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Part I. Individual Neuromuscular Disorders 1

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Part I. Individual Neuromuscular Disorders 1 PART I. INDIVIDUAL NEUROMUSCULAR DISORDERS 1. MOTOR NEURONOPATHIES AMYOTROPHIC LATERALS SCLEROSIS (ALS) Etiology " heterogeneous etiology " most are sporadic " 5-10 % are hereditary, both dominant and recessive inheritance has been described: " one hereditary form is linked to chromosome 2q33-q35, another is Cu/Zn superoxide dismutase (SOD1) mutation on chromosome 21q22 " degeneration of both upper and lower motor neurons Clinical features " incidence around 2/100 000 " usually onset in the older age groups around 60 years but may present earlier " males>females " painless weakness " upper limb muscles affected more frequently than lower limb muscles " bulbar muscles may be involved; slurring of speech, dysphagia, " extraocular muscles and anal or urethral sphincters are rarely clinically affected " upper motor neuron signs, increased tendon reflexes and positive Babinski sign, often present " average survival after diagnosis 3 years,;in patients presenting with bulbar symptoms shorter survival Strategy " confirm neurogenic EMG findings in muscles in three regions of the body (the regions are (1) brainstem, (2) brachial, (3) thorax, (4) trunk and (5) crural " exclude polyneuropathy " differentiate from multifocal motor neuropathy with conduction block (MMN) " differentiate from spinal hereditary motor neuronopathies (spinal muscular atrophies) " differentiate from previous polio Diagnostic criteria " The diagnosis of ALS requires the presence of: (1) lower motor neuron signs (LMS), (2) upper motor neuron signs (UMS) and (3) progression of the disorder 1. definite ALS: LMS in three regions and UMS 2. probable ALS: LMS in two regions and UMS 3. possible ALS: LMS in one region and UMS 4. suspected ALS: LMS in two or three regions Expected abnormal findings EMG " subacute neurogenic muscle findings in at least 3 regions. Preferentially the findings should be asymmetric without any definite proximal or distal predominance. Neurography " MCS often show reduced amplitudes " If the AMPL is reduced significantly the conduction velocity may be reduced (loss of fastest conducting axons) Central motor conduction time " often abnormal Expected normal findings Neurography "SCS " MCS: if AMPL is normal or only moderately reduced, CV should be normal " no motor conduction block " normal number of F-waves in mildly affected muscles (indicating lack of proximal conduction block) Evoked potentials " VEP " BAEP " SEP (may rarley be abnormal) Procedure EMG (if normal findings on one side examine both sides!) " m.orbicularis oris/m.masseter/m.genioglossus (insert electrode below chin) " m.trapezius " interosseus dorsalis I / m.biceps brachii / m.deltoideus " m.tibialis anterior / m.gastrocnemius caput mediale / m.vastus lateralis " if the patient presents with dysarthria and there are no other EMG abnormalities, test m.chricothyreoideus Neurography MCS (bilaterally) " n.medianus " n.ulnaris (also including supraclavicular stimulation) " n.peroneus " n.tibialis Neurography SCS (bilaterally) " n.suralis " n.radialis References " Behnia M, Kelly JJ. Role of electromyography in amyotrophic lateral sclerosis. Muscle Nerve 1991;14:1236-1241 " Bromberg MB. Motor unit estimation: reproducibility of the spike-triggered averaging technique in normal and ALS subjects. Muscle Nerve. 1993;16:466-471 2 " Carvalho M, Schwartz MS, Swash M. Involvement of the external anal sphincter in amyotrophic lateral sclerosis. Muscle Nerve 1995;18:848-853 " Cascino GD, Ring SR, PJL King, Brown RH, Chiappa KH. Evoked potentials in motor system diseases. Neurology 1988;38:231-238 " Cornblath DR, Kuncl RW, Mellits ED, Quaskey SA, Clawson L, Pestronk , Drachman DB. Nerve conduction studies in amyotrophic lateral sclerosis. Muscle Nerve 1992;15:1111-1115 " Dengler R, Konstanzer A, Kuther G, Hesse S, Wolf W, Struppler A Amyotrophic lateral sclerosis: Macro-EMG and twitch forces of single motor units. Muscle Nerve 1990;13:545-50 " Haverkamp LJ, Appel V, Appel SH. Natural history of amyotrophic lateral sclerosis in a database population. Validation of a scoring system and a model for survival prediction. Brain 1995;118:707-19 " Ingram DA, Swash M. Central motor conduction time is abnormal in motor neuroopn disease. J Neurol Neurosurg Psychiatry 1987;50:159-166 " Kang DX, Fan DS. The electrophysiological study of differential diagnosis between amyotrophic lateral sclerosis and cervical spondylotic myelopathy. Electromyogr Clin Neurophysiol 1995;35:231-8 " Kelly JJ, Thibodeau L, Andres PL, Finison LJ. Use of electrophysiologic tests to measure disease progression in ALS therapeutic trials. Muscle Nerve. 1990;13:471-9 " Killian JM, Wilfong AA, Burnett L, Appel SH, Boland D. Decremental motor responses to repetitive nerve stimulation in ALS. Muscle Nerve. 1994;17:747-754 " McComas AJ. Motor unit estimation: anxieties and achievements. Muscle Nerve 1995;18:369-79 " Nakanishi T, Tamaki M, Arasaki K. Maximal and minimal motor nerve conduction velocities in amyotrophic lateral sclerosis. Neurology 1989;39:580-583 " Shefner JM, Tyler HR, Krarup C. Abnormalities in the sensory action potential in patients with amyotrophic lateral sclerosis. Muscle Nerve 1991;14:1242-1246 " Stålberg E, Schwartz MS, Trontelj JV. Single fibre electromyography in various processes affecting the anterior horn cell. J Neurol Sci 1975;24:403-15 " Stålberg E. Electrophysiological studies of reinnervation in ALS. Adv Neurol 1982;36:47-59 " Swasch M, Shaw CED, Leigh PN. Familial amyotrophic lateral sclerosis. In Emery AEH (editor). Diagnostic criteria for neuromuscular disorders. Royal Society of Medicine Press, London 1997. " Ugawa Y, Shimpo T, Mannen T. Central motor conduction in cerebrovascular disease and motor neuron disease. Acta Neurol Scand 1988;78:297-306 Modified " BF 25.3.1997 ES 2.4.97 POLIO, ACUTE Etiology " following infection by poliovirus most patients will have fever and gastrointestinal symptoms, but 1-2 % develope paralysis " due to vaccination polio has been eradicated from developed countries " attenuated virus used for vaccination may cause paralysis, estimated risk is 1 per million " sometimes coxackie and eccho virus may cause a similar paralysis Clinical features " around 1-2 weeks after an episode of febrile illness 1-2 % of patients with a polio virus infection will develop a paralytic disorder " the risk of paralysis increases with age, adults are about 10 times as likely to develop paralysis than children " any group of motor neurons may be affected, the distribution of weakness varies " after the initial paralysis a varying degree of restitution takes place " some patients with polio perceive after a stable period of more than 15 years new loss of muscle function (often called post- polio syndrome, see Polio, sequale following previous infection Strategy " show acute neurogenic involvement of several muscles usually in several regions of the body " assess distribution of abnormalities and degree of involvement " differentiate from polyradiculitis Expected abnormal findings EMG " acute neurogenic EMG findings in muscles " distribution not confined to one segment or nerve; if local - reconsider diagnosis Neurography " MCS: reduced amplitudes in weak muscles " if the amplitude is severely reduced the MCV may be reduced Expected normal findings Neurography "SCS Procedure EMG " weak muscles should be studied Neurography The following motor nerves should be studied bilaterally " n.medianus " n.ulnaris " n.peroneus " n.tibialis The following sensory nerves should be tested " n.suralis " n.radialis Note " although vaccination has largely eradicated acute polio from countries with a good vaccination program, polio may still occur in some parts of the world. In industrialized countries there are minorities that are negative to vaccinations and refugees that may still lack vaccination against polio. 3 References " ParryG. Myelopathies affecting anterior horn cells. 88-898. In Dyck PJ, Thomas PKGriffin JW, Low PA, Puduslo FA. Peripheral Neuropathy. WB Saunders Company , Philadelphia 1993. " Wiechers D. Electrophysiology of acute polio revisited. Utilizing newer EMG techniques in vaccine-associated disease. Ann N Y Acad Sci 1995;753:111-9 Modified " 2.4.1997, ES 3.4.97, BF 15.4.1997 POLIO, SEQUALE FOLLOWING PREVIOUS PARALYSIS Etiology " previously suffered from polio, the patient has recovered from the acute episode to various degrees " the causes of sequele vary considerably: (1) normal aging with loss of contractile strength contributesloss of motor units with aging, (2) pain from joints and tendons and (3) psycho-social factors " there are no well defined biological parameters that define this disorder Clinical features " after a stable period of more than 15 years after the initial paralysis some patients develop subjective new loss of muscle function (often called post-polio syndrome) " the distribution of weakness varies considerably and depends on the distribution and severity of the initial affection Strategy " show inactive neurogenic involvement of several muscles usually in several regions of the body " make sure the polio diagnosis is correct " assess distribution of abnormalities and degree of involvement " beware of additional diseases: radiculopathy, CTS, polyneuropathy, polymyositis Expected abnormal findings EMG " inactive neurogenic findings in weak and often also in strong muscles depending on involvement " distribution not confined to one segment or nerve (if findings are focal - reconsider diagnosis) Neurography " MCS may show reduced amplitudes and if the amplitude is severely
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