Manajemen Perawatan Neurointensif pada Miastenia Gravis

Myasthenia gravis (MG) is an autoimmune disorder that affects neuromuscular transmission, causing generalized or localized weakness characterized by fatigue. Myasthenia gravis is most commonly associated with antibodies to the acetylcholine receptor (AChR) on the motor end plate in the postsynaptic neuron. This article aims to determine the appropriate neurointensive management in patients with myasthenia gravis with complications of myasthenic crisis. The writing of this article includes various sources originating from scientific journals and government guidelines and related agencies. Source searches were carried out on online portals for journal publications such as MedScape, Google Scholar (scholar.google.com) and the National Center for Biotechnology Information (ncbi.nlm.nih.gov), with the keyword “Myasthenia Gravis”. The management of myasthenia gravis can be done in various ways, namely, mechanical intubation and ventilation, non-invasive ventilation, pridostigmine as an anticholinesterase inhibitor, immunosuppressant therapy, short term immunotherapy, intravenous immunoglobulin, and surgical therapy. In the treatment of myasthenia gravis, the main goal is to restore muscle condition, especially patient productivity where the management of myasthenia gravis consists of management of myasthenic crisis, cholinergic crisis, symptoms, immunosuppressant therapy, and thymectomy surgical therapy if a tumor is indicated.

Universal Glia to Neurone Lactate Transfer in the Nervous System: Physiological Functions and Pathological Consequences

Whilst it is universally accepted that the energy support of the brain is glucose, the form in which the glucose is taken up by neurones is the topic of intense debate. In the last few decades, the concept of lactate shuttling between glial elements and neural elements has emerged in which the glial cells glycolytically metabolise glucose/glycogen to lactate, which is shuttled to the neural elements via the extracellular fluid. The process occurs during periods of compromised glucose availability where glycogen stored in astrocytes provides lactate to the neurones, and is an integral part of the formation of learning and memory where the energy intensive process of learning requires neuronal lactate uptake provided by astrocytes. More recently sleep, myelination and motor end plate integrity have been shown to involve lactate shuttling. The sequential aspect of lactate production in the astrocyte followed by transport to the neurones is vulnerable to interruption and it is reported that such disparate pathological conditions as Alzheimer’s disease, amyotrophic lateral sclerosis, depression and schizophrenia show disrupted lactate signalling between glial cells and neurones.

Olanzapine-Induced Withdrawal Oculogyric Crisis in an Adolescent With a Neurodevelopmental Disorder

This case report describes an adolescent female with a complex psychiatric history and Fragile X syndrome who developed an antipsychotic-withdrawal emergent oculogyric crisis (OGC) in approximately 12 hours following reduction in olanzapine dose from 20 mg total daily dose to 5 mg twice daily. The team concluded that the OGC was likely related to olanzapine withdrawal based on the following clinical factors: 1) prior treatment with olanzapine 20 mg for 4 to 5 days/week for several months, without such reaction; 2) proximity of the OGC to the olanzapine dose reduction (within 12 hours); and 3) lack of recurrence with olanzapine dose increase. Additionally, her neurodevelopmental disorder and age were identified as risk factors for an acute dystonic reaction. Published case reports describe withdrawal emergent dystonia, including OGC, following abrupt discontinuation of clozapine in adults. Given structural similarities of clozapine and olanzapine it can be postulated that this phenomenon is based in muscarinic receptor function—specifically, super-sensitized muscarinic receptors may react to excessive acetylcholine upon antipsychotic discontinuation, resulting in muscle motor end plate hyperactivity. Providers caring for pediatric patients with neurodevelopmental disorders should carefully consider risks for withdrawal emergent dystonia, obtain clear medication histories, and consider slow, conservative tapers when discontinuing antipsychotics.

COMPARISON OF INTUBATING CONDITIONS BETWEEN ATRACURIUM PRIMING, MAGNESIUM SULPHATE PRE-TREATMENT AND COMBINATION OF TWO METHODS ON ONSET AND DURATION OF NEUROMUSCULAR BLOCKADE: A RANDOMIZED DOUBLE BLIND CONTROLLED STUDY

Introduction: Magnesium inhibits acetylcholine release from the presynaptic membrane at the motor end plate; and thus it enhances the effect of non-depolarising muscle relaxants. Priming technique shortens the time of onset of non depolarising neuromuscular relaxants. Thus, the combination of magnesium pre-treatment and priming may be an effective method for achieving an early tracheal intubating condition. We studied the effect of magnesium sulphate pretreatment in combination with atracurium priming on onset and duration of neuromuscular blockade, compared with these methods when used alone. Materials and Methods: 100 patients scheduled for elective surgical procedures under general anaesthesia were divided into 4 groups. Group A (n=25) recieved priming with 0.05 mg/kg atracurium, three minutes before the intubating dose of atracurium 0.5 mg/kg, group M (n=25) was given 50 mg/kg magnesium sulphate as infusion over 10 mins before intubating dose of atracurium, group MA (n=25) received both the magnesium sulphate pretreatment and the priming dose of atracurium. Group N (n = 25) were given 0.5mg/kg atracurium alone as part of general anaesthesia. Tracheal intubation was done when the TOF stimulation showed single twitch which was measured at intervals of every 30 seconds. Parameters studied were the time to onset of neuromuscular blockade and the duration of neuromuscular blockade. Results: The MA group had the shortest onset time (mean±SD) 114.30±20.19 sec (p < 0.001) compared to the other groups. The duration of blockade was prolonged in both Group MA and Group M compared to other groups (P<0.001). Few adverse effects were reported in groups receiving magnesium, but were clinically not significant. Conclusion: Magnesium sulphate pretreatment in combination with atracurium priming shortens the time of onset of neuromuscular blockade when compared to magnesium sulphate pretreatment or priming used alone. Keywords: Atracurium priming, magnesium sulphate, neuromuscular blockade

Myofascial Pain

Myofascial pain syndromes arise from acute and chronic musculoskeletal pain and often have a referred neuropathic component. It affects more than three quarters of the world's population and is one of the most important and overlooked causes of disability. The origins of pain are thought to reside anywhere between the motor end plate and the fibrous outer covering of the muscle, with involvement of microvasculature and neurotransmitters at the cellular level. Diagnosis is made by clinical examination for the presence of myofascial trigger points, though some ancillary tests may provide supportive evidence. The mainstay of treatment is regular physical therapy with the goal of restoration of normal muscle laxity and range of motion. Adjunct therapies including pharmacologic and nonpharmacologic interventions provide varying degrees of benefit in refractory cases, and onabotulinum toxin A injection has the most evidence of efficacy for these patients. Here, we discuss the epidemiology, pathophysiology, and diagnostic and therapeutic options for the evaluation and treatment of myofascial pain syndrome.

Comment on Ultrasound Guidance for Botulinum Neurotoxin Chemodenervation Procedures. Toxins 2017, 10, 18—Quintessential Use of Ultrasound Guidance for Botulinum Toxin Injections—Muscle Innervation Zone Targeting Revisited

Recently, the importance of targeting structures during botulinum neurotoxin applications has been discussed in a variety of disorders, including spasticity and dystonia. In this respect, the advantages of ultrasound imaging to traditional techniques have been emphasized. We would like underscore the importance of ultrasound guidance, with targeting innervation zone(s) of the over-active muscles to achieve effective clinical outcomes. Additionally, we also clarify the difference between the terms—innervation zone (motor end plate) and motor point—which have been used by the authors as if they were the same. Further, we disagree with the authors about the intramuscular botulinum neurotoxin application techniques i.e., in-plane vs. out-of-plane whereby the former is, for sure, superior.