Schlosspark Klinik

Berlin, Germany

Schlosspark Klinik

Berlin, Germany
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Radtke A.,Charité - Medical University of Berlin | Von Brevern M.,Parkklinik Weissensee | Neuhauser H.,Robert Koch Institute Hn | Hottenrott T.,Albert Ludwigs University of Freiburg | Lempert T.,Schlosspark Klinik
Neurology | Year: 2012

Objective: The aim of the study was to assess the evolution of clinical symptoms and vestibulocochlear function in patients with definite vestibular migraine (dVM). Methods: We reassessed 61 patients (54 women, 7 men, aged 24-76 years) with dVM according to validated diagnostic criteria after a median follow-up time of 9 years (range, 5.5-11). Assessment comprised a clinical interview and neurotologic examination, including pure-tone audiometry and caloric testing. Results: The majority of patients (87%) had recurrent vertigo at follow-up. Frequency of vertigo was reduced in 56%, increased in 29%, and unchanged in 16%. Impact of vertigo was severe in 21%, moderate in 43%, and mild in 36%. Eighteen percent reported mild persistent unsteadiness. Interictal ocular motor abnormalities had increased from 16% initially to 41% of patients at follow-up. The most frequent finding was positional nystagmus (PN), in 28%, including definite central-type PN in 18%. However, only 1 of 9 patients with ocular motor abnormalities at initial presentation showed similar findings on follow-up. Concomitant cochlear symptoms with vertigo had increased from 15% initially to 49%. Eleven patients (18%) had developed mild bilateral sensorineural hearing loss, which also involved the low-frequency range. Conclusions: The majority of patients continue to have recurrent vertigo in the long-term evolution of VM, and the impact of vertigo may remain severe. Whereas interictal ocular motor abnormalities may show some variation over time, vestibulo-cochlear dysfunction progresses slowly in some patients with VM. Interictal central-type PN may help distinguishVMfrom peripheral vestibular disorders such as Méniére disease. © 2012 by AAN Enterprises, Inc.

Kohler S.,Charité - Medical University of Berlin | Gaus S.,Charité - Medical University of Berlin | Bschor T.,Schlosspark Klinik | Bschor T.,University Hospital Dresden
Pharmacopsychiatry | Year: 2014

Bipolar depression and its clinical presentation is a frequent but complex psychiatric disease. Despite the high prevalence and the clinical and economic relevance of bipolar depression, few treatments are proven to be highly and consistently effective. In practice, the treatment of bipolar depression typically includes complex treatment decision-making. The best evidence for a pharmacological treatment exists for quetiapine. Alternatives with limitations are lamotrigine (also in the combination with lithium), carbamazepine and olanzapine. The effectiveness and recommendation of antidepressants in the treatment of bipolar depression remains controversial. Initially, depressive episodes should been treated with one of the named substances with antidepressant properties. In non-responders, a combination of lithium and lamotrigine, or antidepressants in combination with either lithium, an antiepileptic drug or atypical antipsychotics, may be necessary. If a depressive episode occurs under ongoing mood-stabilizing treatment, combination treatments of different substances, even with antidepressants, can be necessary. In the case of treatment-resistant depressive episodes, complex treatment strategies (combination therapies, MAO inhibitors) should be considered. This review describes the treatment recommendations of different guidelines for bipolar depression and emphasizes their differences. Furthermore, alternative pharmacological treatment strategies and complex treatment situations are discussed. © Georg Thieme Verlag KG Stuttgart · New York ·.

Radtke A.,Charité - Medical University of Berlin | Neuhauser H.,Robert Koch Institute | Von Brevern M.,Parkklinik Weissensee | Hottenrott T.,Charité - Medical University of Berlin | Lempert T.,Schlosspark Klinik
Cephalalgia | Year: 2011

Background: Clinical recognition of vestibular migraine (VM) is still hampered by the lack of consensus diagnostic criteria. The aim of this study is a long-term evaluation of clinical criteria for definite (dVM) and probable (pVM) vestibular migraine.Methods: We re-assessed 75 patients (67 women, age 24-76 years) with dVM (n-=-47) or pVM (n-=-28) according to previously published criteria after a mean follow-up of 8.75-±-1.3 years. Assessment included a comprehensive neurotological clinical examination, pure tone audiometry and caloric testing.Results: dVM was confirmed in 40 of 47 patients with a prior diagnosis of dVM (85%). Fourteen of 28 patients initially classified as pVM met criteria for dVM (50%), nine for pVM (32%). Six additional patients with dVM and two with pVM had developed mild sensorineural hearing loss, formally fulfilling criteria for bilateral Menière's disease (MD), but had clinical features atypical of MD. Seven of these also met criteria for dVM at follow-up. The initial diagnosis was completely revised for four patients.Conclusion: Although VM diagnosis lacks a gold standard for evaluation of diagnostic criteria, repeated comprehensive neurotological evaluation after a long follow-up period indicates not only high reliability but also high validity of presented clinical criteria (positive predictive value 85%). Half of patients with pVM evolve to meet criteria for dVM. However, in a subgroup of VM patients with hearing loss, criteria for dVM and MD are not sufficiently discriminative. © International Headache Society 2011.

Gobel K.,Schlosspark Klinik | Erb C.,Augenklinik Am Wittenbergplatz
Klinische Monatsblatter fur Augenheilkunde | Year: 2014

Due to the anatomic location of the N. opticus to the brain and its embryological development as a bulging part of the brain, a close connection between the opticoneuropathy and certain neurological diseases exists. Glaucoma is a chronic neurodegenerative disorder and many cellular and molecular mechanisms of the chronic neurodegenerative diseases are common in the brain. For example, elevated levels of multiple biomarkers of Alzheimer's disease were found in the aqueous humor of patients with primary open-angle glaucoma. Also a decreased cerebrospinal fluid pressure (CSFP) has been demonstrated in patients with glaucoma and Alzheimer's disease. The resulting translaminar pressure difference is seen as one of the pathogenic mechanisms of the formation of the optic neuropathy in both diseases. Other hypotheses, such as the influence of oxidative stress, excitotoxicity, mitochondrial dysfunction, genetic factors and vascular factors play additional roles in the pathogenesis of the different diseases. Experimental studies have shown that dopaminergic amacrine cells are present in the retina. The dopamine in the retina is necessary for the light adaptation and the signal processing in the rods and cones. Parkinson's disease is characterised by a loss of dopaminergic neurons in the basal ganglia-substantia nigra pars compacta of the midbrain. These decreased levels of dopamine also have an effect on the eye and the afferent signal processing. So there are reductions in visual acuity, disturbances in colour vision and contrast sensitivity and reduction of the retinal nerve fiber layer in patients affected with Parkinson's disease. With the examples of Alzheimer's disease, Parkinson's disease and the chronic inflammatory disease multiple sclerosis, we demonstrate the association between the neurological diseases and the opticoneuropathy in primary open-angle glaucoma. © Georg Thieme Verlag KG Stuttgart. New York.

Body dysmorphic disorder (BDD) is a hard-to-treat disorder that often coincides with depression and suicidal tendency. We investigate the correlations between depression and BDD in an idiographic study of 5 patients receiving treatment in the psychiatric ward of a general hospital in 2008. Among these patients we found common triggering factors - mainly separation - that were associated with humiliation, childhood stresses, worries in regard to attractiveness and masculinity, and personality structures showing dependent-avoidant, self-insecure and sensitive traits, as described by Kretschmer. It transpired that their BDD had developed out of a self-aggravating cycle of shame, controlling actions, alienation and self-disempowerment. After a certain period their self-disempowerment then gradually transforms into a depressive cycle of despair, increased withdrawal, inward-directed anger and self-depreciation. These correlations indicate that the depressive symptomatology among these patients can be better classified as adjustment disorder in regard to their BDD than as independent major depression. Finally, we present dance/movement therapy as a promising additional psychotherapeutic approach that can complement the recognized therapy forms (serotonin re-uptake inhibitors and cognitive behavioral therapy). Copyright © 2011 S. Karger AG, Basel.

Lempert T.,Schlosspark Klinik
CONTINUUM Lifelong Learning in Neurology | Year: 2012

Purpose of Review: This article describes the common causes of recurrent vertigo and dizziness that can be diagnosed largely on the basis of history.Recent Findings: Ninety percent of spontaneous recurrent vertigo and dizziness can be explained by six disorders: (1) Ménière disease is characterized by vertigo attacks, lasting 20 minutes to several hours, with concomitant hearing loss, tinnitus, and aural fullness. Aural symptoms become permanent during the course of the disease. (2) Attacks of vestibular migraine may last anywhere from minutes to days. Most patients have a previous history of migraine headaches, and many experience migraine symptoms during the attack. (3) Vertebrobasilar TIAs affect older adults with vascular risk factors. Most attacks last less than 1 hour and are accompanied by other symptoms from the posterior circulation territory. (4) Vestibular paroxysmia is caused by vascular compression of the eighth cranial nerve. It manifests itself with brief attacks of vertigo that recur many times per day, sometimes with concomitant cochlear symptoms. (5) Orthostatic hypotension causes brief episodes of dizziness lasting seconds to a few minutes after standing up and is relieved by sitting or lying down. In older adults, it may be accompanied by supine hypertension. (6) Panic attacks usually last minutes, occur in specific situations, and are accompanied by choking, palpitations, tremor, heat, and anxiety. Less common causes of spontaneous recurrent vertigo and dizziness include perilymph fistula, superior canal dehiscence, autoimmune inner ear disease, otosclerosis, cardiac arrhythmia, and medication side effects.Summary: Neurologists need to venture into otolaryngology, internal medicine, and psychiatry to master the differential diagnosis of recurrent dizziness. Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Erb C.,Schlosspark Klinik | Heinke M.,Schlosspark Klinik
Frontiers in Bioscience - Elite | Year: 2011

Glaucoma is the second leading cause of blindness worldwide and is still a mysterium. Despite some risk factors are known, like individually elevated intraocular pressure, myopia, age, genetic factors, as well as vascular risk factors and smoking, the exact mechanism developing a glaucomatous optic neuropathy are still unknown. In the pathogenesis of glaucoma oxidative stress seems to play an important role. The mitochondria have an abnormal DNS and the antioxidative capacity is reduced. In addition, in the anterior segment, e.g. trabecular meshwork as well as in the posterior pole glaucoma patients show an increased oxidative stress. Therefore oxidative stress should be considered in therapeutic approaches to glaucoma patients.

Lempert T.,Schlosspark Klinik | Bronstein A.,Imperial College London
Current Opinion in Otolaryngology and Head and Neck Surgery | Year: 2010

Purpose of Review This article reviews the current literature on neurological disorders causing vestibular signs and symptoms. The review focusses on vestibular migraine, vestibular stroke syndromes, and supratentorial gait disorders. Recent Findings: A familiar type of vestibular migraine with autosomal dominant inheritance has been linked to chromosome 5q35. In patients with vestibular migraine, vestibular testing in the asymptomatic interval, including VEMPs, produces heterogeneous and often only minor abnormalities. Migraine headaches can be triggered by vestibular stimulation suggesting that the relation of migraine and vestibular symptoms is bidirectional.Peripheral audiovestibular loss is a common accompaniment of anterior inferior cerebellar artery occlusion. Various brainstem and cerebellar stroke syndromes may mimic acute peripheral vestibular loss but can be differentiated clinically.The periventricular region and the anterior corpus callosum have been identified as specific localizations of cerebral white matter disease that interfere with gait and balance. Summary: Although vestibular migraine has been well delineated as a clinical syndrome, knowledge on its pathophysiology is scarce. To date, recommendations for treatment are based on clinical case series rather than randomized trials. Our understanding of ischemic vertigo has improved since stroke registers have provided large patient series with specific cerebellar and brainstem stroke syndromes. Cerebral white matter disease produces different clinical syndromes according to its severity and anatomical predilection. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Bronstein A.M.,Imperial College London | Lempert Th.,Schlosspark Klinik
Restorative Neurology and Neuroscience | Year: 2010

In this review we present a pragmatic approach to the patient with chronic vestibular symptoms. Even in the chronic patient a retrospective diagnosis should be attempted, in order to establish how the patient reached the current situation. Simple questions are likely to establish if the chronic dizzy symptoms started as benign paroxysmal positional vertigo (BPPV), vestibular neuritis, vestibular migraine, Meniere's disease or as a brainstem stroke. Then it is important to establish if the original symptoms are still present, in which case they need to be treated (e.g. repositioning maenouvres for BPPV, migraine prophylaxis) or if you are only dealing with chronic dizzy symptoms. In addition the doctor or physiotherapist needs to establish if the process of central vestibular compensation has been impeded due to additional clinical problems, e.g. visual problems (squints, cataract operation), proprioceptive deficit (neuropathy due to diabetes or alcohol), additional neurological or orthopaedic problems, lack of mobility or confidence, such as fear of falling or psychological disorders. A general neurological examination should also be conducted, amongst other reasons to make sure your patient's 'chronic dizziness' is not due to a neurological gait disorder. Treatment of the syndrome of chronic dizziness is multidisciplinary but rehabilitation and simple counselling should be available to all patients. In contrast, vestibular suppressants or tranquilisers should be reduced or, if possible, stopped. © 2010 - IOS Press and the authors. All rights reserved.

Protein kinase inhibitors represent a novel and promising approach to the treatment of rheumatoid arthritis (RA). By targeting intracellular signaling pathways of cytokine-mediated reactions, these substances are able to interfere with critical immune processes that underly the pathology of RA. With tofacitinib, the first Janus kinase (JAK) inhibitor has been approved in the USA, as well as in Switzerland and other countries. Several other substances are currently undergoing phase II or phase III trials. A crucial question that will shape the future of these new drugs is whether they are safe and in particular, whether they are safer than biological therapies. This article provides an overview on current data concerning the efficacy and safety of the most promising substances and discusses the potential future role of intracellular kinase inhibitors. © 2013 Springer-Verlag Berlin Heidelberg.

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