[Analysis of the prevalence of anticoagulant therapy in patients with cognitive disorders and cerebral amyloid angiopathy (CAA)]. / Analyse zur Häufigkeit einer gerinnungshemmenden Medikation bei Patientinnen mit kognitiven Störungen und zerebraler Amyloidangiopathie (CAA).

OBJECTIVES: To investigate the prevalence of coincident anticoagulation in patients with cognitive disorders and possible or probable cerebral amyloid angiopathy (CAA) as well as the relationship between the presence of oral anticoagulation and CAA-specific lesion load. MATERIALS AND METHODS: Patients with subjective cognitive decline (SCD), amnestic and non-amnestic mild cognitive impairment (aMCI/naMCI), Alzheimer's disease (AD), mixed dementia (MD) and vascular dementia (VD) who presented to our outpatient dementia clinic between February 2016 and October 2020 were included in this retrospective analysis. Patients underwent cranial magnetic resonance imaging (MRI). MRI data sets were analyzed regarding the presence of CAA-related MRI biomarkers to determine CAA prevalence. Presence of anticoagulant therapy was determined by chart review. RESULTS: Within the study period, 458 patients (209 male, 249 female, mean age 73.2 ± 9.9 years) with SCD (n = 44), naMCI (n = 40), aMCI (n = 182), AD (n = 120), MD (n = 68) and VD (n = 4) were analyzed. A total of 109 patients (23.8%) were diagnosed with possible or probable CAA. CAA prevalence was highest in aMCI (39.4%) and MD (28.4%). Of patients with possible or probable CAA, 30.3% were under platelet aggregation inhibition, 12.8% were treated with novel oral anticoagulants and 3.7% received phenprocoumon treatment. Regarding the whole study cohort, patients under oral anticoagulation showed more cerebral microbleeds (p = 0.047). There was no relationship between oral anticoagulation therapy and the frequency of cortical superficial siderosis (p = 0.634). CONCLUSION: CAA is a frequent phenomenon in older patients with cognitive disorders. Almost half of CAA patients receive anticoagulant therapy. Oral anticoagulation is associated with a higher number of cortical and subcortical microbleeds.

[Prognostic and diagnostic value of cerebrospinal fluid analysis in neurodegenerative dementia diseases]. / Prognostischer und differenzialdiagnostischer Stellenwert der Liquordiagnostik bei neurodegenerativen Demenzerkrankungen.

Cerebrospinal fluid (CSF) analysis is an important diagnostic tool in the assessment of dementia. For the differentiation of Alzheimer's disease from other etiologies of dementia syndromes, established biological markers could be helpful to confirm a distinctive neuropathology. Whereas negative CSF findings can rule out the majority of primarily neurodegenerative disorders, overlapping biomarker profiles remain a diagnostic challenge. Therefore, it is important to interpret CSF results within a specific clinical context. Furthermore, atypical CSF data can be challenging and require profound knowledge of preanalytics, biomarker profiles and the broad spectrum of diseases associated with cognitive decline. Beyond the Alzheimer's disease clinical spectrum, current studies aim at investigating CSF biomarkers to better differentiate tauopathies, TDP43(Transactive response DNA binding protein 43 kDa)-proteinopathies and synucleinopathies.

[Current findings on the coincidence of cerebral amyloid angiopathy and Alzheimer's disease]. / Aktuelle Befunde zur Koinzidenz von zerebraler Amyloidangiopathie und Alzheimer-Erkrankung.

Cerebral amyloid angiopathy (CAA) is closely related to Alzheimer's disease (AD) despite having distinct pathomechanisms. The CAA modulates cognitive impairment within AD by synergistic effects. The pathophysiologic relations are complex and incompletely understood, possibly due to the heterogeneous nature of CAA with its different subtypes. Both diseases are characterized by a pathologic amyloid metabolism but the pathologic processing of amyloid precursor proteins is distinct. The manifestation of vascular and parenchymal amyloid deposits can either overlap or occur independently and isolated. The investigation of the specific contribution of co-occurring CAA within AD to cognitive deficits requires diagnostic methods that sufficiently identify CAA severity and complexity as well as detailed neuropsychological testing to precisely characterize the cognitive deficits and to draw conclusions regarding their etiology.

[Intracerebral hemorrhage under platelet inhibition and oral anticoagulation in patients with cerebral amyloid angiopathy]. / Intrazerebrale Blutungen unter Plättchenaggregationshemmung und oraler Antikoagulation bei Patienten mit zerebraler Amyloidangiopathie.

Oral anticoagulation in patients with cerebral amyloid angiopathy is a therapeutic challenge. The association of cerebral amyloid angiopathy with intracerebral hemorrhage, a high mortality of intracerebral hemorrhage especially under oral anticoagulation and the high risk of recurrent bleeding require a multidisciplinary approach and a thorough risk-benefit analysis. Vitamin K antagonists increase the risk of intracerebral bleeding and the accompanying mortality by 60% and should be avoided if possible or reserved for special clinical situations (e.g. mechanical aortic valve replacement). Treatment with novel oral anticoagulants and antiplatelet drugs also increases the risk of cerebral bleeding and therefore needs a thorough risk-benefit evaluation. An interventional left atrial appendage closure is a promising therapeutic option especially in patients with an absolute arrythmia with atrial fibrillation. Furthermore, other clinical implications in patients with cerebral amyloid angiopathy are the subject of this review of the literature, such as special characteristics after acute ischemic stroke and the necessary secondary prophylaxis, with previous intracerebral hemorrhage and in patients with cognitive deficits.

Modafinil in obstructive sleep apnea-hypopnea syndrome: a pilot study in 6 patients.

We studied the effects of modafinil, a vigilance-enhancing drug, on excessive daytime sleepiness, memory, night sleep and respiration in 6 patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) using a double-blind random cross-over design with 24-hour polysomnography, verbal memory test and a 5-week sleep-wake diary kept by the patients. There were two 2-week treatment periods in which either modafinil or placebo was used; they were separated by a 1-week wash-out period. Our results show that modafinil reduces daytime sleep duration, lengthens the duration of subjective daytime vigilance and improves long-term memory in patients with OSAHS without modifying night sleep and respiration events.

[Electrophysiologic study in a patient presenting with expanding cerebral lacunae]. / Etude électrophysiologique chez un patient présentant des lacunes cérébrales expansives.

A 42-year-old man was affected with multiple cerebral lesions suggesting expanding lacunae. He had suffered for about 15 years of headaches and blurred vision. Neurological examination showed a Parinaud syndrome and a skew deviation. Magnetic resonance imaging showed an enlargement of the third and lateral ventricles and multiple intraparenchymatous lesions with a signal similar to that of the cerebrospinal fluid. These lesions were located in the mesencephalon and right thalamic region. Important discrepancies between the topography of the lesion and the clinical data were observed. Neurological examination, ocular movements during wake and neuropsychological testing suggested sub-cortical dysfunction. These results suggest functional rather than lesional repercussion of expansive lacunae.

A special form of cerebral lacunae: expanding lacunae.

The case of a 42 year old man with headache, blurred vision, and diplopia allowed the description of a particular form of cerebral lacunae-that is, expanding lacunae. Brain MRI showed hydrocephalus and multiple lesions in the thalamomesencephalic region. The radiological features of these lesions were similar to the histological brain coronal section of a case reported in 1983 in which expanding lacunae were related to a dilatation of the perivascular spaces and a focal segmental necrotising angiitis. The role of the lymphatic drainage of the brain is discussed to explain the dilatation of the perivascular spaces. The hypothesis of a hydrodynamic factor being responsible for the expanding character of the lacunae was suggested by the location of the lesions and the influence of various clinical events on the symptomatology.

Suppression of Ottoson waves in the isolated olfactory bulb during sleep in the pontine cat.

In the chronic pontine cat, in which the olfactory bulbs are isolated from the brain stem, the Ottoson and/or Adrian-induced waves are suppressed during paradoxical sleep. This phenomenon cannot be explained by a central centrifugal control. The suppression of olfactory electrical activity was found to correlate with vasodilatation of the nasal mucosa. It is likely, therefore that control of the olfactory bulb activity might be mediated through the vasomotor innervation of the nasal mucosa originating from the medulla.