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Berlin, Germany

Kohler S.,Charite - Medical University of Berlin | Gaus S.,Charite - 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 ·. Source

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. Source

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. Source

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. Source

Radtke A.,Charite - Medical University of Berlin | Neuhauser H.,Robert Koch Institute | Hottenrott T.,Charite - 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. Source

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