Tae Mo Chung

Botulinum Neurotoxin Type A in Neurology: Update

This paper reviews the current and most neurological (central nervous system, CNS) uses of the botulinum neurotoxin type A. The effect of these toxins at neuromuscular junction lends themselves to neurological diseases of muscle overactivity, particularly abnormalities of muscle control. There are seven serotypes of the toxin, each with a specific activity at the molecular level. Currently, serotypes A (in two preparations) and B are available for clinical purpose, and they have proved to be safe and effective for the treatment of dystonia, spasticity, headache, and other CNS disorders in which muscle hyperactivity gives rise to symptoms. Although initially thought to inhibit acetylcholine release only at the neuromuscular junction, botulinum toxins are now recognized to inhibit acetylcholine release at autonomic cholinergic nerve terminals, as well as peripheral release of neuro-transmitters involved in pain regulation. Its effects are transient and nondestructive, and largely limited to the area in which it is administered. These effects are also graded according to the dose, allowing individualized treatment of patients and disorders. It may also prove to be useful in the control of autonomic dysfunction and sialorrhea. In over 20 years of use in humans, botulinum toxin has accumulated a considerable safety record, and in many cases represents relief for thousands of patients unaided by other therapy.

Botulinum toxin therapy for treatment of spasticity in multiple sclerosis: review and recommendations of the IAB-Interdisciplinary Working Group for Movement Disorders task force.

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.

Strategies for treatment of dystonia

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.

Defining spasticity: a new approach considering current movement disorders terminology and botulinum toxin therapy

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.

Poster 187 Is There a Correlation Between Tremor and Other Symptoms of Cervical Dystonia? An Analysis of Data from the Ongoing INTEREST IN CD2 Study

Case/Program Description: Thirty-one-year-old woman with chronic right lateral elbow pain for three years was referred to our hospital for surgical treatment after previous standard conservative managements and extracorporeal shock-wave therapy (ESWT) had failed. Tenderness was prominent over the right lateral epicondyle and the pain was aggravated by resisted wrist extension. Laboratory findings were normal. Plain x-ray and T2-weighted fat-suppressed magnetic resonance imaging (MRI) showed the curvilinear calcification around lateral epicondyle of elbow. Numeric rating scale (NRS) was 7 and Roles-Maudsley score (RMS) “poor” grade. The patient received USguided barbotage and additional 3 sessions of ESWT (0.15 mJ/mm, 600 shocks, weekly). Setting: Tertiary care hospital. Results: After US-guided barbotage combined ESWT, pain and tenderness started to dramatically decrease. Two months after, additional three sessions of ESWT were given to reduce residual pain (NRS 3). At 8 months and 12 months follow-up, pain scores were NRS 1 and NRS 0, and RMSs were good and excellent, respectively. Calcific deposits nearly disappeared on X-ray at 8 months follow-up. Discussion: This is the first reported case, to our knowledge, of chronic intractable calcific tendinitis of the common extensor tendon which was successfully treated with US-guided barbotage combined with ESWT. Conclusions: US-guided barbotage combined with ESWT may be a good non-surgical therapeutic option for managements of chronic intractable calcific tendinitis of the common extensor tendon. Level of Evidence: Level V