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The Sensitivity of Electromyoneurography in The Med Pregl 2011; LXIV (1-2): 11-14. Novi Sad: januar-februar. 11 ORIGINALNI NAUČNI RADOVI ORIGINAL STUDIES Clinical Centre of Vojvodina Novi Sad Originalni naučni rad Department of Neurology Original study UDK 616.379-008.64:616.833-073.7 DOI: 10.2298/MPNS1102011C THE SENSITIVITY OF ELECTROMYONEUROGRAPHY IN THE DIAGNOSIS OF DIABETIC POLYNEUROPATHY SENZITIVNOST ELEKTROMIONEUROGRAFIJE U RANOJ DIJAGNOSTICI DIJABETESNE POLINEUROPATIJE Milan CVIJANOVIĆ, Miroslav ILIN, Petar SLANKAMENAC, Sofija BANIĆ HORVAT and Zita JOVIN Summary – Diabetic polyneuropathy is a complex set of clinical syndromes, which deplete various regions of the nervous system. The process leading to diabetic neuropathy is multi-factorial. Its symptoms are paresthesia, dysesthesia and pain. The signs of damage to the peripheral neurons are hypoesthesia, hypoalgesia, hyperesthesia and hyperalgesia, decreased tendon reflexes, and, possibly, weakness and muscle atrophy. There is no universal classification. Electromyoneurography is indispensable in the diagnosis of dia- betic polyneuropathy. However, there is no agreement on the most sensitive parameter for an early diagnosis. One hundred patients with diabetes mellitus were examined in order to investigate the sensitivity of different electromyographic parameters. Electromyo- graphic techniques proved to be entirely sensitive for the early diagnosis of diabetic polyneuropathy. Some of the parameters are more suitable for an early detection of peripheral nerve damage, and others, which are not so sensitive but easy to use and stable, are suitable to follow up the course of diabetic polyneuropathy. Key words: Diabetic Neuropathies; Signs and Symptoms; Electromyography; Early Diagnosis; Sensitivity and Specificity Introduction Pathophysiology of diabetic polyneuropathy Diabetic polyneuropathy is a complex set of clini- In agreement with the results of retrospective and cal syndromes, which deplete various regions of the prospective studies suggesting a strong association be- nervous system, either individually or in a combina- tween hyperglycemia and the development and severi- tion [1]. It is the most common complication of diabe- ty of diabetic polyneuropathy (DPN), its prevalence is tes mellitus, leading to major morbidity and mortality highest among people with poorly controlled diabetes. and producing huge costs [2]. A simple and widely Until recently, there were two theories explaining the used clinical definition is that diabetic polyneuropathy mechanism of diabetic neuropathy –metabolic and is the presence of symptoms and/or signs of peripheral vascular. It seems most probable, however, that an in- nervous dysfunction in diabetic patients when other teraction between the two mechanisms leads to neu- possible causes have been excluded. The prevalence of ropathy [8]. More recently, it has become generally neuropathy in diabetes varies widely in literature, be- recognized that the process leading to diabetic neu- tween 0.1% and 100% [3], and most frequently the es- ropathy is multi-factorial [9], although dominated by timates are 10-100% [4]. The wide prevalence rates re- metabolic factors involving the polyol pathway and ported are due to different diagnostic criteria used, vascular disorders. Other factors that are related to different methodological approaches adopted [5] and those previously mentioned, such as accumulation of populations studied [6]. Approximately 10% of pa- end-products of non-enzymatic glycosylation in the tients have polyneuropathy at the time they are diag- nerve and blood vessel proteins have also been recog- nosed with diabetes. The data on such a high preva- nized [10]. Furthermore, decreased n-6-essential fatty lence of polyneuropathy in newly-diagnosed diabetics acids and prostaglandin result in damage to the nerve and data estimating the prevalence rate at 100% result sheath and microvascular and blood abnormalities. In from electrophysiological studies [7]. Since a timely addition, a significant role is played by nitric oxides diagnosis is a prerequisite for the adequate treatment (oxidative stress), decreased neurotrophic factors, in and prevention of more severe damage to peripheral particular nerve growth factor but also neurotrophin–3 neurons, it is of utmost importance to identify the most and insulin-like growth factor, which affects axonal sensitive electromyographic technique for the early transport, decreased protein kinase C activity and im- detection of diabetic polyneuropathy. munological factors. Laminin has also been frequently Corresponding Author: Doc. dr Milan Cvijanović, Clinic of Neurology, Clinical Centre of Vojvodina, 21000 Novi Sad, Hajduk Veljkova 1-11, E-mail: [email protected] 12 Cvijanović M, et al. Pathophysiology of diabetic polyneuropathy Abbreviations Subclinical neuropathy DPN – diabetic polyneuropathy Rapid reversible phenomena: CHRD – chronodispersion 1) Distal sensory symptoms SCV – sensory conduction velocity 2) Reduced nerve conduction velocity implicated lately. Laminin, a large heterotrimeric pro- 3) Resistance to ischemia-associated conduction di- tein of basement membranes, appears to have a signif- sturbances icant role in the nerve regulation and manifestations of neuropathy [11]. It promotes neurite extension in cul- Clinically manifest neuropathy tured neurons. An abnormal expression of laminin Focal and multifocal neuropathy: beta 2 gene (laminin is composed of one large alpha 1) Cranial neuropathy and two small beta chains – beta 1 and beta 2) may 2) Thoracoabdominal neuropathy contribute to the pathogenesis of diabetic neuropathy. 3) Focal neuropathy of the extremities 4) Motor asymmetric neuropathy of the proximal Clinical picture of DPN part of lower extremities (diabetic amyotrophy) The most common symptoms of DPN are pare- Symmetric neuropathy sthesias, and dysesthesias, which are described as 1) Sensory/(sensory-motor)/autonomous neuropathy feelings of walking on water, or cotton or wool stro- 2) Proximal motor neuropathy of the lower extremities kes over the soles, or similar. Cramps are also com- mon and usually occur in the lower leg, in particular Electromyoneurography in the diagnosis the calf and toe flexors. Pain is usually described as of diabetic neuropathy sudden and poignant pain resembling piercing by a sharp tool, but also as dull and tormenting, as if The foundations of clinical electromyography were holding legs in the freezing cold water [12]. It may laid by Buchthal and Clemmesen in 1941 [13]. However, occur at any stage of disease and is difficult to ob- this electrophysiological technique, including peripheral jectify. By its characteristics, this small fibre pain nerve studies in diabetic patients, has become more has all characteristics of neuropathic pain. Due to widely used only in the last decades. Early studies fo- its unpleasant manifestations with the paresthetic cused on the analysis of electromyographic findings, modalities, it severely impairs the quality of life and i.e. firing patterns. In diabetic neuropathy, the pattern is frequently resistant to treatment. is usually thin and there is an increased percentage of Impaired vibration sensitivity is frequently report- polyphasic potentials. However, a significantly more ed as a convincing sign of DPN. Hypoesthesia and sensitive parameter is the nerve conduction velocity hypoalgesia also occur and are frequently preceded study, including both sensory and motor nerve fibres, by hyperesthesia and hyperalgesia. Decreased tendon which belongs to the domain of conventional elec- reflexes, almost invariably the Achilles reflex, occur troneurography. Compared to diabetics with no clini- subsequently or simultaneously. Muscle paresis and cal signs of neuropathy, in diabetics with signs of neu- atrophies, more often in the lower extremities, occur ropathy, motor conduction velocities are more de- in advanced disease. These signs are followed by the creased and reduction of the evoked potential ampli- signs of vegetative neuropathy, but the latter is not tude occurs earlier [14]. Tibial and peroneal nerves discussed in the present paper. show more abnormality than ulnar and medial nerves, i.e., the lower extremities are more sensitive to diabetic Classification of diabetic neuropathy damage than the upper extremities. The involvement of peripheral nerves is diffuse, more distal than proxi- Recognition of various clinical syndromes of pe- mal parts. However, some authors have long consid- ripheral neuron damage and their likely overlapping ered that distal latency in axonal neuropathies, includ- prevents us from adopting a universal classification. ing diabetic neuropathy, does not reflect only dysfunc- There have been many attempts at systematizing tion of the distal segment. Namely, the loss of alpha different manifestations, using different criteria, motor neurons leads firstly to decreased motor electric both clinical and topographic, as well as subclinical, conduction velocity in the distal part of the peripheral morphometric and neurophysiological signs of pe- nerve. Sensory conduction velocity is considered a ripheral nerve damage. This has produced a great more sensitive study than the motor conduction velo- number of classifications of diabetic neuropathy. city [15]. Burke et al. consider that sensory conduction However, there are classifications that are widely ac- velocity study of the sural nerve is the most sensitive cepted, such as Thomas’ classification [10], which electrodiagnostic method for the detection of polyneu- differentiates between
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