No abstract

Spasticity is a symptom occurring in many neurological conditions including stroke, multiple sclerosis, hypoxic brain damage, traumatic brain injury, tumours and heredodegenerative diseases. It affects large numbers of patients and may cause major disability. So far, spasticity has merely been described as part of the upper motor neurone syndrome or defined in a narrowed neurophysiological sense. This consensus organised by IAB-Interdisciplinary Working Group Movement Disorders wants to provide a brief and practical new definition of spasticity-for the first time-based on its various forms of muscle hyperactivity as described in the current movement disorders terminology. We propose the following new definition system: Spasticity describes involuntary muscle hyperactivity in the presence of central paresis. The involuntary muscle hyperactivity can consist of various forms of muscle hyperactivity: spasticity sensu strictu describes involuntary muscle hyperactivity triggered by rapid passive joint movements, rigidity involuntary muscle hyperactivity triggered by slow passive joint movements, dystonia spontaneous involuntary muscle hyperactivity and spasms complex involuntary movements usually triggered by sensory or acoustic stimuli. Spasticity can be described by a documentation system grouped along clinical picture (axis 1), aetiology (axis 2), localisation (axis 3) and additional central nervous system deficits (axis 4). Our new definition allows distinction of spasticity components accessible to BT therapy and those inaccessible. The documentation sheet presented provides essential information for planning of BT therapy.

Botulinum toxin (BT) therapy is a complex and highly individualised therapy defined by treatment algorithms and injection schemes describing its target muscles and their dosing. Various consensus guidelines have tried to standardise and to improve BT therapy. We wanted to update and improve consensus guidelines by: (1) Acknowledging recent advances of treatment algorithms. (2) Basing dosing tables on statistical analyses of real-life treatment data of 1831 BT injections in 36 different target muscles in 420 dystonia patients and 1593 BT injections in 31 different target muscles in 240 spasticity patients. (3) Providing more detailed dosing data including typical doses, dose variabilities, and dosing limits. (4) Including total doses and target muscle selections for typical clinical entities thus adapting dosing to different aetiologies and pathophysiologies. (5) In addition, providing a brief and concise review of the clinical entity treated together with general principles of its BT therapy. For this, we collaborated with IAB—Interdisciplinary Working Group for Movement Disorders which invited an international panel of experts for the support.

Botulinum toxin (BT) therapy is an established treatment of spasticity due to stroke. For multiple sclerosis (MS) spasticity this is not the case. IAB-Interdisciplinary Working Group for Movement Disorders formed a task force to explore the use of BT therapy for treatment of MS spasticity. A formalised PubMed literature search produced 55 publications (3 randomised controlled trials, 3 interventional studies, 11 observational studies, 2 case studies, 35 reviews, 1 guideline) all unanimously favouring the use of BT therapy for MS spasticity. There is no reason to believe that BT should be less effective and safe in MS spasticity than it is in stroke spasticity. Recommendations include an update of the current prevalence of MS spasticity and its clinical features according to classifications used in movement disorders. Immunological data on MS patients already treated should be analysed with respect to frequencies of MS relapses and BT antibody formation. Registration authorities should expand registration of BT therapy for spasticity regardless of its aetiology. MS specialists should consider BT therapy for symptomatic treatment of spasticity.

IncobotulinumtoxinA treatment resulted in significant improvements in facial symmetry in patients with facial nerve injury following neurosurgical interventions. Treatment was effective for the correction of the compensatory hyperactivity of mimic muscles on the unaffected side that develops in the acute period of facial nerve palsy, and for the correction of synkinesis in the affected side that develops in the long-term period. Appropriate dosing and patient education to perform exercises to restore mimic muscle function should be considered in multimodal treatment.

Treatment of dystonias is generally symptomatic. To produce sufficient therapy effects, therefore, frequently a multimodal and interdisciplinary therapeutic approach becomes necessary, combining botulinum toxin therapy, deep brain stimulation, oral antidystonic drugs, adjuvant drugs and rehabilitation therapy including physiotherapy, occupational therapy, re-training, speech therapy, psychotherapy and sociotherapy. This review presents the recommendations of the IAB-Interdisciplinary Working Group for Movement Disorders Special Task Force on Interdisciplinary Treatment of Dystonia. It reviews the different therapeutic modalities and outlines a strategy to adapt them to the dystonia localisation and severity of the individual patient. Hints to emerging and future therapies will be given.

Botulinotherapy and Actual Neurology; Build. 1B, 6 Marshala Rokossovskogo Bul'var, Moscow 107370, Russia; 3 Center of Interdisciplinary Dentistry and Neurology; Build. 2, 32 Komsomol'skiy Prospekt, Moscow 119146, Russia Bruxism is stereotypical movements of the mandibula accompanied by grinding or clenching of teeth. Bruxism has 2 circadian manifestations: during sleep (nocturnal bruxism) and during wakefulness (diurnal bruxism). Etiology of the disease is unclear but occlusal disharmony, stress management, basal ganglia dysfunction, and genetic factors are being discussed. An association between bruxism and other motor disorders such as Parkinson's disease, oromandibular dystonia, Huntington's disease, as well as some drugs, is observed. For bruxism diagnosis, questionnaires, clinical examination, polysomnography, electromyography, and brux checkers are used. The leading treatment method for bruxism and accompanying dysfunction of the temporomandibular joint is local administration of botulinum neuroprotein into the temporal, masseter, and lateral pterygoid muscles. Key words: bruxism, motor disorder, masseter muscles, botulinum toxin therapyFor citation : Orlova O.R., Alekseeva A.Yu., Mingazova L.R., Konovalova Z.N. Bruxism as a neurological problem (literature review). Nervno-myshechnye bolezni = Neuromuscular Diseases 2018;8(1):20-7. Введение Термин «бруксизм» происходит от греческого слова «бругмос» -скрежетать. Marie и Pietkiewicz в 1907 г. первыми описали бруксизм в научной литературе и определили его как «la bruxomanie». Бруксизм -сте-реотипные движения нижней челюсти, сопровождаю-щиеся трением или сжатием зубов [1]. Бруксизм имеет 2 циркадных проявления: во время сна (ночной брук-сизм (НБ)) и во время бодрствования (дневной брук-сизм (ДБ)) [2]. Феноменологически между ними име-ются различия: ДБ -полупроизвольные «сжимающие» движения челюстей под влиянием тревоги и стресса во время бодрствования, тогда как НБ -стереотипные непроизвольные движения нижней челюсти, возника-

A.I. Burnazyan Federal Medical and Biological Center, FMBA of Russia; 23 Marshala Novikova St., Moscow 123098, Russia; 3