On the other hand, neuroimaging is not always totally reliable for determining a diagnosis, and MRI cannot assess the functional involvement of the spinal cord. Thus, neurophysiological evaluation by various types of electrodiagnostic procedures may be regarded as a necessary reconcile between clinical assessment and radiographic investigations [12, 13].
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Muscle biopsy and electromyography (EMG) were performed for the diagnosis of ACM.13, 14, 15, 16, 17, 18, 19 Muscle biopsy shows direct evidence of muscle damage from ACM.20 EMG is an electrodiagnostic study and is performed to confirm ACM from a functional point of view.12 To increase the accuracy of the diagnosis of ACM, both measurements were applied in the cases reported.
EMG showed abnormal spontaneous activities at 2 and 4 weeks in those patients treated with MP and underwent EMG studies (except the patient in case 3 who refused EMG). In cases 2, 4 and 5, EMGs demonstrated abnormal spontaneous activities at above and below the SCI levels. For the patient in case 1, his SCI level was so high (at C4) that EMG could only be performed below his SCI level and showed abnormal spontaneous activities. It is difficult to evaluate recruitment and motor unit potentials in the muscles below the SCI level because of the lack of voluntary muscle contraction. In cases 2, 4 and 5, recruitment patterns could only be tested in the muscles above the SCI levels and showed increased recruitment and decreased amplitudes of the motor unit potentials. Recruitment could not be tested in the patient in case 1 because all the testing muscles were below the SCI level and were not voluntarily moveable. In the three patients who did not receive i.v. MP (cases 6, 7 and 8), EMGs were normal. Nerve conduction studies were performed in all the patients participated in this study and did not show peripheral nerve injury. These data, from an electrodiagnostic point of view, suggest that the muscles in the patients who received MP were undergoing myopathic changes.
Quantitative EMG (qEMG), to determine whether the EMG findings were myopathic or neuropathic in nature, is not possible in dogs due to the need for volitional activity. Human qEMG reports in sIBM are conflicting, with some cases appearing myopathic, several labeled as neuropathic and others having mixed results [2, 12, 26, 30]. In this case, peroneal and ulnar MNCV examination revealed changes suggestive of a mild motor neuropathy. As is the case in humans, whether these changes are age-related or a feature of sIBM in dogs is unclear. Similarly, the SNCV findings were of interest. Of the three SNCV studies performed, only the ulnar sensory nerve action potential was dispersed and decreased in amplitude. Dabby [12] describes a subset of 9 cases out of a group of 70 sIBM patients that were originally diagnosed with motor neuron disease based on clinical presentations and electrodiagnostic findings. In all nine, both motor and sensory conduction velocities were normal, but two had reduced CMAP.
This observational cross-sectional study from a neuromuscular disorders center included individuals whose electrodiagnostic tests performed between 2008 and 2017 confirmed a diagnosis of polyneuropathy. Through analysis of medical records, polyneuropathies were classified according to etiology and neurophysiological aspect.
Due to discussions regarding the indication of electrodiagnostic tests and due to the lack of information related to the epidemiology of polyneuropathies33. Felix EPV, Oliveira A de SB. Guidelines for the diagnosis of neuropathies in a Reference Center for Neuromuscular diseases. Rev Neurocienc. 2010 Jan 1;18(1):74-80. ,1010. Azhary H, Farooq MU, Bhanushali M, Majid A, Kassab MY. Peripheral neuropathy: differential diagnosis and management. Am Fam Physician. 2010 Apr 1;81(7):887-92., the aim of this study was to determine the main etiologies of polyneuropathy confirmed by electrodiagnostic tests within a single specialized tertiary center of Southern Brazil. The main clinical manifestations, risk factors, and associated electrophysiological findings are reported.
In our hospital, patients with suspected polyneuropathy are determined by the examination of the neurologist. Nerve conduction studies and needle electromyography (EMG) are performed in all patients according to standard protocols1111. England JD, Gronseth GS, Franklin G, Miller RG, Asbury AK, Carter GT, et al. Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2005 Jan 25;64(2):199-207. ,1212. Dumitru D, Amato A, Zwarts M. Eletrodiagnostic medicine. 2nd ed. Hanley & Belfus; 2001. 1536p. . Reference values of the nerve conduction studies are based on previously published standard protocols1212. Dumitru D, Amato A, Zwarts M. Eletrodiagnostic medicine. 2nd ed. Hanley & Belfus; 2001. 1536p. .
The electrophysiological criterion used for definition of polyneuropathy was an abnormality in at least one parameter in two or more peripheral nerves of two or more extremities1111. England JD, Gronseth GS, Franklin G, Miller RG, Asbury AK, Carter GT, et al. Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2005 Jan 25;64(2):199-207. ,1313. Fuglsang-Frederiksen A, Pugdahl K. Current status on electrodiagnostic standards and guidelines in neuromuscular disorders. Clin Neurophysiol. 2011 Mar;122(3):440-55. . All EDX tests were retrospectively reviewed by the authors to verify the fulfillment of this criterion.
Polyneuropathies were classified as motor or sensory if disturbances were present only in motor or sensitive nerve fibers, respectively. Sensorimotor polyneuropathy was defined by abnormalities involving motor and sensitive nerve fibers1212. Dumitru D, Amato A, Zwarts M. Eletrodiagnostic medicine. 2nd ed. Hanley & Belfus; 2001. 1536p. .
Considering that only patients with electrodiagnostic test compatible with polyneuropathy were included, this study did not evaluate small fiber polyneuropathies, which have as a diagnostic criterion a normal EDX test1515. Gondim F de AA, Barreira AA, Claudino R, Cruz MW, da Cunha FMB, de Freitas MRG, et al. Definition and diagnosis of small fiber neuropathy: consensus from the Peripheral Neuropathy Scientific Department of the Brazilian Academy of Neurology. Arq Neuropsiquiatr. 2018 Mar;76(3):200-8. -282x20180015 -282x2018001... ,1616. Terkelsen AJ, Karlsson P, Lauria G, Freeman R, Finnerup NB, Jensen TS. The diagnostic challenge of small fibre neuropathy: clinical presentations, evaluations, and causes. Lancet Neurol. 2017 Nov 1;16(11):P934-44. -4422(17)30329-0 -4422(17)30... .
The five main causes of polyneuropathy confirmed by EDX testing were inflammatory, hereditary, idiopathic, multifactorial, and diabetic polyneuropathy. From these data, our study indicates that polyneuropathies submitted to electrodiagnostic testing are those recently advocated by the AANEM in its official position: polyneuropathies that show a severe, atypical, rapidly progressing course, with predominant motor involvement, a positive family history, or when no cause is identified despite initial assessment99. American Association of Neuromuscular & Electrodiagnostic Medicine. AANEM policy statement on electrodiagnosis for distal symmetric polyneuropathy. Muscle Nerve. 2018 Feb;57(2):337-9. .
From the EDX tests performed on suspicion of polyneuropathy, 48.9% confirmed this condition and 17.7% revealed a different diagnosis. This corroborates the fact that EDX not only confirms polyneuropathy but also detects other associated neuromuscular diseases and reveals other diagnoses, specially mononeuropathies and radiculopathies. Ginsberg and Morren recently found similar results2828. Ginsberg MR, Morren JA. Utility of electrodiagnostic studies in patients referred with a diagnosis of polyneuropathy. Muscle Nerve. 2020 Mar;61(3):288-92. ; the EDX of patients with suspected diabetic polyneuropathy presented an alternative diagnosis in about 20% of patients, and in 25% of those patients, it detected other overlapping diseases. Thus, it would be interesting to explore polyneuropathies due to common causes to better determine the origin of symptoms and the outcome2828. Ginsberg MR, Morren JA. Utility of electrodiagnostic studies in patients referred with a diagnosis of polyneuropathy. Muscle Nerve. 2020 Mar;61(3):288-92. ,2929. Geiger CD, Preston DC. The value of electrodiagnostic studies in patients with suspected polyneuropathy. Muscle Nerve. 2020 Mar;61(3):263-4. .
Optimal care of patients with NA requires the integrated management of a team that may include a physiatrist, electrodiagnostician, pediatrician, neurologist, physical and occupational therapist, and pain specialist. Referral to surgery may be indicated in certain cases.
Thirty-two patients diagnosed with non-traumaic CPM were retrospective reviewed. The patients with diabetes mellitus or polyneuropathy were excluded. The patients who undertook the electrodiagnostic examination before 7 days after onset were also excluded. Finally, 25 patients with CPM in the knee were included. The delay between the onset of symptom and electrophysiologic evaluation was 10 days to 4 months. The studies conducted on the patients were segmental motor conduction study of the common peroneal nerve (ankle-fibular head-popliteal fossa), tibial motor nerve conduction study, and sensory conduction studies of the common peroneal mixed nerve, the superficial peroneal nerve, and the sural nerve. Needle EMG of the lower extremity muscles was also performed.
The CPM was diagnosed if the electrodiagnostic findings fulfilled one of common peroneal motor conduction study with or without abnormal superficial SNAP and needle electromyographic findings (1, 12): 1) absent or low CMAP with fibular head stimulation in EDB and/or TA recordings, 2) a decrease in CMAP negative potential amplitude from fibular head to popliteal fossa greater than 20% with or without an segmental slowing of fibular head-popliteal fossa segment (greater than 10 m/sec slower than ankle to fibular head segment), 3) significant change in CMAP configuration at the popliteal fossa site compared to the fibular site with or without a segmental slowing of fibular head-popliteal fossa segment (>10 m/sec than ankle to fibular head segment), 4) absent or low superficial SNAP, and 5) abnormal spontaneous activities and/or polyphasic motor unit potentials (MUPs) with reduced recruitment patterns in common peroneal innervated muscles. 2ff7e9595c
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