, the project provides conditions to further describe the treatment modalities 
pressure elevation and endoluminal spasmolysis respectively and can contribute to a better 
understanding regarding their therapeutic potential and guide better and individualized 
treatment. 
Primary Measurement Method: 

• 
Transcranial Doppler (TCD): Measurement of blood flow velocities and derived 
variables in the brain's vessels. Continuous, robotized TCD is the first choice, 
intermittent manual TCD is the second choice. This is the mandatory measurement for 
all patients. 
Secondary Measurement Methods (Multimodal Monitoring): 
• 
Neurological Monitoring: 
o Frequent clinical neurological examinations (in awake patients)  
• 
Neuromonitoring data: Available, already established invasive and non-invasive 
neuromonitoring data. This includes:  
o Quantitative EEG (including A/D ratio), Pupillometry, ICP, CPP, PRx, 
Cerebral microdialysis, Cerebral partial pressure of oxygen or local saturation, 
Local blood flow (rCBF). 
• 
Physiological monitoring data: 
o MAP, Cardiac output with capnographic method, HRV, ECG. 
• 
Imaging: 
o Angiographic data and intervention protocols (dose, location), Interventionist's 
subjective assessment of effect, Follow-up MRI- or CT-angiography. 
• 
Biomarkers (on clinical indication): 
o Brain injury markers: S100b and GFAP in plasma. Cardiac stress 
markers (specifically during pressure elevation): Troponin and pro-BNP. 
3.8 Project Plan  
The project aims to study the effect of two clinical treatments – endovascular 
spasmolysis and elevation of cerebral perfusion pressure – in patients suffering from 
severe vasospasm or local flow disturbances after acute SAH. The goal is to, with advanced 
supervision (multimodal monitoring), describe the treatments' effect size and duration on the 
brain's blood flow, as well as their possibility to reduce the risk of DCI after SAH. 
The project is a prospective observational study conducted in two steps: an initial pilot study 
followed by a larger cohort study with two arms. Since the treatments are acute measures 
often initiated during on-call hours, the project has a pragmatic approach rather than a strict, 
inflexible protocol. A combination of clinically available methods will be used to 
continuously monitor the patients before, during, and up to 12-24 hours after initiated 
treatment. 
Project Phases 
• 
Pilot trial (3–5 patients): Aims to validate the study's feasibility, test logistics 
regarding data collection, and get a first idea of how long after treatment TCD data 
needs to be collected to see if/when blood flow returns to a baseline level. 
• 
Subsequent prospective cohort study spasmolysis (goal 45-50 patients, 120-150 
measurement occasions). Aims to collect data from a larger patient group based on 
experiences from the pilot study. 
• 
Subsequent prospective cohort study pressure elevation (goal 100-110 patients 
where the spasmolysis group is expected to be included as a subgroup). 

Feasibility With the current frequency of spasmolysis at Karolinska University Hospital, and 
considering TCD is not anatomically possible on all patients, we estimate being able to 
include approx. 10-12 patients annually to the spasmolysis analysis. Each patient may 
undergo approximately 1–5 treatments. For the pressure elevation cohort, approx. 25 
patients/year are expected to undergo pressure elevation after aSAH at the department, most 
with some form of invasive intracranial monitoring. Both study arms assume that patients can 
be included and that data can be collected even at inconvenient hours, made possible by good 
coverage of research-active physicians and research nurses. 
3.9 Patient Selection Criteria 
Inclusion Criteria 
• 
Adult individuals, 18 years or older 
• 
Ongoing neurocritical care after subarachnoid hemorrhage  
• 
Source of bleeding secured surgically or endovascularly  
• 
Suspicion of developing or established severe cerebral vasospasm  
Exclusion Criteria 
• 
Expected survival less than 5 days, according to clinician's assessment. 
• 
Not possible to perform TCD (too dense temporal bone, unclear or unstable TCD 
signal)  
• 
Pregnancy  
3.10 Case Report Form – CRF  
eCRF is established with pseudonymized data on a platform approved by the Region and 
Karolinska Institutet, REDCap, an encrypted database with authentication and two-step 
verification. Patient key is stored in a local safe with a code within the operation's research 
premises where access is pass-card protected in two steps. 
• 
Baseline variables including age, sex, comorbidities, and medications. Time of 
hemorrhage, clinical condition at admission according to GCS and injury grading 
according to Hunt & Hess, Modified Fisher, WFNS, Vasograde, and other relevant 
SAH-related variables collected in the existing quality database for SAH at Karolinska 
University Hospital. 
• 
Baseline variables including cardiopulmonary data including biomarkers such as 
troponin and NT-proBNP, ECG & echocardiography for assessment of left and right 
ventricular function. 
• 
Daily ordinary laboratory analyses and patient-related data and findings in the 
intensive care Patient Data Monitoring System, such as, for example, drainage rate of 
CSF from ventricular drains, microdialysis values, blood gas analyses, end-tidal 
carbon dioxide, fluid balance, electrolyte levels. 
• 
Physiological monitoring via the software ICM+, including intracranial pressure 
(ICP), brain oxygenation (PbtO2), brain saturation (SbtO2), estimated cerebral blood 
flow (eCBF), flow velocities at continuous TCD, central temperature (brain and 
bladder), Pressure Reactivity Index (PRx), quantitative EEG (qEEG) including 
alpha/delta-ratio, ECG-analysis including heart-rate variability (HRV), pulse, intra-

arterial blood pressure, saturation (SaO2), ventilator settings including fraction of 
oxygen. 
• 
ICM+ annotation tools. Time-stamped changes in sedation, vasopressor or inotropic 
treatment, clinical or nursing intervention. 
• 
Procedure-related information regarding endoluminal spasmolysis including time of 
decision for treatment, time of treatment, choice of drug, dose, potential stent 
treatment. 
• 
Procedure-related information regarding endoluminal spasmolysis in the form of a 
questionnaire to the treating interventionist regarding treatment outcome including 
both subjective and objective parameters. 
• 
Procedure-related information regarding pressure elevation and pressure reduction 
respectively, including time of decision for treatment, time of initiation of treatment, 
choice of drug for treatment, baseline value regarding cerebral perfusion pressure, 
target pressure and time duration to reach target pressure, causes and extent of 
deviation from target pressure. 
• 
Procedure-related information and outcome at determination of cardiac output with 
capnodynamic method, cardiac output estimated through effective pulmonary blood 
flow (CO EPBF). 
• 
Relevant drug treatment, including sedatives, beta-agonists, vasopressors, inotropic 
drugs, antihypertensive drugs, cardiodepressive drugs, diuretics, and electrolytes. 
• 
Diagnostic basis for establishment and grading of cerebral vasospasm as well as 
associated phenomena such as cerebral salt wasting syndrome. 
• 
Daily symptoms, clinical signs, neurological assessment. 
3.11 Follow-up  
Extended Glasgow Outcome Scale (GOSE) questionnaire and/or assessment at 3, 6, and 12 
months respectively. When applicable; date of death. 
3.12 Planned Analyses  
Data will be presented descriptively as time series and by Granger causality analysis. Primary 
analysis will focus on describing the treatments' effect size and duration of effect. The 
association between treatment effect and ischemic burden (DCI) as well as relations to other 
collected parameters related to flow, metabolism, and injury will be evaluated. Extended 
analysis is expected to include dimensionality reduction of data with PCA and cluster 
methods, tree regressions, and other AI methods to identify composite patterns. Each patient 
will constitute their own cross-over control (comparisons are made before spasm, during 
spasm, and after treatment). 
4 Ethical Considerations  
Ethical application has been approved by the Swedish Ethical Review Authority, diary 
number 2025-05434-01. Many research subjects are unable to apprehend information or 
contribute to consent before inclusion. Consent with the patient is sought before inclusion 
when possible. In cases where the patient's condition does not allow consent, consultation 
occurs with the next of kin. This normally occurs before inclusion if the situation allows but 
shall be carried out at the latest the following day. Information regarding consent to the study 
is discussed at a separate meeting in a private room. 

We apply a an opt-out procedure, where patients who improve during the care period and are 
assessed to be able to apprehend information will be informed and asked about study 
participation retrospectively. Patients who cannot apprehend information in such a situation 
shall be assessed, if possible, at outcome follow-up and then given information and a request 
for participation. This conversation is held by a physician or research nurse. If the patient or 
relative opposes participation and wishes to withdraw from the study, the research subject is 
excluded. Already collected data is retained within the framework of the study, but no further 
data is then collected. Research data is handled and saved pseudonymized in a secure 
environment. Research data is presented at the group level without the possibility of 
identifying specific patients. 
This study has the conditions to add significant information regarding diagnostics and 
treatment of patients with severe cerebral vasospasm after subarachnoid 
hemorrhage. Improved and individualized treatment strategies have the possibility to limit 
infarction extent and secondary brain injury as well as improve functional neurological 
outcome. Study results have the possibility to also benefit patients with a lower degree of 
cerebral vasospasm as well as other cerebrovascular disease conditions. 
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