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Artykuły w czasopismach na temat „Sensorimotor polyneuropathy”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Sedlić, Marija, Gordana Sičaja, Krešimir Luetić, and Hrvoje Budinčević. "Cryoglobulinemia and sensorimotor polyneuropathy." Infektološki glasnik 40, no. 1 (2020): 35–37. http://dx.doi.org/10.37797/ig.40.1.5.

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Secondary cryoglobulinemia is the most common extrahepatic manifestation of hepatitis C. There are different genotypes of hepatitis C, and the ones that are most frequently associated with cryoglobulinemia are genotypes 1b and 2a. Cryoglobulinemia affects various organs and can cause vasculitis, arthralgia, skin changes, glomerulonephritis and neurological manifestations, including peripheral neuropathy. The aim of this report was to emphasize the importance of early diagnosis of hepatitis C infection in patients who are presenting with sensomotor polyneuropathy.

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Gorczyca, Daiva, and Ulrike Schwirten. "Sensorimotor polyneuropathy after hexavalent vaccination." Scandinavian Journal of Infectious Diseases 46, no. 1 (2013): 66–68. http://dx.doi.org/10.3109/00365548.2013.831183.

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Nardone, Raffaele, Thomas Buratti, Stefan Golaszewski, et al. "Delayed Oxaliplatin-Induced Sensorimotor Polyneuropathy." Onkologie 32, no. 5 (2009): 10. http://dx.doi.org/10.1159/000209321.

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Ocampo-Navia, Maria Isabel, María Andrea Negret Noreña, Luis Rafael Chaparro Santos, José Ricardo Morera Afanador, Ricardo Andrés Quintero Farías, and José Luis Bustos Sánchez. "POEMS Syndrome Diagnosis in a Patient with Mixed Polyneuropathy: Case Report." Prague Medical Report 123, no. 1 (2022): 27–34. http://dx.doi.org/10.14712/23362936.2022.3.

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POEMS syndrome is a rare condition of paraneoplasic origin characterized by the presence of a sensorimotor polyneuropathy associated with the presence of a proliferative disorder of plasmatic monoclonal cells and overproduction of vascular endothelial growth factor. The acronym “POEMS” represents multisystem findings including polyneuropathy, organomegaly, endocrinopathy, monoclonal plasma cell disorder and skin changes; nevertheless, clinical presentation is heterogeneous. We describe a clinical case, the diagnostic and therapeutic approach in a patient with sensorimotor polyneuropathy in who

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Jastrzębski, Karol, Nina Romanowska, Marta Rek-Pacześ, et al. "Stiff-person syndrome with sensorimotor polyneuropathy – case report." Aktualności Neurologiczne 21, no. 1 (2021): 47–55. http://dx.doi.org/10.15557/an.2021.0007.

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Stiff-person syndrome (SPS) is a rare disorder with an estimated prevalence in the general population of 1–2 cases/1,000,000. It is 2–3 times more common in females, with symptom onset at the age of 20–50 years in most cases. Although stiff-person syndrome is associated with antibodies against glutamic acid decarboxylase and amphiphysin, their presence is not necessary for the diagnosis. The treatment should be multidirectional and include immunomodulation, symptomatic treatment as well as monitoring and treatment of overlapping autoimmune, and surgery. We present a case report of a patient di

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Puri, Vinod, AshishKumar Duggal, and Neera Chaudhry. "Idiopathic CD4 lymphocytopenia with sensorimotor polyneuropathy." Annals of Indian Academy of Neurology 19, no. 3 (2016): 381. http://dx.doi.org/10.4103/0972-2327.165470.

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Dunnigan, S. K., H. Ebadi, A. Breiner, et al. "Conduction Slowing in Diabetic Sensorimotor Polyneuropathy." Diabetes Care 36, no. 11 (2013): 3684–90. http://dx.doi.org/10.2337/dc13-0746.

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A. Kles, Keri, and Vera Bril. "Diagnostic Tools for Diabetic Sensorimotor Polyneuropathy." Current Diabetes Reviews 2, no. 3 (2006): 353–61. http://dx.doi.org/10.2174/157339906777950598.

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Cornblath, D. R., A. Vinik, E. Feldman, R. Freeman, and A. J. M. Boulton. "Surgical Decompression for Diabetic Sensorimotor Polyneuropathy." Diabetes Care 30, no. 2 (2007): 421–22. http://dx.doi.org/10.2337/dc06-2324.

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Choi, Jong Kyoung, Won Jun Kim, and Jae Yong Jeon. "Paraneoplastic sensorimotor polyneuropathy in prostatic adenocarcinoma." Medicine 97, no. 15 (2018): e0030. http://dx.doi.org/10.1097/md.0000000000010030.

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Heckmann, Josef G., Wenke Dietrich, Werner Hohenberger, Peter Klein, Bert Hanke, and Bernhard Neund�rfer. "Hypoglycemic sensorimotor polyneuropathy associated with insulinoma." Muscle & Nerve 23, no. 12 (2000): 1891–94. http://dx.doi.org/10.1002/1097-4598(200012)23:12<1891::aid-mus17>3.0.co;2-y.

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Gurieva, I. V. "Diabetic sensorimotor polyneuropathy – a cholistic approach." Endocrinology: News, Opinions, Training 11, no. 4 (2022): 26–47. http://dx.doi.org/10.33029/2304-9529-2022-11-4-26-47.

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De Carolis, G. "Effectiveness of 10-kHz High-frequency spinal cord stimulation in diabetic polyneuropathy refractory to medical management: two case reports." Journal of AMD 24, no. 3 (2021): 224. http://dx.doi.org/10.36171/jamd21.24.1.6.

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The sensorimotor diabetic polyneuropathy represents a serious health problem, as it is responsible for an increased risk of mortality and substantial morbidity, resulting from foot ulceration, amputations, and impaired quality of life. Appropriate drug treatments are often unsuccessful at providing adequate pain relief and the use of minimally invasive procedures such as spinal cord stimulation (SCS) represents a valid therapeutic choice. Patient’s medical history and characteristics as well as clinical indication for the procedure influence the clinician in choosing the right type of therapy.

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14

García-Mesa, Yolanda, Jorge Feito, Mario González-Gay, et al. "Involvement of Cutaneous Sensory Corpuscles in Non-Painful and Painful Diabetic Neuropathy." Journal of Clinical Medicine 10, no. 19 (2021): 4609. http://dx.doi.org/10.3390/jcm10194609.

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Distal diabetic sensorimotor polyneuropathy (DDSP) is the most prevalent form of diabetic neuropathy, and some of the patients develop gradual pain. Specialized sensory structures present in the skin encode different modalities of somatosensitivity such as temperature, touch, and pain. The cutaneous sensory structures responsible for the qualities of mechanosensitivity (fine touch, vibration) are collectively known as cutaneous mechanoreceptors (Meissner corpuscles, Pacinian corpuscles, and Merkel cell–axonal complexes), which results are altered during diabetes. Here, we used immunohistochemi

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15

Ekiz, Esra, Abdullah Ozkok, and Nazan Kader Ertugrul. "Paraneoplastic Mononeuritis Multiplex as a Presenting Feature of Adenocarcinoma of the Lung." Case Reports in Oncological Medicine 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/457346.

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Paraneoplastic neurologic syndromes are observed in less than 0.1% of cancer patients. Neurologic syndromes in lung cancer include Lambert-Eaton myasthenic syndrome, polyneuropathy, cerebellar degeneration, and rarely mononeuritis multiplex. In this case, a patient presenting with bilateral asymmetrical sensorimotor polyneuropathy who was diagnosed with adenocarcinoma of the lung is reported.

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16

Vasku, Marketa, Thomas Papathemelis, Nicolai Maass, Ivo Meinhold-Heerlein, and Dirk Bauerschlag. "Endometrial Carcinoma Presenting as Vasculitic Sensorimotor Polyneuropathy." Case Reports in Obstetrics and Gynecology 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/968756.

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Paraneoplastic syndromes (PNS) are a heterogeneous group of symptoms which are indirectly caused by primary or metastatic tumor. Paraneoplastic polyneuropathy (PNP) is mostly related to small cell lung cancer (5%), prostate, gastric, and breast cancer. Only sporadic cases have been reported to be associated with endometrial cancer. We present a case of a premenopausal woman with severe vasculitic, asymmetric sensorimotor polyneuropathy that developed in conjunction with an endometrial carcinoma responding to surgical therapy of primary tumor combined to steroid therapy. Neurological symptoms s

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17

Braund, K. G., M. Toivio-Kinnucan, J. M. Vallat, J. R. Mehta, and D. C. Levesque. "Distal Sensorimotor Polyneuropathy in Mature Rottweiler Dogs." Veterinary Pathology 31, no. 3 (1994): 316–26. http://dx.doi.org/10.1177/030098589403100304.

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A polyneuropathy recognized in mature Rottweiler dogs is characterized by paraparesis that progresses to tetraparesis, spinal hyporeflexia and hypotonia, and appendicular muscle atrophy. Although signs may appear acutely, the course tends to be gradually progressive (up to 12 months or longer in some dogs) and may be relapsing. Nerve and muscle biopsies were examined from eight affected Rottweilers (six male and two female) between ages 1.5 and 4 years. Pronounced neurogenic atrophy was present in skeletal muscle samples. Changes in sensory and motor peripheral nerves included loss of myelinat

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18

Park, Kee Hong, Sung-Yeon Sohn, Jung-Joon Sung, Kwang-Woo Lee, and Yoon-Ho Hong. "Subacute Sensorimotor Polyneuropathy Associated with Autoimmune Hepatitis." Journal of Clinical Neurology 12, no. 1 (2016): 123. http://dx.doi.org/10.3988/jcn.2016.12.1.123.

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BRONSTER, DAVID J., PAUL YONOVER, JEFF STEIN, STEPHEN N. SCELSA, CHARLES M. MILLER, and PATRICIA A. SHEINER. "DEMYELINATING SENSORIMOTOR POLYNEUROPATHY AFTER ADMINISTRATION OF FK506." Transplantation 59, no. 7 (1995): 1066???1067. http://dx.doi.org/10.1097/00007890-199504000-00029.

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Bronster, David J., Paul Yonover, Jeff Stein, Stephen N. Scelsa, Charles M. Miller, and Patricia A. Sheiner. "DEMYELINATING SENSORIMOTOR POLYNEUROPATHY AFTER ADMINISTRATION OF FK506." Transplantation 59, no. 7 (1995): 1066–68. http://dx.doi.org/10.1097/00007890-199504150-00029.

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Vedanarayanan, V. V., S. Smith, S. H. Subramony, G. O. Bock, and O. B. Evans. "Lethal neonatal autosomal recessive axonal sensorimotor polyneuropathy." Muscle & Nerve 21, no. 11 (1998): 1473–77. http://dx.doi.org/10.1002/(sici)1097-4598(199811)21:11<1473::aid-mus16>3.0.co;2-1.

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Hong, Sang-Wook, Hye Ryoun Kim, and Suk-Won Ahn. "Inflammatory Polyneuropathy Associated with Myelodysplastic Syndrome." Journal of the Korean Neurological Association 40, no. 4 (2022): 338–42. http://dx.doi.org/10.17340/jkna.2022.4.11.

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Inflammatory polyneuropathy may be associated with various tumorous diseases, including hematological malignancy. A 50-year-old man visited neurologic department complaining of bilateral lower extremities weakness, tingling sensation and weight loss. Initially he was diagnosed as demyelinating sensorimotor polyneuropathy after performing the nerve conduction study, furthermore myelodysplastic syndrome was revealed by the hematologic tests and bone marrow examination. Conclusively, high-dose steroid therapy, intravenous immunoglobulin and chemotherapy improved neurological symptoms. This case s

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23

Armakov, Sergey. "Diabetic Polyneuropathy." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 6 (June 1, 2020): 33–38. http://dx.doi.org/10.33920/med-10-2006-04.

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Diabetes mellitus is a chronic disease that develops against the background of insulin deficiency as a result of a decrease in its production or impaired receptor perception by target cells. As a result of impaired glucose metabolism, a state of chronic hyperglycemia develops, which has a detrimental effect on a number of organs and systems. One of such systems that are negatively affected by an increase in glucose concentration against the background of a general violation of all types of metabolism is the nervous system, in particular, its peripheral part. Approximately every second patient

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Ducci, Renata Dal-Prá, Camila Lorenzini Tessaro, Cláudia Suemi Kamoi Kay, et al. "Peripheral polyneuropathy from electrodiagnostic tests: a 10-year etiology and neurophysiology overview." Arquivos de Neuro-Psiquiatria 80, no. 3 (2022): 270–79. http://dx.doi.org/10.1590/0004-282x-anp-2020-0561.

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ABSTRACT Background: Polyneuropathies are characterized by a symmetrical impairment of the peripheral nervous system, resulting in sensory, motor and/or autonomic deficits. Due to the heterogeneity of causes, an etiological diagnosis for polyneuropathy is challenging. Objective: The aim of this study was to determine the main causes of polyneuropathy confirmed by electrodiagnostic (EDX) tests in a tertiary service and its neurophysiological aspects. Methods: This observational cross-sectional study from a neuromuscular disorders center included individuals whose electrodiagnostic tests perform

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Pal, PramodKumar, YashaT Chickabasaviah, RajaniR Battu, SanjuP Joy, Samhita Panda, and GirishB Kulkarni. "Incontinentia pigmenti with sensorimotor polyneuropathy: A novel association." Neurology India 57, no. 6 (2009): 813. http://dx.doi.org/10.4103/0028-3886.59490.

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Song, Joo Mee, Soonwook Kwon, Juhyeon Kim, Byoung Joon Kim, and Ju-Hong Min. "Anti-Ma2-Associated Encephalitis with Axonal Sensorimotor Polyneuropathy." Journal of the Korean Neurological Association 37, no. 2 (2019): 191–94. http://dx.doi.org/10.17340/jkna.2019.2.14.

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Bril, V., T. Hirose, S. Tomioka, and R. Buchanan. "Ranirestat for the Management of Diabetic Sensorimotor Polyneuropathy." Diabetes Care 32, no. 7 (2009): 1256–60. http://dx.doi.org/10.2337/dc08-2110.

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Yosifova, Lili, and Klara Dokova. "MLS laser in diabetic sensorimotor polyneuropathy—late effects." Varna Medical Forum 11, no. 1 (2022): 91. http://dx.doi.org/10.14748/vmf.v0i0.8517.

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Zubair, Adeel S., Melissa Rethana, and Benison Keung. "Brentuximab-Induced Sensorimotor Polyneuropathy With Acquired Demyelinating Features Resembling Chronic Inflammatory Demyelinating Polyneuropathy." Journal of Clinical Neuromuscular Disease 23, no. 3 (2022): 166–68. http://dx.doi.org/10.1097/cnd.0000000000000352.

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Tan, Cheng-Yin, Thaarani Arumugam, Siti Nur Omaira Razali, Mohd Azly Yahya, Khean-Jin Goh, and Nortina Shahrizaila. "Nerve ultrasound can distinguish chronic inflammatory demyelinating polyneuropathy from demyelinating diabetic sensorimotor polyneuropathy." Journal of Clinical Neuroscience 57 (November 2018): 198–201. http://dx.doi.org/10.1016/j.jocn.2018.08.031.

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Muradova, Malika Saidakhrorovna Raimova Malika Mukhamedjanovna. "PECULIARITIES OF COGNITIVE DISFUNCTION IN PATIENTS WITH CHRONIC KIDNEY DISEASE (LITERATURE REVIEW)." EURASIAN JOURNAL OF MEDICAL AND NATURAL SCIENCES 2, no. 11 (2022): 47–53. https://doi.org/10.5281/zenodo.7155171.

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The review article deals with the clinical features of neurological disorders in patients with chronic kidney disease. It is emphasized that at the initial stages the changes in the central nervous system are manifested by the disturbances of attention, memory, and psycho-motor functions. However, as the underlying disease progresses, the frontal defect becomes clinically more pronounced. There is a significant prevalence of polyneuropathic disorders in this category of patients. Polyneuropathy in chronic kidney disease is similar in its manifestations to other mixed sensorimotor axonal polyne

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Beal, Jules C., Yishan Cheng, Sabiha Merchant, and Reza Zarnegar. "An Acute, Severe Axonal Sensorimotor Polyneuropathy in the Setting of Nitrous Oxide Abuse." Neurohospitalist 10, no. 4 (2020): 293–96. http://dx.doi.org/10.1177/1941874420910648.

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Nitrous oxide, often used as an anesthetic agent, is also increasingly a drug of abuse due to its euphoric and anxiolytic effects. Frequent exposure to nitrous oxide can lead to neurologic complications, including B12 deficiency and resultant subacute myeloneuropathy, as well as direct neurotoxicity. A clinical presentation of acute sensorimotor polyneuropathy mimicking Guillain-Barré syndrome after chronic nitrous oxide abuse has been reported only rarely. Here we present a 17-year-old previously healthy girl presented with 10 days of progressive ascending sensory loss and weakness in the leg

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Hasan, Abdullah Al, Mohshina Abedin, Md Robed Amin, Shah Habibur Rahman, Salina Daisy, and Mansur Habib. "Role of Nerve Conduction Study in Polyneuropathy." Bangladesh Journal of Medicine 31, no. 1 (2019): 3–8. http://dx.doi.org/10.3329/bjm.v31i1.44746.

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Background: Polyneuropathy has many different causes. It is often very difficult to find out the cause. Nerve conduction study (NCS) can classify neuropathy as axonal and demyelinatig variety and direct the search for cause. Methodology: Purposively selected 80 patients from the department of Neurology Dhaka Medical College during the period of January 2009 to June 2010 were taken for NCS whose were compatible with polyneuropathy by history and clinical examination. Clinical, electrophysiological feature and pattern of polyneuropathy were analyzed. Results: Mean age of the patients

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Wathurapatha, Wasundara, B. G. A. Rathnamali, and Upul Dissanayake. "Sensory-Motor Polyneuropathy and Digital Ischemia: A Rare Presentation of Granulomatosis with Polyangiitis." Case Reports in Rheumatology 2021 (October 30, 2021): 1–6. http://dx.doi.org/10.1155/2021/5353575.

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Granulomatosis with polyangiitis (GPA) typically presents with upper or lower respiratory tract symptoms and/or with renal involvement. Although it can affect the peripheral nervous system frequently, with mononeuritis multiplex being the most common pattern, the occurrence of peripheral sensory-motor polyneuropathy as a presenting manifestation is distinctly rare. Prevalence of digital gangrene is also extremely rare in GPA. We describe a 46-year-old woman presenting with severe peripheral sensorimotor polyneuropathy affecting bilateral lower limbs preceded by a purpuric skin rash and multipl

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Ling, Hua chan, Chiew sern Ong, Kaavya Narasimhalu, James Xinzhe Cai, and You Jiang Tan. "A treatable case of hereditary transthyretin amyloidosis with polyneuropathy masquerading as motor neuron disease." Neurology Asia 29, no. 2 (2024): 483–87. http://dx.doi.org/10.54029/2024ptd.

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Hereditary transthyretin amyloidosis is a progressive, life-threatening disease that typically presents as length-dependent symmetric axonal sensorimotor polyneuropathy, restrictive cardiomyopathy, or a combination of both. In this case report, we describe a 50-year-old gentleman with a rare motor phenotypic variant of hereditary transthyretin amyloidosis with polyneuropathy (hATTR-PN) masquerading as motor neuron disease. This case represents the first reported association between the motor phenotypic variants of hATTR-PN and mutations involving p.Ala117Ser, a mutation prevalent in the Chines

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Oliveira, Aline Pinheiro Martins de, Raquel Campos Pereira, Patrícia Toscano Onofre, et al. "Clinical and neurophysiological features of the hereditary neuropathy with liability to pressure palsy due to the 17p11.2 deletion." Arquivos de Neuro-Psiquiatria 74, no. 2 (2016): 99–105. http://dx.doi.org/10.1590/0004-282x20160010.

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ABSTRACT The hereditary neuropathy with liability to pressure palsies (HNPP) is an autossomal dominant disorder manifesting recurrent mononeuropathies. Objective Evaluate its clinical and nerve conduction studies (NCS) characteristics, searching for diagnostic particularities. Method We reviewed the neurological manifestations of 39 and the NCS of 33 patients. Results Family history was absent in 16/39 (41%). The onset complaints were weakness in 24, pain in 6, sensory deficit in 5 and paresthesias in 4. Pain was seen in 3 other patients. The following neuropathy patterns were found: multiple

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Weiman, Daniel I., Meredith K. Gillespie, Taila Hartley, et al. "Neurophysiological Characteristics of Allgrove (Triple A) Syndrome: Case Report and Literature Review." Child Neurology Open 8 (January 2021): 2329048X2110310. http://dx.doi.org/10.1177/2329048x211031059.

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Allgrove or “Triple A” syndrome is characterized by alacrima, achalasia, and adrenocorticotropic hormone-resistant adrenal insufficiency, as well as central and peripheral nervous system involvement. Patients demonstrate heterogeneity with regard to their age of symptom onset, disease severity, and nature of clinical symptoms. Neurophysiological testing has also shown variability ranging from: motor neuron disease with prominent bulbar involvement, motor-predominant neuropathy, or sensorimotor polyneuropathy with axonal or mixed axonal and demyelinating features. We report an 11-year-old boy w

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Barantsevich, E. R., E. E. Smirnov, A. A. Potapchuk, A. V. Artyomova, and Y. V. Emanuel. "Possibilities of using neuromuscular electrostimulation for treating polyneuropathy in gluten intolerance (clinical observation)." Medical alphabet, no. 5 (June 15, 2020): 59–64. http://dx.doi.org/10.33667/2078-5631-2020-5-59-64.

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The article presents a clinical observation of a 54-year-old patient with sensorimotor polyneuropathy and newly diagnosed celiac disease. It was shown that laboratory methods for examining patients with polyneuropathy are required to identify the etiology of the process in most cases. Attention is drawn to the possibility of developing polyneuropathy with gluten intolerance without obvious pathological manifestations of the gastrointestinal tract. The importance of not only observing a gluten-free diet for treatment, but also the use of pulsed currents in the form of an exponent to reduce pain

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Lizwan, Marco, Shawn Zhi Zheng Lin, and Sumit Kumar Sonu. "Rare case of anti-CV2 paraneoplastic polyneuropathy associated with lung adenocarcinoma." BMJ Case Reports 16, no. 2 (2023): e253686. http://dx.doi.org/10.1136/bcr-2022-253686.

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We describe the first case of anti-CV2 paraneoplastic polyneuropathy associated with lung adenocarcinoma. Our patient presented with progressive unsteadiness and numbness involving bilateral upper and lower limbs. He had symmetrical length-dependent lower motor neuron pattern of weakness and numbness involving both small and large fibres with prominent sensory ataxia. An extended workup for the polyneuropathy involving a serum paraneoplastic antineuronal antibody panel showed a positive reaction for anti-CV2 antibody. CT scan of the thorax, abdomen and pelvis revealed a right upper lung nodule

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Orzheshkovskyi, V. V. "CLINICAL AND NEUROPHYSIOLOGICAL CHARACTERISTICS OF POLYNEUROPATHY ASSOCIATED WITH RHEUMATOID ARTHRITIS." National Journal of Neurology 2, no. 10 (2016): 21–26. http://dx.doi.org/10.61788/njn.v2i16.03.

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The article presents the clinical and electromyographic characteristics of 35 patients with polyneuropathy associated with rheumatoid arthritis compared with 30 healthy patients. The results of the analysis of different variants of the disease, and conducted a correlation analysis of clinical, laboratory and neurophysiological parameters. It is shown that predominantly affects the motor nerve fibers are the most vulnerable - the ulnar and peroneal, and diffuse sensory fibers, and that the distal symmetrical sensorimotor polyneuropathy can be combined with other variants of disorders of the per

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진동관, 김봉제, 문희수, 정필욱, 서범천, and 김용범. "A Case of Leprosy with Subacute Progressive Sensorimotor Polyneuropathy." Jouranl of Korean Association of EMG Electrodiagnostic Medicine 12, no. 1 (2010): 57–60. http://dx.doi.org/10.18214/jkaem.2010.12.1.57.

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Brola, Waldemar, Renata Pejas-Dulewicz, Jarosław Wasiński, Jolanta Paszkiewicz, and Małgorzata Fudala. "Sensorimotor polyneuropathy as an initial clinical manifestation of sarcoidosis." Medical Studies 2 (2014): 111–14. http://dx.doi.org/10.5114/ms.2014.43603.

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Bril, V., Y. Ono, and R. A. Buchanan. "Sural Nerve Sorbitol in Patients With Diabetic Sensorimotor Polyneuropathy." Diabetes Care 27, no. 5 (2004): 1160–63. http://dx.doi.org/10.2337/diacare.27.5.1160.

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Sato, Shinji, Shigeru Nogawa, Michito Hirakata, et al. "Sensorimotor polyneuropathy as an initial clinical manifestation of sarcoidosis." Modern Rheumatology 15, no. 2 (2005): 144–47. http://dx.doi.org/10.3109/s10165-005-0381-2.

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Shin, Dae Youp, Bora Lee, Won Sang Yoo, Joo Won Park, and Jung Keun Hyun. "Prediction of Diabetic Sensorimotor Polyneuropathy Using Machine Learning Techniques." Journal of Clinical Medicine 10, no. 19 (2021): 4576. http://dx.doi.org/10.3390/jcm10194576.

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Diabetic sensorimotor polyneuropathy (DSPN) is a major complication in patients with diabetes mellitus (DM), and early detection or prediction of DSPN is important for preventing or managing neuropathic pain and foot ulcer. Our aim is to delineate whether machine learning techniques are more useful than traditional statistical methods for predicting DSPN in DM patients. Four hundred seventy DM patients were classified into four groups (normal, possible, probable, and confirmed) based on clinical and electrophysiological findings of suspected DSPN. Three ML methods, XGBoost (XGB), support vecto

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HONG, YOUNG BIN, JA HYUN LEE, HYUNG JUN PARK, et al. "A family with axonal sensorimotor polyneuropathy with TUBB3 mutation." Molecular Medicine Reports 11, no. 4 (2014): 2729–34. http://dx.doi.org/10.3892/mmr.2014.3047.

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Hengstman, Gerald J. D., Karlijn F. de Laat, Bram Jacobs, and Baziel G. M. van Engelen. "Sensorimotor Axonal Polyneuropathy Without Hepatic Failure in Erythropoietic Protoporphyria." Journal of Clinical Neuromuscular Disease 11, no. 2 (2009): 72–76. http://dx.doi.org/10.1097/cnd.0b013e3181b0a7a5.

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Mancuso, M., M. Filosto, M. Bellan, et al. "POLG mutations causing ophthalmoplegia, sensorimotor polyneuropathy, ataxia, and deafness." Neurology 62, no. 2 (2004): 316–18. http://dx.doi.org/10.1212/wnl.62.2.316.

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Chroni, E., A. Monastirli, E. Pasmatzi, et al. "Sensorimotor Polyneuropathy After a Three-Month Oral Acitretin Therapy." Clinical Neuropharmacology 25, no. 6 (2002): 310–12. http://dx.doi.org/10.1097/00002826-200211000-00006.

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Binfalah, M., S. Alsadadi, and M. Mattar. "Solitary plasmacytoma presenting as sensorimotor polyneuropathy: A case report." Journal of the Neurological Sciences 405 (October 2019): 60. http://dx.doi.org/10.1016/j.jns.2019.10.538.

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