Berk Orakcioglu

Stroke magnetic resonance imaging within 6 hours after onset of hyperacute cerebral ischemia.

We studied the diagnostic and prognostic value of diffusion‐ and perfusion‐weighted magnetic resonancce imaging (DWI and PWI) for the initial evaluation and follow‐up monitoring of patients with stroke that had ensued less than 6 hours previously. Further, we examined the role of vessel patency or occlusion and subsequent recanalization or persistent occlusion for further clinical and morphological stroke progression so as to define categories of patients and facilitate treatment decisions. Fifty‐one patients underwent stroke magnetic resonance imaging (DWI, PWI, magnetic resonance angiography, and T2‐weighted imaging) within 3.3 ± 1.29 hours, and, of those, 41 underwent follow‐up magnetic resonance imaging on day 2 and 28 on day 5. In addition, we assessed clinical scores (on the National Institutes of Health Stroke Scale, Scandinavian Stroke Scale, Barthel Index, and Modified Rankin Scale) on days 1, 2, 5, 30, and 90 and performed volumetric analysis of lesion volumes. In all, 25 patients had a proximal, 18 a distal, and 8 no vessel occlusion. Furthermore, 15 of 43 patients exhibited recanalization on day 2. Vessel occlusion was associated with a PWI‐DWI mismatch on the initial magnetic resonance imaging, vessel patency with a PWI‐DWI match (p < 0.0001). Outcome scores and lesion volumes differed significantly between patients experiencing recanalization and those who did not (all p < 0.0001). Acute DWI and PWI lesion volumes correlated poorly with acute clinical scores and only modestly with outcome scores. We have concluded on the basis of this study that early recanalization saves tissue at risk of ischemic infarction and results in significantly smaller infarcts and a significantly better clinical outcome. Patients with proximal vessel occlusions have a larger amount of tissue at risk, a lower recanalization rate, and a worse outcome. Urgent recanalization seems to be of utmost importance for these patients. Ann Neurol 2001;49:460–469

Stroke MRI in Intracerebral Hemorrhage. Is There a Perihemorrhagic Penumbra

Background and Purpose— Cerebral ischemia has been proposed as a contributing mechanism to secondary neuronal injury after intracerebral hemorrhage (ICH). The search for surrogate parameters that allow treatment stratification for spontaneous ICH continues. We sought to assess the presence and prognostic effect of perihemorrhagic ischemic changes and hypoperfusion in a prospective stroke MRI study. Methods— We performed stroke MRI in 32 patients with hyperacute ICH (mean, 16.9±17.2 mL) within 6 hours after symptom onset (mean, 3.1±1.3 hours). Clinical data at baseline (National Institutes of Health Stroke Scale) and on day 90 (Barthel Index, modified Rankin Scale) were assessed. Perihemorrhagic perfusion- and diffusion-weighted imaging changes were assessed in a 1-cm-wide area around the clot. Results— Despite a mild perihemorrhagic mean transit time prolongation of 0.7±1.1 second, there were no significant perihemorrhagic apparent diffusion coefficient or mean transit time changes indicating irreversible ischemia or hypoperfusion. ICH size, time to imaging, or clinical severity at baseline or outcome were not reflected by changes of relative apparent diffusion coefficient or perfusion-weighted imaging. ICH size correlated with baseline clinical severity (r =0.51, P =0.005). There was a significant association (P =0.0494) and a significant negative correlation (r =−0.468, P =0.0103) of perihemorrhagic perfusion change with time from symptom onset not associated with ICH size. Conclusions— Perihemorrhagic hypoperfusion probably is a consequence of reduced metabolic demand (diaschisis) rather than a sign of ischemia. We found no evidence for a perihemorrhagic and potentially salvageable ischemic penumbra in hyperacute ICH. Further studies should address metabolic, toxic, apoptotic, and microvascular aspects.

Evidence Against a Perihemorrhagic Penumbra Provided by Perfusion Computed Tomography

Background and Purpose— Several recent studies analyzing perfusion changes in acute intracerebral hemorrhage fed the debate whether there is secondary ischemic tissue damage in the vicinity of intracerebral hemorrhage. We used perfusion CT to address this question. Methods— We examined 36 patients between 2001 and 2002 with acute intracerebral hemorrhage (within 24 hours after symptom onset). A subgroup of 8 patients was examined serially on day 1, between days 2 and 4, and after day 5. Nonenhanced CT images and maps of cerebral blood flow, cerebral blood volume, and time to peak were evaluated by region of interest analysis. Results— In comparison to the contralateral hemisphere, perfusion values were clearly reduced around the hematoma (relative values: cerebral blood flow 0.51, cerebral blood volume 0.62, time to peak 1.7 seconds). There was no difference in size between the area of reduced perfusion and the area of edema (5.17 versus 5.75 cm2, respectively) surrounding the hematoma. At time point 2, the edema grew significantly. Conclusions— In accordance with previous studies, we found reduced perfusion as well as edema surrounding acute intracerebral hemorrhage. Regarding ischemic tissue damage, we did not detect an initial mismatch between the perfusion deficit and the edema and therefore could not identify any tissue at risk of ischemia. We therefore interpret the reduced perfusion as a secondary phenomenon, ie, reduced oxygen demand of tissue damaged by pressure and clot components, not as the cause of any tissue damage associated with acute intracerebral hemorrhage.

Intracerebral Hemorrhage With Severe Ventricular Involvement Lumbar Drainage for Communicating Hydrocephalus

Background and Purpose— The objective was to analyze the feasibility of a lumbar drainage (LD) for a communicating malresorptive hydrocephalus in patients with supratentorial hemorrhage (intracerebral hemorrhage) accompanied by severe ventricular involvement (intraventricular hemorrhage) who required an external ventricular drain (EVD). Methods— In this retrospective study, 16 patients received an EVD and concurrent LD and were compared with 39 historical patients treated with EVD alone. The duration of required EVD and need for permanent ventriculoperitoneal-shunt were analyzed. Results— LD was inserted after 12 (4 to 18) days. In LD-treated patients, the LD was capable to replace repeated EVD exchanges, resulting in a shorter EVD-duration (12 versus 16 days) compared with patients treated with EVD alone. The overall duration of extracorporal cerebrospinal fluid drainage was longer (16 days EVD versus 21 days EVD+LD) and the frequency of ventriculoperitoneal-shunt lower (18.75% versus 33%; P<0.03) in LD-treated patients. Conclusion— Our data suggest that LD is safe and feasible for treatment of nonpersistent communicating hydrocephalus after intracerebral hemorrhage. After adequate treatment of the occlusive hydrocephalus using an EVD in the acute phase, LD discloses an alternative for further extracorporal cerebrospinal fluid drainage.

Brain tissue oxygen monitoring and hyperoxic treatment in patients with traumatic brain injury.

Cerebral ischemia is a well-recognized contributor to high morbidity and mortality after traumatic brain injury (TBI). Standard of care treatment aims to maintain a sufficient oxygen supply to the brain by avoiding increased intracranial pressure (ICP) and ensuring a sufficient cerebral perfusion pressure (CPP). Devices allowing direct assessment of brain tissue oxygenation have showed promising results in clinical studies, and their use was implemented in the Brain Trauma Foundation Guidelines for the treatment of TBI patients in 2007. Results of several studies suggest that a brain tissue oxygen-directed therapy guided by these monitors may contribute to reduced mortality and improved outcome of TBI patients. Whether increasing the oxygen supply to supraphysiological levels has beneficial or detrimental effects on TBI patients has been a matter of debate for decades. The results of trials of hyperbaric oxygenation (HBO) have failed to show a benefit, but renewed interest in normobaric hyperoxia (NBO) in the treatment of TBI patients has emerged in recent years. With the increased availability of advanced neuromonitoring devices such as brain tissue oxygen monitors, it was shown that some patients might benefit from this therapeutic approach. In this article, we review the pathophysiological rationale and technical modalities of brain tissue oxygen monitors, as well as its use in studies of brain tissue oxygen-directed therapy. Furthermore, we analyze hyperoxia as a treatment option in TBI patients, summarize the results of clinical trials, and give insights into the recent findings of hyperoxic effects on cerebral metabolism after TBI.

Intracranial dermoid cysts: variations of radiological and clinical features

BackgroundIntracranial dermoid cysts are uncommon, and their clinical features as well as surgical management differ from patient to patient. Dermoids are generally benign lesions, but may cause spontaneous complications such as meningitis and/or hydrocephalus due to rupture and epileptic seizures depending on their location. Little has been reported about characteristic imaging findings with resulting therapeutic considerations, and only a few reports exist about associated hydrocephalus. Imaging modalities have changed and can facilitate differential diagnosis and follow-up if applied correctly. In this paper, we attempt to contribute our clinical experience with the management of dermoid cysts.Patients and methodsThe charts of five men and two women with intracranial dermoid cysts were retrospectively reviewed. The patients were treated between September 1993 and September 2006. Selected patients are presented in detail.ResultsTumour location, size and radiographic characteristics varied in each patient. Clinical presentations comprised focal neurological deficits as well as epileptic seizures, persistent headache, mental changes and psycho-organic syndromes. One patient underwent delayed ventriculo-peritoneal shunting after ruptured fatty particles caused obstructive hydrocephalus. Despite dermoid rupture into the subarachnoid space, three patients never developed hydrocephalus. Diffuse vascular supra-tentorial lesions were seen in one patient as a result of aseptic meningitis. Diffusion-weighted imaging (DWI) hyperintensity in dermoids is related to decrease of water proton diffusion and should be used for both the diagnosis and follow-up of this lesion.ConclusionAlthough dermoid cysts are known to be benign entities per se, their rupture can cause a wide range of symptoms including aseptic meningitis and/or hydrocephalus. This may be due to intraventricular obstruction and/or paraventricular compression. While rupture does not necessarily bring about hydrocephalus, radical removal of the tumour and close monitoring of ventricular size is required. Although not widely recognised as such, DWI is considered to be a useful imaging modality in the diagnosis and follow-up of dermoids.

Evolution of early perihemorrhagic changes:Ischemia vs. edema : An MRI study in rats

OBJECTIVES Cerebral ischemia has been proposed as a contributing mechanism to secondary neuronal injury after intracranial hemorrhage (ICH). The search for surrogate parameters that allow treatment stratification for spontaneous ICH continues. We aimed to examine perihemorrhagic ischemic changes with an animal experimental MRI study. METHODS A high field MRI compatible setup for male Wistar rats was established using a double injection model. ICH was stereotactically placed into the right basal ganglia of 29 Wistar rats. Coronal T2-WI, T2*-WI and DWI were generated with a 2.35 T animal MRI scanner 15 min, 60 min and 210 min after ICH. Clot signal characteristics, clot volumes and normalized ADC values were analyzed in four hematoma regions (core, periphery, outer rim, healthy ipsilateral tissue) in all sequences. RESULTS T2*-WI and DWI reliably demonstrated ICH in 100% with only small deviation from the applied volume (-20% to +26%) whereas T2-WI failed to conspicuously show ICH. There were no perihemorrhagic ADC decreases consistent with ischemic cytotoxic edema but a mild vasogenic edema surrounding the ICH could be observed. CONCLUSION T2*-WI and DWI are accurate for the diagnosis of hyperacute ICH. According to serial and crossectional ADC analysis, there is no hint towards the existence of a perihemorrhagic ischemic area that might be saved by early intervention. Future studies should focus on perfusion and metabolic/neurotoxic studies of this particular area and neurotoxic properties of the surrounding edema.

Evaluation of a novel brain tissue oxygenation probe in an experimental swine model.

BACKGROUND: Cerebral microdialysis, cerebral blood flow, and cerebral oxygenation (PbrO2) measurements using intraparenchymal probes are widely accepted as invasive diagnostic monitoring for early detection of secondary ischemia. OBJECTIVE: To evaluate a novel PbrO2 probe for continuous and quantitative oxygenation assessment compared with the existing gold standard PbrO2 probe. METHODS: In 9 pigs, 2 PbrO2 probes (Neurovent-TO vs Licox) were implanted into the subcortical white matter. An intracranial pressure probe was inserted contralaterally. The PbrO2 probes were tested during (1) baseline measurements followed by (2) hyperoxygenation (fraction of inspired oxygen [Fio2] = 1.0), medically induced (3) hypo- and (4) hypertension, (5) hyperventilation, (6) tris-hydroxymethylaminomethane application, and (7) hypoxygenation (Fio2 < 0.05). For statistical analyses, Bland-Altman plots were used. RESULTS: The Neurovent-TO probe is easy to handle and does not need a specific storage or calibration. Bland-Altman analyses revealed good comparability of both technologies under baseline conditions (meandiff 2.09 mm Hg, standard deviation 0.04 mm Hg, range 1.98-2.20 mm Hg), but measurement dynamics during hyperoxygenation (Fio2 = 1.0) revealed significantly different profiles, eg Neurovent-TO probe reached up to 1.53-fold higher PbrO2 values than the Licox probe. During hypoxygenation (Fio2 < 0.05), the Neurovent-TO probe detected the hypoxic level of 8.5 mm Hg 1.5 minutes earlier than did the Licox probe. All other maneuvers showed similar responses in both technologies. CONCLUSION: The Neurovent-TO PbrO2 device comparably measures PbrO2 under most conditions tested compared with the Licox device. The Neurovent-TO is more sensitive to rapid Fio2 changes. Further studies are necessary to clarify these differences. It is questionable whether existing knowledge of Licox tissue oxygenation, ie, hypoxic threshold, can be directly transferred to the Neurovent-TO.

Telemetric ICP Measurement with the First CE-Approved Device: Data from Animal Experiments and Initial Clinical Experiences

The objective was to evaluate the qualification of the new telemetric intracranial pressure (ICP) measurement (t-ICP) device Raumedic(®) NEUROVENT P-Tel and S-Tel. The proof of concept was examined in a pilot animal study measuring intraperitoneal pressure with a telemetric and a conventional ICP measurement probe at five rates for 1 h each. Moderate external pressure load allowed measuring values between 0 and 40 mmHg. To estimate long-term performance 18 t-ICP devices were implanted subdurally or intraparenchymally into minipigs. Reference measurements were performed regularly using conventional ICP probes. From the short-term as well as from the long-term perspective t-ICP proved to have excellent dynamic ICP signal components perception (e.g. pulse amplitude). Some zero drift of static ICP was found, ranging between 5 and 8 mmHg. While all telemetric, intraparenchymal probes kept their functionality throughout the follow-up, 33% of the subdurals failed for reasons detailed in another paper. Raumedics NEUROVENT(®) P-Tel/S-Tel proved to provide reliable data over periods of up to 18 months. Minor zero drift can be well tolerated as the dynamic ICP signal is measured with excellent stability. Clinicians should focus more on such ICP dynamic signal information than on static ICP when using the device over longer follow-up periods.

Intracranial haemorrhage in patients treated with direct oral anticoagulants

INTRODUCTION Direct oral anticoagulants (DOAC) are increasingly used for the prevention and treatment of thromboembolic events. However, only little evidence is available regarding the management of patients who are treated with DOAC and present with potentially life-threatening intracranial haemorrhage. Herein, we describe our experience with respective patients treated at our institution. METHODS We retrospectively analysed all consecutive patients with DOAC intake and intracranial haemorrhage treated at our institution from 09/2011 to 03/2015. Patient characteristics were analysed with specific focus on results of laboratory studies, treatment modalities and patient outcomes. Findings were compared between survivors (SV) and non-survivors (NSV) on day 30 after admission. RESULTS A total of 55 patients were identified. The 30-day mortality rate in this patient cohort was 20.0%. Neurosurgical procedures were carried out in 37 patients (67%). Median values of international normalized ratio (INR) did not differ significantly between SV (1.11) and NSV (1.09). Renal function was significantly lower in NSV (median serum creatinine: 115μmol/l) than in SV (median serum creatinine: 69μmol/l; p<0.05) and all patients with serum creatinine levels >125μmol/l died during in-hospital treatment. Pro-haemostatic therapy with prothrombin complex concentrates (PCC) had no effect on INR in repeated measurements. CONCLUSION Our experience demonstrates that successful neurosurgical management of patients with intracranial haemorrhage and DOAC intake is feasible. However, drastic deterioration was observed in some patients, particularly when impaired renal function was present. The role of pro-haemostatic therapy with PCC is unclear. These findings underscore the urgent need of improving treatment modalities for these patients.