Martin Furtner

The osteoprotegerin/RANK/RANKL system: a bone key to vascular disease

Owing to the common coincidence of osteoporosis and vascular disease, pathophysiological links between both disorders have long been sought. The osteoprotegerin (OPG)/receptor activator of NF-κB (RANK)/receptor activator of NF-κB ligand (RANKL) cytokine network, a key regulatory system in bone homeostasis, has been implicated recently in vascular calcification, changes in matrix composition and diabetic macroangiopathy, aortic aneurysm development, heart failure and, most importantly, advanced atherosclerosis, plaque destabilization and manifestation of cardiovascular diseases. The concept of an active role of RANKL and OPG in vascular pathophysiology is intriguing and is gaining increasing support from both epidemiological and basic research. OPG serum level is considered to be a stable and reliable indicator of the overall activity of the OPG/RANK/RANKL axis and may find application as a biomarker of vascular risk and prognosis. RANKL in turn may be a suitable target for novel therapies. Pharmacological strategies for specific interference with the OPG/RANK/RANKL axis are currently being developed and evaluated in osteoporosis therapy.

REM sleep behavior disorder in 703 sleep-disorder patients: the importance of eliciting a comprehensive sleep history.

OBJECTIVES The aim of our study was to evaluate the frequency of REM sleep behavior disorder (RBD) in a mixed sleep laboratory population and to assess potential associations. Moreover, we investigated referral diagnoses of patients subsequently diagnosed with RBD and assessed the frequency of incidental RBD. METHODS Charts and polysomnographic reports of 703 consecutive patients comprising the full spectrum of ICSD-2 sleep disorders [501 males, 202 females; mean age, 51.0+/-14.1 years (range: 10-82 years)] were carefully reviewed. The vast majority of patients were adults (98.7%). Patients were categorized into those with and without RBD. For associations, all concomitant sleep and neurological diagnoses and medications were evaluated. RESULTS Thirty-four patients (4.8%) were diagnosed with RBD (27 men; 7 women, mean age, 57.7+/-12.3 years). RBD was idiopathic in 11 patients (1.6%; 9 men) and symptomatic in 23 patients (3.3%; 18 men) secondary to Parkinsonian syndromes (n=11), use of antidepressants (n=7), narcolepsy with cataplexy (n=4), and pontine infarction (n=1). Six out of 34 patients were referred for suspected RBD, 20 reported RBD symptoms only on specific questioning, and 8 patients had no history of RBD but showed typical RBD behavioral manifestations in the video-polysomnography. Logistic regression analysis revealed significant associations between RBD and the presence of Parkinsonian syndromes (odds ratio [OR] 16.8, 95%CI: 6.4-44.1; P<0.001), narcolepsy with cataplexy (OR 10.7, 95%CI: 2.9-40.2; P<0.001), SSRI use (OR 3.9, 95%CI: 1.6-9.8; P=0.003), and age (OR 1.5/10-year increase, 95%CI: 1.0-2.0; P=0.039). CONCLUSION In this population of 703 consecutive sleep-disorder patients, RBD was uncommon. Its etiology was predominantly symptomatic. The majority of RBD patients reported RBD symptoms on specific questioning only, underlining the importance of eliciting a comprehensive sleep history for the diagnosis of RBD.

Cerebral vasoreactivity decreases overnight in severe obstructive sleep apnea syndrome: A study of cerebral hemodynamics

BACKGROUND OSAS has been associated with surrogate markers of atherosclerosis and is a known risk factor for stroke. However, there is limited data on the effects of recurring apneas in severe OSAS on cerebral circulation and their consequences on cerebrovascular reactivity and compliance. OBJECTIVE To evaluate cerebral blood flow velocity (CBFV) changes and vascular compliance in patients with severe obstructive sleep apnea syndrome (OSAS) using transcranial Doppler sonography (TCD) and cerebral pulse transit time (PTT). METHODS Seven patients (1 woman, 6 men, mean age 57.4 years) with severe OSAS underwent polysomnography at the sleep laboratory of the Neurology Department of Innsbruck Medical University. TCD was performed continuously during the whole night using a pulsed wave probe and was co-registered with routine polysomnography. Cerebrovascular reactivity was assessed by calculation of apnea and hypopnea-related CBFV changes. Arterial compliance was characterized by PTT derived from phase difference analysis between ECG and TCD signals. Sleep time was dichotomized into periods with high density of consecutive respiratory events (CRE) vs. periods with low density of consecutive respiratory events (non-CRE). TCD measurements of CBFV showed a regular, undulating pattern with flow minima immediately before apneas or hypopneas and maxima closely after their termination, reciprocally to peripheral O(2) saturation. CBFV reactivity was significantly diminished in CRE compared to non-CRE periods. PTT phase differences were reduced in non-CRE, and even more so in CRE periods, compared to initial wake phases. CONCLUSION We found severe disturbances of cerebrovascular reactivity in OSAS patients. Our data demonstrate loss of vasoreactivity and increase of arterial stiffness, indicated by CBF hyporeactivity and PTT reduction, especially during CRE periods. These changes are likely to impair cerebral circulation and may be detrimental to the endothelium.

Basilar Artery Dissection: Series of 12 Consecutive Cases and Review of the Literature

Background: Current knowledge on primary or isolated basilar artery dissection (IBAD) is limited to case vignettes and small patient series. Objective: To delineate the frequency and clinical presentations of IBAD along with short-term outcome, specific prognosis and targeted management. Methods: Data were derived from a series of 12 consecutive patients and a review of 88 cases reported in the literature. In all the cases, the dissection was confined to the basilar artery. Results: Disease incidence was estimated at 0.25 per 100,000 person-years. IBAD accounted for roughly 1.0% of all subarachnoid hemorrhage events and for no less than 10.5 and 4.5% of posterior circulation and brain-supplying artery dissections, respectively. The main clinical presentations were subarachnoid hemorrhage (46%) and posterior circulation brain ischemia (42%). Subarachnoid hemorrhage typically manifested at a higher age than brain ischemia (mean age, 48.9 vs. 41.4 years) and was more prevalent among women. Rebleedings related to pseudoaneurysm formation in patients with subarachnoid hemorrhage and recurrent ischemia in stroke patients were common in the acute phase (26.1 and 33.3%, respectively) but were rare in the long term. The outcome was generally favorable in stroke patients but variable in subarachnoid hemorrhage (case fatality rate, 21.7%). The mainstay of therapy for subarachnoid hemorrhage related to IBAD was endovascular occlusion of the aneurysm pouch whereas stroke patients were usually put on anticoagulants. Conclusions: IBAD is probably an underrecognized disease with heterogeneous clinical presentation and prognosis. It should be considered as a differential diagnosis in peritruncal subarachnoid hemorrhage, classic subarachnoid hemorrhage and posterior circulation stroke, especially in young individuals. Case management is challenging and has to be tailored to each patient.

Iatrogenic Creutzfeldt–Jakob disease 22 years after human growth hormone therapy: clinical and radiological features

Creutzfeldt–Jakob disease (CJD) is a human transmissible spongiform encephalopathy or prion disease. Although CJD is most frequently sporadic, numerous acquired or iatrogenic CJD (iCJD) cases have been reported, about half of which are attributable to prion-contaminated human growth hormone (hGH) preparations.1 Cadaveric hGH was provided by public and commercial sources up to 1985, when recombinant GH became available. Incubation periods of hGH-iCJD peak at a median of 12 (range 5–30) years after exposure.2 3 We report the first Austrian case of hGH-associated autopsy-proven iCJD and discuss clinical features and serial magnetic resonance imaging (MRI) findings. ### Clinical history A 39-year-old man presented with right-sided clumsiness and dysaesthesia, which had started in his leg 3 weeks prior to admission and had spread to his right arm. No impairment of cognitive function and no involuntary movements were present. There was no family history of neurological disease. The patient had been healthy until the age of 11 years, when progressive obesity and growth impairment had been noticed and a diagnosis of Cushing syndrome had been made. The patient moved to Austria at the age of 15 years (1982) and was subsequently diagnosed with a hormone-producing pituitary adenoma, which was removed by transsphenoidal hypophysectomy. The frontal skull base defect was covered with autologous connective tissue (fascia lata). Due to persistent Cushing syndrome symptoms, bilateral adrenalectomy was performed. To promote body growth (height <3rd percentile), he received commercially manufactured cadaveric hGH (Crescormon®, Kabi Pharma, now discontinued) from September 1984 (2 IU IM three times per week, which was later reduced to 2 IU IM twice a week). The treatment was continued until November 1985 …

Fibrokartilaginäre Embolie des Rückenmarks

ZusammenfassungDie spinale fibrokartilaginäre Embolie (FKE) ist eine seltene Ursache für ischämische Rückenmarksschädigungen. In der vorliegenden Arbeit wird der Fall eines 13-jährigen Patienten mit wahrscheinlicher posttraumatischer FKE in Anamnese, Klinik, differenzialdiagnostischer Aufarbeitung und Verlauf geschildert. Die Diagnose einer FKE als Ursache eines akuten Querschnittssyndroms ist in der Regel nur per exclusionem möglich. Ein möglicher Hinweis auf das Vorliegen einer Rückenmarksischämie ist neben einem Trauma in der Anamnese der Nachweis eines Wirbelkörperödems angrenzend an die spinale Läsion in der Magnetresonanztomographie. Zudem ist der Ausschluss systemischer Emboliequellen sowie anderer Rückenmarksschädigungen notwendig, um die Verdachtsdiagnose einer FKE stellen zu können. Des Weiteren werden mögliche Pathomechanismen, durchzuführende Untersuchungen, Therapie und Prognose in diesem Artikel besprochen.SummaryFibrocartilaginous embolism (FCE) of the spinal cord is a rare cause of ischemic myelopathy. We describe a 13-year-old patient with probable post-traumatic FCE. History of disease, clinical presentation, diagnostic workup, and disease course are outlined. Diagnosing FCE in the living often seems to be merely conjectural. Therefore, vertebral edema adjacent to the level of the spinal lesion is a possibly valuable diagnostic hint of spinal ischemia. Furthermore, exclusion of systemic embolism and other etiologies of myelopathy is necessary to corroborate the diagnosis of FCE. The postulated pathomechanism, diagnostic procedures, therapy, and prognosis of FCE are discussed in this article.

Prognostic Relevance of Limb Shaking in Symptomatic Carotid Artery Occlusion

Background: Internal carotid artery (ICA) occlusion, present in up to 15% of stroke patients, may cause low-flow transient ischemic attacks (TIAs) like limb shaking (LS) or retinal claudication (RC). Reliable data on the frequency of these phenomena and their potential prognostic relevance are still sparse. Aims: To provide more data about the frequency of low-flow TIA and investigate their influence on outcome. Material and Methods: Medical records of 260 consecutive patients with symptomatic ICA occlusion were carefully reviewed (survey period: January 2000 to December 2006). Baseline stroke severity and outcome at 90 days and in the long term were assessed. All patients were specifically questioned about symptoms of LS and RC, were exposed to bright light (pupillary testing) and carefully watched during testing of posture/gait and early mobilization. Results: LS, RC or both occurred in 28.6, 9.5 and 2.7%, respectively, of patients eligible for a thorough assessment of low-flow TIAs (n = 147). An adverse outcome was more likely in patients with LS than in those without at day 90 (modified Ranking Scale ≧4, 45.2 vs. 21.9%, p = 0.005) and in the long term (median, 37 months) (52.7 vs. 23.1%, p < 0.001). In a multivariable analysis, prognostic relevance was found to be independent of baseline stroke severity (National Institutes of Health Stroke Scale). There was also a tendency towards higher rates of recurrent stroke and TIA in limb shakers. RC had no prognostic relevance regarding functional outcome and recurrent events. Conclusion: In patients with ICA occlusion, RC and LS are more common than previously assumed. The presence of LS is associated with a worse outcome independent of initial stroke severity and patient characteristics.

Kaleidoscopic vision and a jerking leg on the ski slope

In March, 2005, a 48-year-old woman was fl own to our hospital by rescue helicopter after she fell while skiing. Shortly before she fell, she started to see objects in a distorted or fragmented way, and to see geometric shapes. The images of the objects and shapes were constantly changing, and she described her experience as like “looking through a kaleidoscope”. She closed her eyes in turn: vision in her right eye was normal; vision in her left eye was monochrome, fragmented, and changing. Her right leg started to jerk briskly and irregu larly, causing her to fall. She did not lose conscious ness; nor was she hurt. She had had migraine attacks, without an aura, for more than 30 years, but had had no attacks for several weeks. She had no risk factors for epilepsy. Nonetheless, the emergency physicians provisionally diagnosed a partial seizure. The patient was right-handed. Blood pressure was normal, at 140/90 mm Hg, as was visual acuity. However, on standing, the patient had vertigo; within seconds, her right arm and leg started to jerk repeatedly. The jerking promptly ceased when she lay down. Fundoscopy and gazing into the sun caused her vision to be as though of a picture with poor resolution, or one consisting of fi ne granules; she would then go blind in her left eye. Vision returned to normal once the patient stopped gazing at bright lights. MRI, magnetic-resonance angiography (MRA), and high-resolution ultrasonography revealed a high-grade (>90%) stenosis of the left carotid artery, caused by dissection of the artery wall (fi gure). Ultrasonography also showed signifi cant impair ment of blood fl ow in the left middle cerebral artery, with a loss of autoregulation. There was evidence of collateral blood supply via the ophthalmic artery, leptomeningeal pathways, and anterior and posterior communicating arteries. The patient was given a plasma expander (hydroxyethyl starch) and norepinephrine to raise her mean arterial pressure above 100 mm Hg, and heparin to reduce the risk of clotting. She was also told to remain lying in bed, and to wear sunglasses. Her symptoms resolved within 48 h, but recurred 4 days after admission; additionally, she now had brief episodes of aphasia and right-sided hemiparesis. Repeat MRI and MRA showed that the wall haematoma had expanded, so the left carotid artery was now blocked. MRI also showed two pinhead-sized diff usion abnormalities, implying small strokes, in the left frontal lobe. Trans cranial duplex ultrasonography showed that mean fl ow velocity in the left middle cerebral artery was now just 60% of the velocity on the right. We considered placing a stent in the carotid artery; however, the patient’s condition rapidly improved, through an increase in collateral blood fl ow. 10 days after admission, treatment with hydroxyethyl starch and norepinephrine was discontinued; 4 days later, heparin was replaced by warfarin, which we prescribed for 12 months. On further assessment, we found no evidence of fi bromuscular dysplasia, polycystic kidney disease, Ehlers-Danlos syndrome, or Marfan’s syndrome, all illnesses associated with arterial dissection. When last seen, in March, 2006, the patient was well. Although the unilateral limb jerks seemed to signify epilepsy, the postural onset of clinical signs indicated that the illness was probably vascular. Low-fl ow transient ischaemic attacks (TIAs) can cause limbs to swing, jerk, or tremble. Such movements are nearly always unilateral; the face is generally unaff ected. These attacks are ascribed to a focal low-perfusion state in the carotid artery territory, and loss of autoregulation. Similarly, our patient’s visual symptoms were caused by a vascular mechanism. Retinal ischaemia delayed regener ation of visual pigments, leading to kaleidoscopic vision and blindness. Transient painless amaurosis precipitated by exposure to bright light is known as retinal claudication. Retinal claudication and TIAs with limb-shaking are thought to occur in 3% and 8%, respectively, of patients with carotid artery occlusion.

[Juvenile stroke--results from the Austrian Stroke Registry].

In recent years, many aspects of juvenile stroke have been addressed in medium-sized case series. We have analyzed stroke severity, etiology, risk factors, and outcome in different age groups in the large dataset of the Austrian Stroke Unit Registry. In the nationwide Austrian Stroke Unit Registry 13,440 men and women with ischemic stroke or transient ischemic attack were recorded between March 2003 and February 2007. A number of important disease characteristics were documented by a stroke specialist upon admission of a patient and at discharge from the stroke unit and during a 3-month follow-up interview. A total of 749 patients (5.6%) were 18 to 45 years old and 1895 (14.1%) 18 to 55 years. Arterial dissection and cardiac/paradoxical embolism were the most common causes of stroke up to an age of 45. With a steeply increasing frequency of standard vascular risk factors, micro- and macroangiopathic causes of stroke substantially gain weight after the fourth decade of life. At 3-month follow-up, good clinical outcome (mRS 0-2) and death were 88.3% and 1.4% in the young (<or=55 years), and 65.3 (9.2%) in subjects aged 56 years and over. In multivariate analysis, young age (<or=55 years) predicted a good clinical outcome (Odds Ratio [95% confidence interval] 3.4 [2.4-5.0]) independently from stroke severity (NIH-SS), concomitant risk factors, stroke etiology, and thrombolytic therapy. Young men experience a significant delay in the onset-to-door time in comparison to other segments of the population. Increasing awareness about the relevance of stroke in the young is a valuable target for future health campaigns.SummaryIn recent years, many aspects of juvenile stroke have been addressed in medium-sized case series. We have analyzed stroke severity, etiology, risk factors, and outcome in different age groups in the large dataset of the Austrian Stroke Unit Registry. In the nationwide Austrian Stroke Unit Registry 13,440 men and women with ischemic stroke or transient ischemic attack were recorded between March 2003 and February 2007. A number of important disease characteristics were documented by a stroke specialist upon admission of a patient and at discharge from the stroke unit and during a 3-month follow-up interview. A total of 749 patients (5.6%) were 18 to 45 years old and 1895 (14.1%) 18 to 55 years. Arterial dissection and cardiac/paradoxical embolism were the most common causes of stroke up to an age of 45. With a steeply increasing frequency of standard vascular risk factors, micro- and macroangiopathic causes of stroke substantially gain weight after the fourth decade of life. At 3-month follow-up, good clinical outcome (mRS 0–2) and death were 88.3% and 1.4% in the young (≤55 years), and 65.3 (9.2%) in subjects aged 56 years and over. In multivariate analysis, young age (≤55 years) predicted a good clinical outcome (Odds Ratio [95% confidence interval] 3.4 [2.4–5.0]) independently from stroke severity (NIH-SS), concomitant risk factors, stroke etiology, and thrombolytic therapy. Young men experience a significant delay in the onset-to-door time in comparison to other segments of the population. Increasing awareness about the relevance of stroke in the young is a valuable target for future health campaigns.ZusammenfassungViele Aspekte des juvenilen Schlaganfalls wurden bereits an kleinen bis mittelgroßen Fallserien beschrieben. Wir analysierten den großen Datensatz des Österreichischen Stroke Unit Registers in Hinblick auf Schweregrad, Ätiologie, Risikofaktoren und Outcome von Schlaganfällen in den verschiedenen Altersgruppen. Im österreichweiten Stroke Unit Register wurden zwischen März 2003 und Februar 2007 13.440 Männer und Frauen mit ischämischem Schlaganfall oder einer transitorisch-ischämischen Attacke jenseits des 18. Lebensjahres registriert. Eine Vielzahl von Parametern wurde bei Aufnahme und Entlassung, sowie in einem 3-Monats-Follow-up erhoben 749 (5,6 %) Patienten waren zwischen 18 und 45 bzw. 1895 (14,1 %) zwischen 18 und 55 Jahre alt. Unter den bekannten Schlaganfallätiologien waren in der jungen Population (18.–45. Lebensjahr) die Dissektion und kardiale paradoxe Embolie die häufigsten. Ab der 4. Lebensdekade nahmen – parallel zum Anstieg der vaskulären Risikofaktoren – die Häufigkeit von arteriosklerotisch bedingter Mikro- und Makroangiopathie zu. Im 3-Monats-Follow-up waren 1.4 % der jungen Schlaganfallpatienten (≤55 Jahre) und 9,2 % der über 55-Jährigen verstorben, eine gutes klinisches Outcome (mRS 0–2) wurde bei 88,3 % bzw. 65,3 % beobachtet. In der multivariaten Analyse war junges Alter (≤55 Jahre) ein signifikanter Prädiktor für Selbständigkeit nach 3 Monaten (Odds Ratio [95 % Konfidenzintervall] 3,4 [2,4–5,0]) unabhängig von Geschlecht, NIH-SS bei Aufnahme, begleitenden Risikofaktoren, erfolgter Lysetherapie und Ätiologie. Bei jungen Männern ist die Zeitspanne zwischen Manifestation des Schlaganfalls und Eintreffen im Krankenhaus signifikant länger als in der restlichen Population, was Anlass zu entsprechenden Aufklärungskampagnen geben sollte.

Juveniler Schlaganfall in Österreich – Daten aus dem Österreichischen Schlaganfallregister

In recent years, many aspects of juvenile stroke have been addressed in medium-sized case series. We have analyzed stroke severity, etiology, risk factors, and outcome in different age groups in the large dataset of the Austrian Stroke Unit Registry. In the nationwide Austrian Stroke Unit Registry 13,440 men and women with ischemic stroke or transient ischemic attack were recorded between March 2003 and February 2007. A number of important disease characteristics were documented by a stroke specialist upon admission of a patient and at discharge from the stroke unit and during a 3-month follow-up interview. A total of 749 patients (5.6%) were 18 to 45 years old and 1895 (14.1%) 18 to 55 years. Arterial dissection and cardiac/paradoxical embolism were the most common causes of stroke up to an age of 45. With a steeply increasing frequency of standard vascular risk factors, micro- and macroangiopathic causes of stroke substantially gain weight after the fourth decade of life. At 3-month follow-up, good clinical outcome (mRS 0-2) and death were 88.3% and 1.4% in the young (<or=55 years), and 65.3 (9.2%) in subjects aged 56 years and over. In multivariate analysis, young age (<or=55 years) predicted a good clinical outcome (Odds Ratio [95% confidence interval] 3.4 [2.4-5.0]) independently from stroke severity (NIH-SS), concomitant risk factors, stroke etiology, and thrombolytic therapy. Young men experience a significant delay in the onset-to-door time in comparison to other segments of the population. Increasing awareness about the relevance of stroke in the young is a valuable target for future health campaigns.SummaryIn recent years, many aspects of juvenile stroke have been addressed in medium-sized case series. We have analyzed stroke severity, etiology, risk factors, and outcome in different age groups in the large dataset of the Austrian Stroke Unit Registry. In the nationwide Austrian Stroke Unit Registry 13,440 men and women with ischemic stroke or transient ischemic attack were recorded between March 2003 and February 2007. A number of important disease characteristics were documented by a stroke specialist upon admission of a patient and at discharge from the stroke unit and during a 3-month follow-up interview. A total of 749 patients (5.6%) were 18 to 45 years old and 1895 (14.1%) 18 to 55 years. Arterial dissection and cardiac/paradoxical embolism were the most common causes of stroke up to an age of 45. With a steeply increasing frequency of standard vascular risk factors, micro- and macroangiopathic causes of stroke substantially gain weight after the fourth decade of life. At 3-month follow-up, good clinical outcome (mRS 0–2) and death were 88.3% and 1.4% in the young (≤55 years), and 65.3 (9.2%) in subjects aged 56 years and over. In multivariate analysis, young age (≤55 years) predicted a good clinical outcome (Odds Ratio [95% confidence interval] 3.4 [2.4–5.0]) independently from stroke severity (NIH-SS), concomitant risk factors, stroke etiology, and thrombolytic therapy. Young men experience a significant delay in the onset-to-door time in comparison to other segments of the population. Increasing awareness about the relevance of stroke in the young is a valuable target for future health campaigns.ZusammenfassungViele Aspekte des juvenilen Schlaganfalls wurden bereits an kleinen bis mittelgroßen Fallserien beschrieben. Wir analysierten den großen Datensatz des Österreichischen Stroke Unit Registers in Hinblick auf Schweregrad, Ätiologie, Risikofaktoren und Outcome von Schlaganfällen in den verschiedenen Altersgruppen. Im österreichweiten Stroke Unit Register wurden zwischen März 2003 und Februar 2007 13.440 Männer und Frauen mit ischämischem Schlaganfall oder einer transitorisch-ischämischen Attacke jenseits des 18. Lebensjahres registriert. Eine Vielzahl von Parametern wurde bei Aufnahme und Entlassung, sowie in einem 3-Monats-Follow-up erhoben 749 (5,6 %) Patienten waren zwischen 18 und 45 bzw. 1895 (14,1 %) zwischen 18 und 55 Jahre alt. Unter den bekannten Schlaganfallätiologien waren in der jungen Population (18.–45. Lebensjahr) die Dissektion und kardiale paradoxe Embolie die häufigsten. Ab der 4. Lebensdekade nahmen – parallel zum Anstieg der vaskulären Risikofaktoren – die Häufigkeit von arteriosklerotisch bedingter Mikro- und Makroangiopathie zu. Im 3-Monats-Follow-up waren 1.4 % der jungen Schlaganfallpatienten (≤55 Jahre) und 9,2 % der über 55-Jährigen verstorben, eine gutes klinisches Outcome (mRS 0–2) wurde bei 88,3 % bzw. 65,3 % beobachtet. In der multivariaten Analyse war junges Alter (≤55 Jahre) ein signifikanter Prädiktor für Selbständigkeit nach 3 Monaten (Odds Ratio [95 % Konfidenzintervall] 3,4 [2,4–5,0]) unabhängig von Geschlecht, NIH-SS bei Aufnahme, begleitenden Risikofaktoren, erfolgter Lysetherapie und Ätiologie. Bei jungen Männern ist die Zeitspanne zwischen Manifestation des Schlaganfalls und Eintreffen im Krankenhaus signifikant länger als in der restlichen Population, was Anlass zu entsprechenden Aufklärungskampagnen geben sollte.