Video-based analysis of the blink reflex in Parkinson's disease patients.

We developed a video-based tool to quantitatively assess the Glabellar Tap Reflex (GTR) in patients with idiopathic Parkinson's disease (iPD) as well as healthy age-matched participants. We also video-graphically assessed the effect of dopaminergic medication on the GTR in iPD patients, as well as the frequency and blinking duration of reflex and non-reflex blinks. The Glabellar Tap Reflex is a clinical sign seen in patients e.g. suffering from iPD. Reliable tools to quantify this sign are lacking. METHODS: We recorded the GTR in 11 iPD patients and 12 healthy controls (HC) with a consumer-grade camera at a framerate of at least 180 images/s. In these videos, reflex and non-reflex blinks were analyzed for blink count and blinking duration in an automated fashion. RESULTS: With our setup, the GTR can be extracted from high-framerate cameras using landmarks of the MediaPipe face algorithm. iPD patients did not habituate to the GTR; dopaminergic medication did not alter that response. iPD patients' non-reflex blinks were higher in frequency and higher in blinking duration (width at half prominence); dopaminergic medication decreased the median frequency (Before medication-HC: p < 0.001, After medication-HC: p = 0.0026) and decreased the median blinking duration (Before medication-HC: p = 0.8594, After medication-HC: p = 0.6943)-both in the direction of HC. CONCLUSION: We developed a quantitative, video-based tool to assess the GTR and other blinking-specific parameters in HC and iPD patients. Further studies could compare the video data to electromyogram (EMG) data for accuracy and comparability, as well as evaluate the specificity of the GTR in patients with other neurodegenerative disorders, in whom the GTR can also be present. SIGNIFICANCE: The video-based detection of the blinking parameters allows for unobtrusive measurement in patients, a safer and more comfortable option.

Treatment of Peripheral Nerve Compression Syndromes of the Upper Extremities: a Systematic Review. / Die Therapie peripherer Nervenkompressionssyndrome der oberen Extremität ­ eine systematische Übersichtsarbeit.

BACKGROUND: Nerve compression syndromes are referred to as chronic irritation or pressure palsies of peripheral nerves in areas of preformed anatomical constriction. Carpal tunnel syndrome is the most common nerve compression syndrome, followed by cubital tunnel syndrome. In addition, less frequent nerve compression syndromes of the upper extremities that affect the median, ulnar or radial nerves have been described. This review provides an overview of current treatment options for nerve compression syndromes of the upper extremities. STUDY DESIGN: Systematic overview. METHODS: Based on established national (AWMF) and international guidelines as well as the Cochrane Library, we performed a systematic literature search on PubMed (NLM), focusing on randomised controlled trials. RESULTS: Over the research period (2012 - 2020), there were 43 randomised trials that investigated surgical carpal tunnel release methods, 68 that compared different conservative therapies and 12 that compared surgical versus conservative treatments. Furthermore, eight studies analysed surgical techniques and four analysed conservative techniques for cubital tunnel syndrome. No randomised trials were conducted on the less common peripheral nerve compression syndromes, but case reports and observational studies were conducted. CONCLUSION: For carpal and cubital tunnel syndromes, there are evidence-based diagnostic methods as well as therapeutic recommendations based on randomised and controlled trials. When diagnosis is made after clinical examination and supported by radiological and electrophysiological evaluation, surgical treatment is considered superior to conservative treatment. In particular, excellent long-term results can be achieved by surgery for carpal and cubital tunnel syndromes. More controlled studies are needed to establish evidence-based therapeutic recommendations for the less common nerve compression syndromes, which are somewhat controversially and inconsistently defined.

Left atrial appendage thrombus in acute stroke: diagnostic accuracy of CT angiography compared to transesophageal echocardiography.

OBJECTIVES: To evaluate the value of an extended emergency computed tomography angiography (CTA) including cardiac imaging in patients with acute ischemic stroke for the detection of left atrial appendage (LAA) thrombus compared to transesophageal echocardiography (TEE) as a reference standard. MATERIALS AND METHODS: We conducted a retrospective case-control study of patients with presumed acute ischemic stroke who had undergone non-ECG-gated CTA for the craniocervical vessels with an extended coverage including the heart in the context of emergency stroke evaluation and for whom TEE was available as part of the routine stroke diagnostic. We selected cases with evidence of LAA thrombus in TEE and controls without LAA thrombus in TEE in a 1:3 ratio. Two independent observers analyzed CTA images for presence of LAA thrombus and were blinded to the presence of thrombus in TEE. RESULTS: Twenty-two patients with LAA thrombus in TEE, and 66 patients without LAA thrombus in TEE were included. The detection of LAA thrombus using CTA showed a sensitivity of 63.6%, a specificity of 81.8%, a positive predictive value of 53.9% and a negative predicted value of 87.1%. Interobserver agreement was only moderate (Cohen´s κ = 0.43). CONCLUSIONS: An extended emergency CTA including cardiac imaging can be helpful in early risk stratification in patients with stroke of cardioembolic origin. However, our data show that a standard CTA of craniocervical vessels with extended coverage of the heart is of limited value when compared to TEE, the standard method of detecting LAA thrombi.

Video-Based Hand Movement Analysis of Parkinson Patients before and after Medication Using High-Frame-Rate Videos and MediaPipe.

Tremor is one of the common symptoms of Parkinson's disease (PD). Thanks to the recent evolution of digital technologies, monitoring of PD patients' hand movements employing contactless methods gained momentum. Objective: We aimed to quantitatively assess hand movements in patients suffering from PD using the artificial intelligence (AI)-based hand-tracking technologies of MediaPipe. Method: High-frame-rate videos and accelerometer data were recorded from 11 PD patients, two of whom showed classical Parkinsonian-type tremor. In the OFF-state and 30 Minutes after taking their standard oral medication (ON-state), video recordings were obtained. First, we investigated the frequency and amplitude relationship between the video and accelerometer data. Then, we focused on quantifying the effect of taking standard oral treatments. Results: The data extracted from the video correlated well with the accelerometer-based measurement system. Our video-based approach identified the tremor frequency with a small error rate (mean absolute error 0.229 (±0.174) Hz) and an amplitude with a high correlation. The frequency and amplitude of the hand movement before and after medication in PD patients undergoing medication differ. PD Patients experienced a decrease in the mean value for frequency from 2.012 (±1.385) Hz to 1.526 (±1.007) Hz and in the mean value for amplitude from 8.167 (±15.687) a.u. to 4.033 (±5.671) a.u. Conclusions: Our work achieved an automatic estimation of the movement frequency, including the tremor frequency with a low error rate, and to the best of our knowledge, this is the first paper that presents automated tremor analysis before/after medication in PD, in particular using high-frame-rate video data.

Arteriovenous malformations of the filum terminale: clinical characteristics, angioarchitecture, and management of a rare spinal vascular pathology.

OBJECTIVE: The goal of this study was to describe clinical and neuroradiological features of arteriovenous malformations of the filum terminale (FT AVMs) and to present the authors' diagnostic and therapeutic management in this rare disease. METHODS: The presented cases were retrieved from a retrospectively collected database of all spinal vascular malformations treated between June 1992 and December 2021 at the Rheinisch-Westfälische Technische Hochschule (RWTH) University Hospital Aachen. Pretreatment and follow-up clinical and neuroradiological data were analyzed for this study. RESULTS: Data in 15 patients with FT AVM with a mean age of 60 years were included, with an overall incidence of FT AVM of 19% among all spinal AVMs in our cohort. Twelve of 15 (80%) patients were men. Nonspecific but typical clinical and MR findings of thoracolumbar congestive myelopathy were found in all patients. Spinal MR angiography, performed in 10 patients, identified in all cases the arterialized FT vein as well as a lumbar/lumbosacral location of an AV shunt. Digital subtraction angiography (DSA) showed an arterial supply solely via the FT artery in 12/15 (80%) patients and via an additional feeder from the lumbosacral region in the other 3/15 (20%) patients. All patients were treated surgically. During 1-year follow-up, 2 patients presented with recurrent FT AVM due to further arterial supply from the lumbosacral region, and were treated surgically. Neurological status was improved in all patients within the 1-year follow-up, with marginal further changes during long-term follow-up. CONCLUSIONS: Congestive myelopathy is the major pathological mechanism of symptoms in these patients, with no evidence for intradural bleeding. Missing the presence of possible multiple arterial supply of FT AVM during DSA may result in misdiagnosis and/or insufficient treatment. Due to the frequently prolonged course of FT artery, resection of the FT AVM may be a favorable treatment modality in comparison with endovascular treatment. Follow-up examinations are obligatory within the first 3 years after treatment, and further MR angiography and DSA examinations are indicated if congestive myelopathy persists.

[Cerebral venous sinus thrombosis : An overview of causes, diagnostics and treatment]. / Sinus- und Hirnvenenthrombose : Ein Überblick über Ursachen, Diagnostik und Therapie.

In some cases, cerebral venous sinus thrombosis shows a fulminant progress but with an incidence of 1.32 cases per 100,000 person-years it is relatively rare. Nevertheless, the disease is responsible for around 0.5-1% of all stroke cases. The neurological examination often reveals nonspecific findings but especially in younger patients with acute to subacute position-dependent headaches, this differential diagnosis should definitely be considered. This article presents the most common causes, including a digression on vaccine-induced immune thrombotic thrombocytopenia (VITT) as well as recommendations for clinical, laboratory testing and imaging diagnostics. In addition, relevant complications with particular reference to epileptic seizures within the framework of the disease entity and guideline-based acute treatment and secondary prophylaxis are presented.

Novel CACNA1A Variant p.Cys256Phe Disrupts Disulfide Bonds and Causes Spinocerebellar Ataxia.

BACKGROUND: Spinocerebellar ataxia (SCA) is a progressive, autosomal dominant neurodegenerative disorder typically associated with CAG repeat expansions. OBJECTIVE: We assessed the pathogenicity of the novel, heterozygous missense variant p.Cys256Phe (C256F) in the pore-forming α1-subunit of the Cav2.1 Ca2+ channel found in a 63-year-old woman with SCA with no CAG repeat expansion. METHODS: We examined the effect of the C256F variant on channel function using whole-cell patch-clamp recordings in transfected tsA-201 cells. RESULTS: The maximum Ca2+ current density was significantly reduced in the mutant compared to wild-type, which could not be explained by lower expression levels of mutant Cav2.1 α1- protein. Together with a significant increase in current inactivation, this is consistent with a loss of channel function. Molecular modeling predicted disruption of a conserved disulfide bond through the C256F variant. CONCLUSIONS: Our results support the pathogenicity of the C256F variant for the SCA phenotype and provide further insight into Cav2.1 structure and function.

[Causes, spectrum, and treatment of the diabetic neuropathy]. / Ursachen, Spektrum und Therapie der diabetischen Neuropathie.

BACKGROUND: Half of all diabetics are affected by a diabetic neuropathy. Microangiopathy, dysfunctional Schwann cell interactions, accumulation of toxic metabolites, and inflammatory processes all contribute to nerve damage. OBJECTIVE: Overview and perspectives of the pathophysiology as well as the current and future treatment implications. METHODS: Literature search (1990-2020). RESULTS: Clinically predominant are sensory and autonomic symptoms; however, muscle weakness can occur as well. Complications such as unrecognized myocardial infarctions and the diabetic foot syndrome are potentially life-threatening and can cause major disability. The pathophysiology of neuropathies in type 1 and type 2 diabetes mellitus differs due to additional risk factors of the metabolic syndrome. To reduce the risk of neuropathy, an intensive insulin therapy is superior compared to the conventional insulin therapy. Oral antidiabetic drugs should be chosen based on individual risk profiles. Metformin can cause an iatrogenic vitamin B12 deficiency. In the treatment of neuropathic pain, the calcium channel blocker pregabalin has the highest recommendation level. The tricyclic antidepressant amitriptyline is considered to be equally effective, but it is contraindicated in autonomic dysregulation and cognitive impairment. Alternatively, the serotonin-norepinephrine reuptake inhibitor duloxetine is approved for the symptomatic treatment of diabetic neuropathies. Controversially discussed medications include alpha-lipoic acid, epalrestat, and L­serine. CONCLUSION: The diabetic neuropathy is frequent and causes severe complications. A good understanding of the underlying pathophysiology can contribute to the development of novel treatment strategies in the future.

Gaze Palsy as a Manifestation of Todd's Phenomenon: Case Report and Review of the Literature.

Background: Though Todd's phenomenon (TP) is a relatively rare occurrence, its correct identification is of key diagnostic and therapeutic importance as a stroke mimic. Here we describe a case of isolated gaze palsy as a manifestation of TP, discuss periictal gaze abnormalities as lateralizing sign involving the frontal eye field (FEF), and present a narrative literature review. Methods: We reviewed the main features of the case and conducted a structured literature search of TP and gaze palsy using PubMed. We restricted the search to publications in English, Spanish, French, and German. Case presentation: A 71-year-old male with a history of right frontotemporal subarachnoid hemorrhage was admitted to the Emergency Department of our institution after suffering a first unprovoked focal to bilateral tonic-clonic seizure with ictal gaze deviation to the left. Cranial imaging showed no signs of ischemia, intracerebral hemorrhage, or tumor. The patient presented the following postictal features: involuntary eye deviation to the right due to left-sided gaze palsy and disorientation in time with preserved responsiveness. Eye movements were normal three days later. We concluded that the patient suffered from new-onset epilepsy due to sequelae following the right frontotemporal subarachnoid hemorrhage, affecting the FEF with contralateral ictal gaze deviation, and postictal gaze palsy with ipsilateral eye deviation as an unusual Todd's phenomenon. Conclusion: Unusual manifestations of TP are uncommon but clinically highly relevant, as they can mimic stroke or epileptic status and are decisive in the diagnostic and therapeutic decision-making process. Though postictal gaze palsy has been reported associated with other deficits, this constitutes, to our knowledge, the first report of isolated gaze palsy as a form of TP. Further research into the underlying causes is needed. Ictal contralateral gaze and head deviation, and probably postictal ipsilateral gaze deviation if present, are very helpful for the lateralization of the seizure-onset zone.

Cardiac stress after electroconvulsive therapy and spontaneous generalized convulsive seizures: A prospective echocardiographic and blood biomarker study.

AIM: Knowledge about cardiac stress related to seizures in electroconvulsive therapy (ECT) and spontaneously occurring generalized convulsive seizures (GCS) is limited. The aim of the present study was to analyze cardiac function and circulating markers of cardiac stress in the early postictal period after ECT and GCS. METHODS: Patients undergoing ECT in the Department of Psychiatry, Psychotherapy and Psychosomatics and patients undergoing diagnostic video-EEG monitoring (VEM) in the Department of Neurology were prospectively enrolled between November 2017 and November 2018. Cardiac function was examined twice using transthoracic echocardiography within 60 min and >4 h after ECT or GCS. Established blood markers (troponin T high-sensitive, N-terminal pro brain natriuretic peptide) of cardiac stress or injury were collected within 30 min, 4 to 6 h, and 24 h after ECT or GCS. In the ECT group, the troponin T values were also correlated with periprocedural heart rate and blood pressure values. Because of organizational or technical reasons, the measurement was not performed in all patients. RESULTS: Twenty patients undergoing ECT and 6 patients with epilepsy with a GCS during VEM were included. Postictal echocardiography showed no wall motion disorders and no change in left ventricular and right ventricular functions. Four of 17 patients displayed a transient increase in high-sensitive cardiac troponin T 4-6 h after the seizure (3 patients with ECT-induced seizure). None of these 4 patients had signs of an acute cardiac event, and periprocedural blood pressure or heart rate peaks during ECT did not significantly differ in patients with and without troponin T elevation. CONCLUSIONS: Signs of mild cardiac stress can occur in some patients following ECT or GCS without clinical complications, probably related to excessive catecholamine release during the seizure.

[Hemiballism-Hemichorea Induced by Non-Ketotic Hyperglycemia]. / Hemiballistisch-choreatiforme Bewegungsstörung durch eine nicht-ketotische Hyperglykämie.

INTRODUCTION: A non-ketotic hyperglycaemia may cause an affection of basalganglia and, in the following, lead to a hemiballism-hemichorea movement-disorder. HISTORY: A 68-year-old male patient was admitted at our ward with a subacute and painless hemichorea-hemiballism movement-disorder. FINDINGS AND DIAGNOSIS: Due to elevated levels of glycated haemoglobin, negative ketone bodies in the urine and characteristic changes of the striatum in MR-imaging the diagnosis of a non-ketotic hyperglycemia induced hemichorea-hemiballism was made. THERAPY AND COURSE: An antidiabetic treatment was applied using Metformin, Insulin glargin and Sitagliptin as well as a symptomatic treatment with Risperidon 3 mg. In the following, blood sugar levels normalized and a beginning regression of symptoms was observed. CONCLUSIONS: The exact pathophysiology of this phenomenon is still not fully understood and will need to be investigated. Nevertheless, this disease should always be taken into consideration if the typical clinical presentation as well as matching laboratory tests and imaging features are found.

The Neurophysiology and Treatment of Motion Sickness.

BACKGROUND: Seasickness and travel sickness are classic types of motion illness. Modern simulation systems and virtual reality representations can also induce comparable symptoms. Such manifestations can be alleviated or prevented by various measures. METHODS: This review is based on pertinent publications retrieved by a PubMed search, with special attention to clinical trials and review articles. RESULTS: Individuals vary in their susceptibility to autonomic symptoms, ranging from fatigue to massive vomiting, induced by passive movement at relatively low frequencies (0.2 to 0.4 Hz) in situations without any visual reference to the horizontal plane. Younger persons and women are considered more susceptible, and twin studies have revealed a genetic component as well. The various types of motion sickness are adequately explained by the intersensory conflict model, incorporating the vestibular, visual, and proprioceptive systems and extended to include consideration of postural instability and asymmetry of the otolith organs. Scopolamine and H1-antihistamines, such as dimenhydrinate and cinnarizine, can be used as pharmacotherapy. The symptoms can also be alleviated by habituation through long exposure or by the diminution of vestibular stimuli. CONCLUSION: The various types of motion sickness can be treated with general measures to lessen the intersensory conflict, behavioral changes, and drugs.

[Risk factors for hypertensive and cerebral amyloid angiopathy associated intracerebral hemorrhage: a retrospective comparison]. / Risikofaktoren für hypertensive und zerebrale Amyloidangiopathie-assoziierte intracerebrale Blutungen: ein retrospektiver Vergleich.

INTRODUCTION: The aim of this study was to compare possible risk factors for the most common forms of spontaneous intracerebral hemorrhage (ICH), namely hypertensive and cerebral amyloid angiopathy (CAA) associated ICH. METHODS: Retrospectively, different parameters and factors were compared in patients with hypertensive ICH (n = 141) and patients with a CAAassociated ICH (n = 95). These included age, INR value and blood pressure at admission, cardiovascular risk factors as well as pre-medication. The Chi-square test with the Yates' continuity correction and the t-test were used as test methods. RESULTS: Patients of the group with CAA-associated ICH were significantly older than patients with a hypertensive ICH (p = 0.001). In addition, there was a significantly higher incidence of acetylsalicylic acid prior treatment (p = 0.042) and a previous stroke (p = 0.048) in the CAA patients. Patients of both groups had a high proportion of arterial hypertension as pre-diagnosis, which was significantly more common in patients with hypertensive ICH (p < 0,001). Patients with a hypertensive ICH also had significantly higher systolic and diastolic blood pressure values (p < 0.001) and higher INR values (p = 0.005) at admission. A subgroup analysis of all patients without anticoagulation (ZAA group: n = 78, hypertensive ICB group: n = 99) showed similar results. However, there was no significant difference (p = 0.037) for a previous stroke, but there was a significant difference in premedication with a statin (p = 0.032). DISCUSSION: Arterial hypertension is a relevant risk factor in both forms of intracerebral hemorrhage and should therefore receive adequate prophylaxis. For a more detailed classification of the other risk factors, further studies with larger cases are necessary.

Can perfusion CT unmask postictal stroke mimics? A case-control study of 133 patients.

OBJECTIVE: To study the diagnostic value of volume perfusion CT (VPCT) in patients with transient focal neurologic deficits following and during epileptic seizures, that mimic symptoms of stroke. METHODS: A retrospective case-control study was performed on 159 patients who presented with a seizure and received an emergency VPCT within the first 3.5 hours of admission, after being misjudged to have an acute stroke. The reference test was a clinical-based, EEG-supported diagnostic algorithm for seizure. RESULTS: We included 133 patients: 94 stroke-mimicking cases with postictal focal neurologic deficits ("Todd phenomenon," n = 67) or ongoing seizure on hospital admission ("ictal patients," n = 27), and 39 postictal controls without focal neurologic deficits. Patients with Todd phenomenon showed normal perfusion (64%), hypoperfusion (21%), and hyperperfusion (14%) on early VPCT. Ictal patients displayed more hyperperfusion compared to postictal patients (p = 0.015). Test sensitivity of hyperperfusion for ictal patients is 38% (95% confidence interval [CI] 20.7%-57.7%), specificity 86% (95% CI 77.3%-91.7%), positive predictive value is 42% (95% CI 27.5%-58.7%), and the negative predictive value 83% (95% CI 78.6%-86.9%). A cortical distribution was seen in all hyperperfusion scans, compared to a cortico-subcortical pattern in hypoperfusion (p < 0.001). A history of complex focal seizure and age were associated with hyperperfusion (p = 0.046 and 0.038, respectively). CONCLUSION: VPCT can differentiate ictal stroke mimics with hyperperfusion from acute ischemic stroke, but not postictal patients who display perfusion patterns overlapping with ischemic stroke. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that VPCT accurately differentiates ictal stroke mimics from acute ischemic stroke.

Early postictal serum lactate concentrations are superior to serum creatine kinase concentrations in distinguishing generalized tonic-clonic seizures from syncopes.

Concentrations of serum creatine kinase (CK) and serum lactate are frequently measured to help differentiate between generalized tonic-clonic seizures (GTCS) and syncope. The aim of this prospective cohort study was to systematically compare these two markers. The primary outcome is the measurement of serum lactate and CK in blood samples drawn within 2 h of the event in patients admitted with either a GTCS (n = 49) or a syncope (n = 36). Furthermore, the specificity and sensitivity of serum lactate and CK are determined as diagnostic markers in distinguishing between GTCS and syncope. GTCS patients have significantly higher serum lactate levels compared to syncope patients (p < 0.001). In contrast, CK does not differ between groups at admission. Regarding the first hour after the seizure, we identify a cut-off for serum lactate of 2.45 mmol/l for diagnosing GTCS as the cause of an impairment of consciousness with a sensitivity of 0.94 and a specificity of 0.93 (AUC: 0.97; 95% CI 0.94-1.0). In the second hour after the event, the ROC analysis yields similar results (AUC: 0.94; 95% CI 0.85-1.0). Serum lactate is a sensitive and specific diagnostic marker to discriminate GTCS from syncope and is superior to CK early after admission to the emergency department.

An unusual agent for an unusual localization of infective endocarditis.

We report on a 32-year-old male patient with acute left-hemispheric stroke caused by embolism due to infective endocarditis affected from the HACEK group. Additionally, atypical findings from the transesophageal echocardiography (TEE) which showed fluttering structures belonging to the papillary muscle could be proven as infectious agents with the help of a glucose positron emission tomography (PET) scan. TEE controls showed increasing vegetation involving the mitral valve so that surgery became necessary. The current work reflects, in detail, the emergent clinical course of this young patient, suffering from both an unusual localization and an infrequent cause of endocarditis and focuses on an actual view to the literature.

Cerebral Amyloid Angiopathy in Stroke Medicine.

BACKGROUND: Cerebral amyloid angiopathy (CAA) is a degenerative vasculopathy that is classically associated with lobar intracerebral or sulcal hemorrhage. Its prevalence is estimated at 30% in the seventh decade and 50% in the eighth and ninth decades. In this review, we summarize the risks linked to CAA with respect to the treatment and prevention of stroke. METHODS: This review is based on pertinent publications retrieved by a selective search employing the terms "amyloid cerebral angiopathy," "stroke," "intra - cerebral bleeding," and "acute stroke therapy." RESULTS: Among patients given systemic lytic treatment for stroke, those who have microhemorrhages tend to have a higher risk of treatment-associated brain hemorrhage. In a meta-analysis, 70% of patients who sustained a hemorrhage after thrombolytic therapy were found to have CAA, compared to only 22% in a control population. Patients with cerebral hemorrhages have microhemorrhages more commonly than patients with transient ischemic attacks (TIA) or infarcts. This was observed among persons under treatment with vitamin K antagonists (odds ratio, 2.7) or platelet aggregation inhibitors (odds ratio, 1.7). Moreover, the apolipoprotein E2 allele is associated with a higher incidence of intracerebral hemorrhage (ICH) under oral anticoagulation. Strict treatment of arterial hypertension can lower the risk of ICH in persons with probable CAA by 77%. On the other hand, the use of statins after a lobar ICH increases the risk for a clinically manifest recurrent hemorrhage from 14% to 22%. CONCLUSION: In patients with CAA, arterial hypertension should be tightly controlled. On the other hand, caution should be exercised in prescribing oral anticoagulants or platelet aggregation inhibitors for patients with CAA, or statins for patients who have already sustained a lobar ICH.