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Also try: distal autonomic neuropathy, paraneoplastic neuropathy, diabetic neuropathy,

204 results of 21 texts with exact phrase : 'neuropathy'.

1. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, Vol. 1, 2005 , , ,

Prevalence of diabetic autonomic neuropathy measured by simple bedside tests.
Dyrberg T, Benn J, Christiansen J, Hilsted J, Nerup J. Prevalence of diabetic autonomic neuropathy measured by simple bedside tests.
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Diagnosing Diabetic Autonomic Neuropathy.
Vinik AI. Diagnosing Diabetic Autonomic Neuropathy.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 1, 2005, No. 2 , , ,

Other are a result of definite choroidal, retinal, optic nerve, visual sensory pathways damage, to wit: central retinal artery or branch central retinal artery occlusion, ischemic optic neuropathy, unilateral venous-stasis retinopathy, ischemic ocular syndrome, contralateral homonymous hemianopias and quadrantanopias.
Various ophthalmologic disorders as an isolated independent manifestation or in combination with concomitant neurologic symptomatology can be observed in patients with carotid occlusive disease (carotid stenosis or thrombosis). Some of these symptoms are transient like amaurosis fugax (transient monocular blindness), which is very frequent predictor of the carotid occlusive disease. Other are a result of definite choroidal, retinal, optic nerve, visual sensory pathways damage, to wit: central retinal artery or branch central retinal artery occlusion, ischemic optic neuropathy, unilateral venous-stasis retinopathy, ischemic ocular syndrome, contralateral homonymous hemianopias and quadrantanopias. Their exact interpretation, especially of the transient ophthalmologic symptoms, supports the early diagnosis of carotid pathology and prevents the late definite neurologic and ophthalmologic complications.
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Vanik A. Neuropathy.
Vanik A. Neuropathy. In The Health Professionnal
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Effects of treatment with antioxidant alpha-lipoic acid cardiac autonomic neuropathy in NIDDM, patients: a 4month random.
Ziegler D. Effects of treatment with antioxidant alpha-lipoic acid cardiac autonomic neuropathy in NIDDM, patients: a 4month random. Controlled multicenter trial |DEKAN Study|.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 1 , , ,

Anterior ischemic optic neuropathy.
Arnold A. Anterior ischemic optic neuropathy.
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Recurrent visual field defect and ischemic optic neuropathy associated with tadalafil rechallenge.
Bollinger K, Lee M. Recurrent visual field defect and ischemic optic neuropathy associated with tadalafil rechallenge.
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glioma of adulthood simulating ischemic optic neuropathy.
glioma of adulthood simulating ischemic optic neuropathy.
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Sildenafil (Viagra) associated anterior ischemic optic neuropathy.
Egan R, Pomeranz H. Sildenafil (Viagra) associated anterior ischemic optic neuropathy.
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Tadalafil associated with anterior ischemic optic neuropathy.
Escaravage G, Wright J, Givre S. Tadalafil associated with anterior ischemic optic neuropathy.
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Posterior ischemic optic neuropathy: case report of a rare complication after general surgery.
Gaillard M, Zambaz B, Borruat F. Posterior ischemic optic neuropathy: case report of a rare complication after general surgery.
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Visual field defects in optic neuritis and anterior ischemic optic neuropathy: distinctive features.
Gerling J, Meyer J, Kommerell G. Visual field defects in optic neuritis and anterior ischemic optic neuropathy: distinctive features.
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Bilateral simultaneous anterior ischemic optic neuropathy in a young, healthy man.
Goff M, Kerrison J. Bilateral simultaneous anterior ischemic optic neuropathy in a young, healthy man.
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Unilateral optic neuropathy associated with sildenafil intake.
Gruhn N, Fledelius H. Unilateral optic neuropathy associated with sildenafil intake.
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Posterior ischaemic optic neuropathy: clinical features, pathogenesis, and management.
Hayreh S. Posterior ischaemic optic neuropathy: clinical features, pathogenesis, and management.
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Non-arteritic ischaemic optic neuropathy (NAION) in patients under
Janaky M, Fulop Z, Palffy A, Benedek K, Benedek G. Non-arteritic ischaemic optic neuropathy (NAION) in patients under
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Levodopa may improve vision loss in recent-onset, nonarteritic anterior ischemic optic neuropathy.
Johnson L, Guy M, Krohel G, Madsen R. Levodopa may improve vision loss in recent-onset, nonarteritic anterior ischemic optic neuropathy.
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Bilateral anterior ischemic optic neuropathy following influenza vaccination.
Kawasaki A, Purvin V, Tang R. Bilateral anterior ischemic optic neuropathy following influenza vaccination.
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Bilateral posterior ischemic optic neuropathy after lumbar spine surgery.
Murphy M. Bilateral posterior ischemic optic neuropathy after lumbar spine surgery.
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Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): a report of seven new cases.
Pomeranz H, Bhavsar A. Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): a report of seven new cases.
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Bilateral, nearly simultaneous anterior ischemic optic neuropathy complicated by diabetes and bilateral, small, crowded optic discs.
Shibayama J, Oku H, Imamura Y, Kajiura S, Sugasawa J., Ikeda T. Bilateral, nearly simultaneous anterior ischemic optic neuropathy complicated by diabetes and bilateral, small, crowded optic discs.
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Hypovolemic ischemic optic neuropathy.
Suzuki D, Ilsen P. Hypovolemic ischemic optic neuropathy.
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Vardizer Y, Linhart Y, Loewenstein A.. Interferon-alpha-associated bilateral simultaneous ischemic optic neuropathy.
Vardizer Y, Linhart Y, Loewenstein A.. Interferon-alpha-associated bilateral simultaneous ischemic optic neuropathy.
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Suspected simultaneous bilateral anterior ischemic optic neuropathy in a patient with Behcet’s disease.
Yamauchi Y, Cruz J, Kaplan H, Goto H, Sakai J, Usui M. Suspected simultaneous bilateral anterior ischemic optic neuropathy in a patient with Behcet’s disease.
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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 2 , , ,

A new approach to the diagnosis of diabetic peripheral autonomic neuropathy.
Aso Y, Inukai T, Takemura Y. Evaluation of skin vasomotor reflexes in response to deep inspiration in diabetic patients by laser Doppler flowmetry. A new approach to the diagnosis of diabetic peripheral autonomic neuropathy.
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of diabetic sympathetic neuropathy demonstrated by laser Doppler flowmetry.
of diabetic sympathetic neuropathy demonstrated by laser Doppler flowmetry.
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Autonomic neuropathy in non insulin dependant (type II) diabetes mel� litus.
Bergstrom B, Lilja B, Osterlin S, Sundqvist, G. Autonomic neuropathy in non insulin dependant (type II) diabetes mel� litus. Possible influence of obesity.
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Cardiac autonomic neuropathy predicts cardio� vascular morbidity and mortality in type 1 diabetic patients with diabetic nephropathy.
Astrup AS, Tarnow L, Rossing P, Hansen BV, Hilsted J, Parving HH. Cardiac autonomic neuropathy predicts cardio� vascular morbidity and mortality in type 1 diabetic patients with diabetic nephropathy.
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The prevalence by staged severity of various types of diabetic neuropathy, reti� nopathy and nephropathy in a population � based cohort: the Rochester Diabetic Neuropathy Study.
Dyck P, Kratz K, Karnes J, Litchy W, Klein R, Pach J, Wilson D, O’Brien P, Melton L 3rd, Service F. The prevalence by staged severity of various types of diabetic neuropathy, reti� nopathy and nephropathy in a population � based cohort: the Rochester Diabetic Neuropathy Study.
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Spectral analysis of heart rate in diabetic autonomic neuropathy.
Freeman R. Saul J, Roberts M, Berger R, Broadbridge C and Cohen R. Spectral analysis of heart rate in diabetic autonomic neuropathy. A comparison with standart tests of autonomic function.
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Diabetic autonomic neuropathy.
Hilsted J, Low P. Diabetic autonomic neuropathy. In: Ph. A. Low (eds). Clinical autonomic disorders. Lippincott�Raven Publishers. Philadelphia � New York, 1997, 487�508.
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Autonomic neuropathy in a diabetic population.
Latini A, Martin L, Limiti G, Magarelli M, Polidori L, Tramutoli R, Papini E, Rinaldi R, Guglielmi R, Petrucci L, Panunzi C, Pagano, A. Autonomic neuropathy in a diabetic population. Validity of cardiovascular tests and correlations with the complications.
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The Association Between Cardiovascular Autonomic Neuropathy and Mortality in Individuals With Diabetes.
Maser R, Mitchell B, Vinik A, Freeman R. The Association Between Cardiovascular Autonomic Neuropathy and Mortality in Individuals With Diabetes. A meta�analysis.
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P. Progression of diabetic autonomic neuropathy over a decade in insulin� dependant diabetics.
P. Progression of diabetic autonomic neuropathy over a decade in insulin� dependant diabetics.
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Diabetic Autonomic Neuropathy.
Vinik A, Maser R, Mitchell B, Freeman R. Diabetic Autonomic Neuropathy.
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Diabetic peripheral neuropathy and quality of life.
Benbow S, Wallymahmed M, Macfarlane I. Diabetic peripheral neuropathy and quality of life.
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Cardiovascular reflexes and autonomic neuropathy.
Ewing D. Cardiovascular reflexes and autonomic neuropathy.
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New insights into the pathogenesis of diabetic neuropathy.
Feldman E. Russell J, Sullivan K, Golovoy D. New insights into the pathogenesis of diabetic neuropathy.
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autonomic neuropathy and QT interval length: a follow-up study in diabetic patiens.
autonomic neuropathy and QT interval length: a follow-up study in diabetic patiens.
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Diabetic peripheral neuropathy and depressive symptoms.
Loretta V, Jeffrey S, Richard R, Adam G, Peter R, Andrew J. Diabetic peripheral neuropathy and depressive symptoms.
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Clinical diagnosis of diabetic polyneuropathy with the diabetic neuropathy symptom and diabetic neuropathy examination scores.
Meijer J, Bosma E, Lefrandt J, Links T, Smit A, Stewart R, Van Der Hoeven J, Hoogenberg K. Clinical diagnosis of diabetic polyneuropathy with the diabetic neuropathy symptom and diabetic neuropathy examination scores.
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Psychological aspects of diabetic peripheral neuropathy.
Vileikyte L. Psychological aspects of diabetic peripheral neuropathy. Diabetes Rev, 1999, 7:387–3945. World Health Organisation Study Group. Tehnical Report Series №727, Geneva, 1985.
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Recognizing and treating diabetic autonomic neuropathy.
Vinik A, Erbas T. Recognizing and treating diabetic autonomic neuropathy.
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1 , , ,

Consensus statement: Report and recommendations of San Antonio confence on diabetic neuropathy.
Consensus statement: Report and recommendations of San Antonio confence on diabetic neuropathy. American Diabetes
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Vinik A, Erbas T. Neuropathy.
Vinik A, Erbas T. Neuropathy. In: Ruderman N, Devlin JT, Schneider SH et al. Handbook of exercise in diabetes. American Diabetes Association. Alexandria, 2002, 463-496.
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Minimizing risks in patients who have neuropathy.
Ward S. Diabetes, exercise, and foot care. Minimizing risks in patients who have neuropathy.
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Alpha-Lipoic Acid in Diabetic Neuropathy.
Ziegler D, Hanefeld M, Ruhnau K, Hasche H, Lobisch M, Schutte K, Kerum G, Malessa R. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a 7-month multicenter randomized controlled trial (ALADIN III Study). ALADIN III Study Group. Alpha-Lipoic Acid in Diabetic Neuropathy.
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 1 , , ,

Has potassium been prematurely discarded as a contributing factor to the development of uraemic neuropathy?
Bostock H, Walters RJL, Andersen KV, Murray NMF, Taube D, Kiernan MC. Has potassium been prematurely discarded as a contributing factor to the development of uraemic neuropathy?
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Incidence of neuropathy in non – dialyzed chronic renal failure patients.
Coomes EN, Berlyne EM, Shaw AB. Incidence of neuropathy in non – dialyzed chronic renal failure patients.
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The relationship between sensory and motor conduction and kidney function, azotemia, age, sex and clinical neuropathy.
Nielsen VK. The peripheral nerve function in chronic renal failure: VI. The relationship between sensory and motor conduction and kidney function, azotemia, age, sex and clinical neuropathy.
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Electrophysiological course of uraemic neuropathy in haemodialysis patients.
Ogura T, Makinodan A, Kubo T, Hayashida T, Hirasava Y. Electrophysiological course of uraemic neuropathy in haemodialysis patients.
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Vibratory perception threshold compared with conduction velocity in the evaluation of uremic neuropathy.
Tegner R, Lindholm B. Vibratory perception threshold compared with conduction velocity in the evaluation of uremic neuropathy.
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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1 , , ,

Reactivity in Distal Autonomic Neuropathy
Reactivity in Distal Autonomic Neuropathy
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Vasomor reactivity in distal autonomic neuropathy
Vasomor reactivity in distal autonomic neuropathy
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Vasomor reactivity in distal autonomic neuropathy
Vasomor reactivity in distal autonomic neuropathy
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Vasomor reactivity in distal autonomic neuropathy
Vasomor reactivity in distal autonomic neuropathy
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Autonomic impairment in painful neuropathy.
Novak V, Freimer ML, Kissel JT, Sahenk Z, Periquet IM, Nash SM, Collins MP, Mendell JR. Autonomic impairment in painful neuropathy.
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Small-fiber neuropathy: answering the burning questions.
Fink E, Oaklander AL. Small-fiber neuropathy: answering the burning questions.
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of diabetic sympathetic neuropathy demonstrated by laser Doppler flowmetry.
of diabetic sympathetic neuropathy demonstrated by laser Doppler flowmetry.
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Selective fiber vulnerability in acute ischemic neuropathy.
Parry GJ, Brown MJ. Selective fiber vulnerability in acute ischemic neuropathy.
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Idiopathic autonomic neuropathy: Clinical, neurophysiologic, and follow-up studies on 27 patients.
Suarez GA, Fealey RD, Camilleri M, Low PA. Idiopathic autonomic neuropathy: Clinical, neurophysiologic, and follow-up studies on 27 patients.
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The roles of oxidative stress and antioxidant treatment in experimental diabetic neuropathy.
Low PA, Nickander KK, Tritschler HJ. The roles of oxidative stress and antioxidant treatment in experimental diabetic neuropathy.
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8. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1 , , ,

Paraneoplastic Neuropathy
Paraneoplastic Neuropathy
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Carcinoma associated paraneoplastic peripheral neuropathy.
Dalmau J. Carcinoma associated paraneoplastic peripheral neuropathy.
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Ataxis vs painful form of paraneoplastic neuropathy.
Oki Y, Koike H, Iijima M, Mori K, Hattori N, Katsuno M, Nakamura T, Hirayama M, Tanaka F, Shiraishi M. Ataxis vs painful form of paraneoplastic neuropathy.
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Skin biopsy in the management of peripheral neuropathy.
Sommer C, Lauria G. Skin biopsy in the management of peripheral neuropathy.
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Symptomatology and differential diagnosis of peripheral neuropathy.
Thomas PK, Ochoa J. Symptomatology and differential diagnosis of peripheral neuropathy. In: Dyck PJ, Thomas PK (eds). Peripheral neuropathy.
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Peripheral neuropathy.
Thomas PK, Ochoa J. Symptomatology and differential diagnosis of peripheral neuropathy. In: Dyck PJ, Thomas PK (eds). Peripheral neuropathy.
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Clinical evaluation and investigation of neuropathy.
Willison HJ, Winer JB. Clinical evaluation and investigation of neuropathy.
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Paraneoplastic Neuropathy
Paraneoplastic Neuropathy
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antineuronal antibodies, paraneoplastic neuropathy, primary neoplasma
antineuronal antibodies, paraneoplastic neuropathy, primary neoplasma
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Subacute sensory neuronopathy is the most frequent presentation of paraneoplastic neuropathies, but sensory-motor neuropathy, autonomic neuropathy and mononeuritis multiplex with vasculitis have been also described.
Paraneoplastic neuropathies are rare diseases related to underlying neoplasma where immunological mechanisms are involved – immune response to onconeural antigens. Many anti-neuronal antibodies have been identified but most of them are not specific except for anti-Hu-antibodies. Subacute sensory neuronopathy is the most frequent presentation of paraneoplastic neuropathies, but sensory-motor neuropathy, autonomic neuropathy and mononeuritis multiplex with vasculitis have been also described. Sometimes the diagnosis is very difficult and includes different imaging studies, laboratory, electromyographic and histologic tests. Diagnostic criteria have been established and divide the patients into two groups: with definite and with probable diagnosis. The treatment of these diseases is complex and depends on the characteristics of primary neoplasm and neuropathy.
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The treatment of these diseases is complex and depends on the characteristics of primary neoplasm and neuropathy.
Paraneoplastic neuropathies are rare diseases related to underlying neoplasma where immunological mechanisms are involved – immune response to onconeural antigens. Many anti-neuronal antibodies have been identified but most of them are not specific except for anti-Hu-antibodies. Subacute sensory neuronopathy is the most frequent presentation of paraneoplastic neuropathies, but sensory-motor neuropathy, autonomic neuropathy and mononeuritis multiplex with vasculitis have been also described. Sometimes the diagnosis is very difficult and includes different imaging studies, laboratory, electromyographic and histologic tests. Diagnostic criteria have been established and divide the patients into two groups: with definite and with probable diagnosis. The treatment of these diseases is complex and depends on the characteristics of primary neoplasm and neuropathy.
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Paraneoplastic Neuropathy
Paraneoplastic Neuropathy
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Paraneoplastic Neuropathy
Paraneoplastic Neuropathy
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Carcinoma associated paraneoplastic peripheral neuropathy.
Dalmau J. Carcinoma associated paraneoplastic peripheral neuropathy.
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Ataxis vs painful form of paraneoplastic neuropathy.
Oki Y, Koike H, Iijima M, Mori K, Hattori N, Katsuno M, Nakamura T, Hirayama M, Tanaka F, Shiraishi M. Ataxis vs painful form of paraneoplastic neuropathy.
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Skin biopsy in the management of peripheral neuropathy.
Sommer C, Lauria G. Skin biopsy in the management of peripheral neuropathy.
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Symptomatology and differential diagnosis of peripheral neuropathy.
Thomas PK, Ochoa J. Symptomatology and differential diagnosis of peripheral neuropathy. In: Dyck PJ, Thomas PK (eds). Peripheral neuropathy.
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Peripheral neuropathy.
Thomas PK, Ochoa J. Symptomatology and differential diagnosis of peripheral neuropathy. In: Dyck PJ, Thomas PK (eds). Peripheral neuropathy.
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Clinical evaluation and investigation of neuropathy.
Willison HJ, Winer JB. Clinical evaluation and investigation of neuropathy.
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9. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 2 , , ,

Diabetic Neuropathy – Correlative Clinical and Electromyographic Study
Diabetic Neuropathy – Correlative Clinical and Electromyographic Study
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They are characterized by imbalance between endothelial-derived vasodilators and constrictors and plays an important role in pathogenesis of diabetic microangiopathy and neuropathy [18].
Up to 75% of patients with diabetes mellitus die from vascular disease. Endothelial dysfunction plays an early (probably even preceding manifested symptoms of diabetes) and important role in this process [2, 7]. Endothelial cells between blood and tissues produce many autocrine and paracrine substances participating in the regulation of vascular tone and local control of blood flow and homeostasis [3, 35]. Endothelial dysfunction might be at the same time the reason and the result of insulin resistance syndrome [25, 38]. Endothelial dysfunction and/or damage are connected to increased cardiovascular risk and an early sign of atherosclerotic process [5, 36]. They are characterized by imbalance between endothelial-derived vasodilators and constrictors and plays an important role in pathogenesis of diabetic microangiopathy and neuropathy [18]. Reactive hyperemia test is an index of endothelial-dependent dilator capacity of blood vessels in norm and pathology [19]. The rate of diabetic polyneuropathy according to different studies reaches 90% from patients with diabetes mellitus. Objectives: Assessment of microvascular endothelial-derived vasodilator reactivity in patients
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Autonomic neuropathy might induce increased blood shunting through skin arterio-venular anastomoses and to disturb nutritious capillary circulation [4, 11, 31].
Our study established increased values of skin perfusion in patients with diabetes mellitus. Skin microvascular blood flow in the limbs at normal temperature pass through arterio-venular shunts and by-passes nutritious capillary bed inducing capillary tissue ischemia [4, 11, 29]. Autonomic neuropathy might induce increased blood shunting through skin arterio-venular anastomoses and to disturb nutritious capillary circulation [4, 11, 31]. Early in the course of the disease microvascular perfusion at rest is increased [18, 29]. In condition of stress – tissue damage or a period of arterial occlusion restricted hyperemic response is observed [26, 28]. Increased skin microvascular perfusion is connected with poor glycemic control [13, 15, 34].
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Diabetic Neuropathy –
Diabetic Neuropathy –
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diabetes mellitus, diabetic neuropathy, electromyography, risk factors
diabetes mellitus, diabetic neuropathy, electromyography, risk factors
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Significant correlation between the type, duration and compensation of DM and the clinical and electromyographic characteristics of diabetic neuropathy were found.
Significant correlation between the type, duration and compensation of DM and the clinical and electromyographic characteristics of diabetic neuropathy were found.
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The late complications are macrovascular (cerebrovascular and cardiovascular diseases) and microvascular (diabetic retinopathy, nephropathy and neuropathy).
Diabetes mellitus (DM) is a socially important disease leading to early (hypoglycemia and ketoacidosis) and late complications. The late complications are macrovascular (cerebrovascular and cardiovascular diseases) and microvascular (diabetic retinopathy, nephropathy and neuropathy). The rate of diabetic neuropathy varies from 16% to 50% in patients with different types of DM [3, 11, 24]. The main risk factors (RF) for its appearance are duration of DM and glicemic control. Important additional factors could be arterial hypertension, hyperlypidemia, cigarette smoking, age etc [6].
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The rate of diabetic neuropathy varies from 16% to 50% in patients with different types of DM [3, 11, 24].
Diabetes mellitus (DM) is a socially important disease leading to early (hypoglycemia and ketoacidosis) and late complications. The late complications are macrovascular (cerebrovascular and cardiovascular diseases) and microvascular (diabetic retinopathy, nephropathy and neuropathy). The rate of diabetic neuropathy varies from 16% to 50% in patients with different types of DM [3, 11, 24]. The main risk factors (RF) for its appearance are duration of DM and glicemic control. Important additional factors could be arterial hypertension, hyperlypidemia, cigarette smoking, age etc [6].
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The complications of DM including diabetic neuropathy, invalidate the patients, worsen the quality of life and diminish life expectancy.
The complications of DM including diabetic neuropathy, invalidate the patients, worsen the quality of life and diminish life expectancy. An active approach for early diagnostics, identification and prophylaxis of RF is needed.
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Examination of nerve conduction velocity by electromyography (EMG) is a reliable, exact and sensitive method for evaluation of peripheral nerves function in diabetic neuropathy [14, 16].
Examination of nerve conduction velocity by electromyography (EMG) is a reliable, exact and sensitive method for evaluation of peripheral nerves function in diabetic neuropathy [14, 16].
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The aim of this study is to look for significant correlation between the frequency, localization and severity of diabetic neuropathy (DN) and the type and degree of peripheral nerves damage estimated by electromyography.
The aim of this study is to look for significant correlation between the frequency, localization and severity of diabetic neuropathy (DN) and the type and degree of peripheral nerves damage estimated by electromyography.
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The influence of different RF for diabetic neuropathy was estimated: duration of DM, age, sex, weight (kg), body mass index (kg/m
– ODSS) [12]. The scale is reproduced in three parts: the arm disability scale (0 – 5 points), the leg disability scale (0 – 7 points) and the scoring system information – from 0 to 12 points (Table 1). The influence of different RF for diabetic neuropathy was estimated: duration of DM, age, sex, weight (kg), body mass index (kg/m
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Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
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The patients with type 2 DM had the highest rates of concomitant diseases (alcohol abuse, intoxications, anemia, neoplasm) – independent RF’s for neuropathy taken alone.
The patients with type 1 DM were considerably younger than the others. The patients with type 2 DM on oral medication were with the shortest DM duration and these with type 2 DM on insulin – the longest disease duration. In all three groups the male predominated. The lowest C-peptide and the highest morning blood sugar levels were found in patients with type 1 DM. The lowest HbA1c levels were measured in patients with type 2 DM on oral therapy, statistically significant in relation to other two groups. The patients with type 2 DM had the highest rates of concomitant diseases (alcohol abuse, intoxications, anemia, neoplasm) – independent RF’s for neuropathy taken alone.
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Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
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Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
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Some studies show that only the disease duration and creatinine and HbA1c levels have a significant relation to neuropathy development [20].
Scientific data about RFs for late microvascular DM complications including neuropathies are controversial. Some studies show that only the disease duration and creatinine and HbA1c levels have a significant relation to neuropathy development [20]. Some authors report a significant correlation between neuropathy and age, sex, DM duration, unsatisfactory glicemic control, obesity, low levels of HDL cholesterol and high levels of triglycerides especially in type 2 DM [10, 14, 19,
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Some authors report a significant correlation between neuropathy and age, sex, DM duration, unsatisfactory glicemic control, obesity, low levels of HDL cholesterol and high levels of triglycerides especially in type 2 DM [10, 14, 19,
Scientific data about RFs for late microvascular DM complications including neuropathies are controversial. Some studies show that only the disease duration and creatinine and HbA1c levels have a significant relation to neuropathy development [20]. Some authors report a significant correlation between neuropathy and age, sex, DM duration, unsatisfactory glicemic control, obesity, low levels of HDL cholesterol and high levels of triglycerides especially in type 2 DM [10, 14, 19,
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Our study shows that the severity of neuropathy correlates significantly only with DM duration and C-peptide levels.
21, 23], others do not find similar relations [1, 14]. Our study shows that the severity of neuropathy correlates significantly only with DM duration and C-peptide levels. This is probably due to the fact that all our patients were not in compensation stage of DM and the level of neuropathy could not be estimated exactly. A close follow up after compensation will show the influence of the therapy on neuropathy severity.
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This is probably due to the fact that all our patients were not in compensation stage of DM and the level of neuropathy could not be estimated exactly.
21, 23], others do not find similar relations [1, 14]. Our study shows that the severity of neuropathy correlates significantly only with DM duration and C-peptide levels. This is probably due to the fact that all our patients were not in compensation stage of DM and the level of neuropathy could not be estimated exactly. A close follow up after compensation will show the influence of the therapy on neuropathy severity.
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A close follow up after compensation will show the influence of the therapy on neuropathy severity.
21, 23], others do not find similar relations [1, 14]. Our study shows that the severity of neuropathy correlates significantly only with DM duration and C-peptide levels. This is probably due to the fact that all our patients were not in compensation stage of DM and the level of neuropathy could not be estimated exactly. A close follow up after compensation will show the influence of the therapy on neuropathy severity.
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In patients with type 1 DM low levels of Cpeptide, associated with specific structural defects and progression of the neuropathy have been detected.
In patients with type 1 DM low levels of Cpeptide, associated with specific structural defects and progression of the neuropathy have been detected. Long-lasting clinical studies have proven that patients with type 1 DM having a small amount of endogenous C-peptide and preserved, insulin secretion are less susceptible to late diabetic complications – neuropathy, retinopathy and nephropathy. The peripheral nerve function, estimated by sensory conduction velocity and quantitative sensory tests, improves with input of exogenous C-peptide in early stages of type 1 DM. C-peptide could become a new opportunity for prevention or even regression of neuropathy in type 1 DM [4].
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Long-lasting clinical studies have proven that patients with type 1 DM having a small amount of endogenous C-peptide and preserved, insulin secretion are less susceptible to late diabetic complications – neuropathy, retinopathy and nephropathy.
In patients with type 1 DM low levels of Cpeptide, associated with specific structural defects and progression of the neuropathy have been detected. Long-lasting clinical studies have proven that patients with type 1 DM having a small amount of endogenous C-peptide and preserved, insulin secretion are less susceptible to late diabetic complications – neuropathy, retinopathy and nephropathy. The peripheral nerve function, estimated by sensory conduction velocity and quantitative sensory tests, improves with input of exogenous C-peptide in early stages of type 1 DM. C-peptide could become a new opportunity for prevention or even regression of neuropathy in type 1 DM [4].
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C-peptide could become a new opportunity for prevention or even regression of neuropathy in type 1 DM [4].
In patients with type 1 DM low levels of Cpeptide, associated with specific structural defects and progression of the neuropathy have been detected. Long-lasting clinical studies have proven that patients with type 1 DM having a small amount of endogenous C-peptide and preserved, insulin secretion are less susceptible to late diabetic complications – neuropathy, retinopathy and nephropathy. The peripheral nerve function, estimated by sensory conduction velocity and quantitative sensory tests, improves with input of exogenous C-peptide in early stages of type 1 DM. C-peptide could become a new opportunity for prevention or even regression of neuropathy in type 1 DM [4].
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Smoking, obesity and high triglyceride levels are accepted by some authors as independent RF for neuropathy [17].
Smoking, obesity and high triglyceride levels are accepted by some authors as independent RF for neuropathy [17]. Half of diabetic patients (53%) have additional causes for distal neuropathy, such as neurotoxic medications, alcohol abuse, kidney diseases, B
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Half of diabetic patients (53%) have additional causes for distal neuropathy, such as neurotoxic medications, alcohol abuse, kidney diseases, B
Smoking, obesity and high triglyceride levels are accepted by some authors as independent RF for neuropathy [17]. Half of diabetic patients (53%) have additional causes for distal neuropathy, such as neurotoxic medications, alcohol abuse, kidney diseases, B
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Our study shows that EMG findings of diabetic neuropathy correlate with the DM duration and C-peptide levels.
Our study shows that EMG findings of diabetic neuropathy correlate with the DM duration and C-peptide levels. Dissociation between the rate of functional disability estimated by ODSS and EMG findings is detected. Combined with other clinical and functional tests, the EMG examination contributes to the exact estimation of the type and severity of diabetic neuropathy.
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Combined with other clinical and functional tests, the EMG examination contributes to the exact estimation of the type and severity of diabetic neuropathy.
Our study shows that EMG findings of diabetic neuropathy correlate with the DM duration and C-peptide levels. Dissociation between the rate of functional disability estimated by ODSS and EMG findings is detected. Combined with other clinical and functional tests, the EMG examination contributes to the exact estimation of the type and severity of diabetic neuropathy.
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Correlation of HgA1c concentration and single fiber EMG findings in diabetic neuropathy.
Chang CW, Chuang LM. Correlation of HgA1c concentration and single fiber EMG findings in diabetic neuropathy.
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P. Risk factors for severity of diabetic polyneuropathy: intensive longitudinal assessment of the Rochester Diabetic Neuropathy Study cohort.
P. Risk factors for severity of diabetic polyneuropathy: intensive longitudinal assessment of the Rochester Diabetic Neuropathy Study cohort.
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The Rochester Diabetic Neuropathy Study: reassessment of tests and criteria for diagnosis and staged severity.
Dyck PJ, Karnes JL, O'Brien PC, Litch WJ, Low PA, Melton LJ. The Rochester Diabetic Neuropathy Study: reassessment of tests and criteria for diagnosis and staged severity.
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Effect of C-Peptide on Diabetic Neuropathy in Patients with Type 1 Diabetes.
Ekberg K, Johansson B-L. Effect of C-Peptide on Diabetic Neuropathy in Patients with Type 1 Diabetes.
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Potential risk factors for diabetic neuropathy: a case control study.
Fargol B, Fatemeh B, Bagher L, Mohammad P, Mahdi Nooraeiand JL. Potential risk factors for diabetic neuropathy: a case control study.
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Diabetic Neuropathy.
Krendel DA. Diabetic Neuropathy. In: Neuromuscular Function
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Impaired glucose tolerance and insulinopenia in the GK-rat causes peripheral neuropathy.
Murakawa Y, Zhang W, Pierson CR, Brismar T, Ostenson CG, Efendic S, Anders A, Sima F. Impaired glucose tolerance and insulinopenia in the GK-rat causes peripheral neuropathy.
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Prevalence of diabetic peripheral neuropathy and relation to glycemic control therapies at baseline in the BARI 2D cohort.
Pop-Busui R, Lu J, Lopes N, Jones TL, BARI 2D Investigators. Prevalence of diabetic peripheral neuropathy and relation to glycemic control therapies at baseline in the BARI 2D cohort.
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Demyelinating neuropathy in diabetes mellitus.
Sharma KR, Cross J, Farronay O, Ayyar DR, Shebert RT, Bradley WG. Demyelinating neuropathy in diabetes mellitus.
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Diabetic neuropathy – a continuing enigma.
Sugimoto K, Murakawa Y, Sima AAF. Diabetic neuropathy – a continuing enigma.
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Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
Diabetic Neuropathy – Correlative Clinical and Electromyographic Studies
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The Eurodiab study: what has this taught us about diabetic peripheral neuropathy?
Tesfaye S, Selvarajah D. The Eurodiab study: what has this taught us about diabetic peripheral neuropathy?
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Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study.
Tesfaye S, Stevens LK, Stephenson JM, Fuller JH, Plater M, Ionescu-Tirgoviste C, Nuber A, Pozza G, Ward JD. Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study.
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on quality of life of peripheral neuropathy with or without neuropathic pain in type 1 and type 2 diabetic patients attending hospital outpatients clinics.
on quality of life of peripheral neuropathy with or without neuropathic pain in type 1 and type 2 diabetic patients attending hospital outpatients clinics.
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Overview of Diabetic Neuropathy.
Younger DS, Bronfin L. Overview of Diabetic Neuropathy.
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10. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 8, 2012, No. 1 , , ,

Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy
Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy
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Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy
Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy
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myosonography, neuropathy
myosonography, neuropathy
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We present a 48-year-old man with hereditary juvenile insulindependent diabetes mellitus complicated by late neuropathy.
We present a 48-year-old man with hereditary juvenile insulindependent diabetes mellitus complicated by late neuropathy. Clinical, electromyographic and myosonographic 4-dimensional studies of triceps surae muscles are performed. The results are compared to a healthy control and a patient with genetic distal myopathy.
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Electromyography objectified a demyelinating multifocal sensorimotor neuropathy.
A polyneuropathic syndrome with more severe involvement of the lower limbs was found: peroneal paralysis and tibial paresis, feet paresthesia and distal hypoesthesia for superficial and deep sensibility in the legs. Electromyography objectified a demyelinating multifocal sensorimotor neuropathy. Sonographic study showed impaired myoarchitectonics of muscle gastrocnemius bilaterally with more severe involvement of the lateral head asymmetrical changes with bundles, differing from normal myosonographies and from the patient with genetic distal myopathy.
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The aim of this study was to analyze myosonographic changes in triceps surae muscles in patients with metabolic neuropathy in the legs.
The aim of this study was to analyze myosonographic changes in triceps surae muscles in patients with metabolic neuropathy in the legs.
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A 48-year-old patient with autosomal dominant (AD) mode of inheritance of insulin-dependent diabetes mellitus (DM) diagnosed at the age of 1 year and 6 months, complicated by neuropathy, established on 33 years of age was studied.
A 48-year-old patient with autosomal dominant (AD) mode of inheritance of insulin-dependent diabetes mellitus (DM) diagnosed at the age of 1 year and 6 months, complicated by neuropathy, established on 33 years of age was studied. The disease debuted with numbness and pain in both feet and difficulty stepping on toes and heels. Ten years later weakness in arms was added. The patient has a brother, a sister and a nephew with diabetes, established in the first two years of their lives.
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Myosonography in metabolic neuropathy
Myosonography in metabolic neuropathy
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. Patient with neuropathy – extremely prolonged CMAP latency and diminished CMAP amplitude
. Patient with neuropathy – extremely prolonged CMAP latency and diminished CMAP amplitude
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, irregular strips hipoehoic strand type atrophy in diabetic neuropathy
, irregular strips hipoehoic strand type atrophy in diabetic neuropathy
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Myosonography in metabolic neuropathy
Myosonography in metabolic neuropathy
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Unlike the netlike myoarchitectonics in healthy individuals, patients with diabetic neuropathy have hipoehoic strips of uneven bundle atrophy as an expression of neurogenic denervation.
Unlike the netlike myoarchitectonics in healthy individuals, patients with diabetic neuropathy have hipoehoic strips of uneven bundle atrophy as an expression of neurogenic denervation. That contrasts with the granular-fibrous structure in genetic distal myopathy, where atrophic muscle fibers are replaced by fatty degeneration and fibrosis tissue (Fig. 3).
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Diabetic neuropathy is a late complication of diabetes observed in 50% of patients.
Diabetic neuropathy is a late complication of diabetes observed in 50% of patients. Most often it is manifested as a symmetric sensorimotor and autonomic neuropathy [9]. Histological studies show neurogenic muscular atrophy with signs of chronic denervation and reinervation angular small muscle fibers, muscle fibers type “target”, grouping of muscle fibers in the form of bundle atrophy (Fig. 4).
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Most often it is manifested as a symmetric sensorimotor and autonomic neuropathy [9].
Diabetic neuropathy is a late complication of diabetes observed in 50% of patients. Most often it is manifested as a symmetric sensorimotor and autonomic neuropathy [9]. Histological studies show neurogenic muscular atrophy with signs of chronic denervation and reinervation angular small muscle fibers, muscle fibers type “target”, grouping of muscle fibers in the form of bundle atrophy (Fig. 4).
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We presented a patient with insulin dependent diabetes with AD mode of inheritance and diabetic neuropathy occurring 30 years after disease onset.
We presented a patient with insulin dependent diabetes with AD mode of inheritance and diabetic neuropathy occurring 30 years after disease onset. The early onset of DM and the presence of family history imposed the differential diagnosis with MODY disease (maturityonset diabetes of the young) [5], characterized by early onset (before age 25), AD mode of inheritance, primary defect in glucose-stimulated insulin secretion and heterogeneity in genetic, metabolic and clinical treatment. Genetic mutations determine the development of MODY and
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In our patient mutations in HNF-4α and HNF-1α gene are suggested because of insulin therapy from an early childhood, poor glycemic control and developed complications diabetic neuropathy and retinopathy [4].
encode proteins responsible for the homeostasis of β-cells in the pancreas. In our patient mutations in HNF-4α and HNF-1α gene are suggested because of insulin therapy from an early childhood, poor glycemic control and developed complications diabetic neuropathy and retinopathy [4]. Genetic studies in this direction have been appointed.
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Rehabilitation treatment and interdisciplinary approach may improve the condition of patients with progressive neurologic disorders such as multiple sclerosis, Parkinson’s disease, amyotrophic lateral sclerosis, muscular dystrophy and neuropathy.
Rehabilitation treatment and interdisciplinary approach may improve the condition of patients with progressive neurologic disorders such as multiple sclerosis, Parkinson’s disease, amyotrophic lateral sclerosis, muscular dystrophy and neuropathy. The choice of a wheelchair is crucial in progressive neurologic disorders [1].
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11. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2012, No. 2 , , ,

„Diabetic Neuropathy“ and others.
„Diabetic Neuropathy“ and others. With great interest the audience followed the contemporary trends and developments in pathogenesis and treatment of diabetes. Early and late complications of diabetes – a major interdisciplinary problem in medicine, bringing together experts from different fields were discussed. Prof. Alexiev from MMA presented specific health, social and law problems of diabetic patients working in aviation field.
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12. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

Orthostatic Reactivity in Patients with Diabetic Neuropathy.
Orthostatic Reactivity in Patients with Diabetic Neuropathy.
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Patients with carotid pathology, neuro-ophthalmic syndromes, neuropathy, myopathy, cervical tumors, calf muscle trauma and chronic spastic paralysis were studied by multimodal 2D/3D/4D sonography.
Patients with carotid pathology, neuro-ophthalmic syndromes, neuropathy, myopathy, cervical tumors, calf muscle trauma and chronic spastic paralysis were studied by multimodal 2D/3D/4D sonography. The results were compared to the findings from other diagnostic methods.
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Different types of triceps surae (TS) muscle disturbances due to traumatic injury, genetic disorders, peripheral neuropathy, chronic spastic hemiparesis, venous pathology and combined hemiparesis after cervical and lumbar spinal surgery were evaluated by EMG and electroneurography.
Different types of triceps surae (TS) muscle disturbances due to traumatic injury, genetic disorders, peripheral neuropathy, chronic spastic hemiparesis, venous pathology and combined hemiparesis after cervical and lumbar spinal surgery were evaluated by EMG and electroneurography. The findings were juxtaposed to corresponding images obtained by simultaneous multimodal 2D/3D/4D myosonography in rest, during maximal plantar flexion and electrical stimulation. The results were compared to EMG findings and myosonograms of healthy persons.
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ORTHOSTATIC REACTIVITY IN PATIENTS WITH DIABETIC NEUROPATHY
ORTHOSTATIC REACTIVITY IN PATIENTS WITH DIABETIC NEUROPATHY
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To assess the effect of a structured physical therapy (PT) programme on the orthostatic reactivity in patients with diabetic neuropathy (DNP).
To assess the effect of a structured physical therapy (PT) programme on the orthostatic reactivity in patients with diabetic neuropathy (DNP).
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13. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

Differentiation between arteritic or embolic central retinal artery (CRA) occlusion is a diagnostic challenge specially in older patients with ischemic optic neuropathy (ION).
Differentiation between arteritic or embolic central retinal artery (CRA) occlusion is a diagnostic challenge specially in older patients with ischemic optic neuropathy (ION). Presence of the so called ‘‘spot sign’’ (hyperechogenic embolic material) in the optic nerve head at the projec-
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14. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 11, 2015, No. 1 , , ,

In older patients with ischemic optic neuropathy the presence of the so called spot sign’’ (hyperechogenic embolic material) in the optic nerve head is a marker for embolic event within
In older patients with ischemic optic neuropathy the presence of the so called spot sign’’ (hyperechogenic embolic material) in the optic nerve head is a marker for embolic event within
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15. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 11, 2015, No. 2 , , ,

Reliable abnormalities in cardiovascular reflexes with sympathetic and parasympathetic dysfunctions suggestive of autonomic neuropathy in scleroderma have been described by other authors [7, 8, 13, 15].
compared to those in primary Raynaud's phenomenon, and healthy persons. During orthostatic, deep breathing and cold tests the patients with scleroderma maintained similar heart rate variability, suggesting impaired baroreceptor and thermoregulatory modulation of the autonomic control and cardiovascular autonomic dysfunction. The sympathetic activity was increased in the patients with scleroderma. A state of sympathetic arousal is suggested because of a reliable reduction of heart rate variability [16]. Reliable abnormalities in cardiovascular reflexes with sympathetic and parasympathetic dysfunctions suggestive of autonomic neuropathy in scleroderma have been described by other authors [7, 8, 13, 15].
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Heinonen E, Farkkila M, Forsstrom J, Antila K, Jalonen J, Korhonen O, Pyykko I Autonomic neuropathy and vibration exposure in forestry workers.
Heinonen E, Farkkila M, Forsstrom J, Antila K, Jalonen J, Korhonen O, Pyykko I Autonomic neuropathy and vibration exposure in forestry workers.
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Autonomic neuropathy in systemic sclerosis.
Klimiuk PS, Taylor L, Baker RD, Jayson MI. Autonomic neuropathy in systemic sclerosis.
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Different types of triceps surae (TS) muscle disturbances due to traumatic injury, genetic disorders, peripheral neuropathy, chronic spastic hemiparesis, venous pathology and combined hemiparesis after cervical and lumbar spinal surgery were evaluated by EMG and electroneurography.
Different types of triceps surae (TS) muscle disturbances due to traumatic injury, genetic disorders, peripheral neuropathy, chronic spastic hemiparesis, venous pathology and combined hemiparesis after cervical and lumbar spinal surgery were evaluated by EMG and electroneurography. The findings were juxtaposed to corresponding images obtained by simultaneous multimodal 2D/3D/4D myosonography in rest, during maximal plantar flexion and electrical stimulation. The results were compared to EMG findings and myosonograms of healthy persons.
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16. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 1 , , ,

Scientific Practical Workshop “Diabetic Neuropathy”
Scientific Practical Workshop “Diabetic Neuropathy”
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Workshop “Diabetic Neuropathy”
Workshop “Diabetic Neuropathy”
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, 2015 in the town of Gotse Delchev a scientific and practical forum on Diabetes Mellitus and diabetic neuropathy, organized and sponsored by W
, 2015 in the town of Gotse Delchev a scientific and practical forum on Diabetes Mellitus and diabetic neuropathy, organized and sponsored by W
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She presented the various neuropathy forms in diabetes mellitus, the reasons for their occurrence and some new treatment approaches, including strict glycemic control using insulin pumps, pathogenetic treatment with benfotiamine and alpha-lipoic acid, symptomatic treatment of neuropathic pain, foot hygiene, combined with appropriate exercise regimen.
On the first day over 80 doctors and pharmacists from the region attended the forum. Dr. Maria Radiykova – Chief Doctor of the local hospital, opened the seminar. Guest speaker at the event was academician Ekaterina Titianova, MD – Head of the “Clinic of Functional Diagnostics of Nervous System” and Head of the Department “Neurology, Psychiatry, Physiotherapy and Rehabilitation, Preventive Medicine and Public Health” of the Medical Faculty of Sofia University “St. Kliment Ohridski”. She presented the various neuropathy forms in diabetes mellitus, the reasons for their occurrence and some new treatment approaches, including strict glycemic control using insulin pumps, pathogenetic treatment with benfotiamine and alpha-lipoic acid, symptomatic treatment of neuropathic pain, foot hygiene, combined with appropriate exercise regimen. It was emphasized that as genetic dis-
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rwag Pharma for the treatment of diabetic neuropathy were presented.
rwag Pharma for the treatment of diabetic neuropathy were presented.
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, 2015 at the House of Science and Technology in the city a specialized training of patients with diabetes mellitus and diabetic neuropathy was held.
, 2015 at the House of Science and Technology in the city a specialized training of patients with diabetes mellitus and diabetic neuropathy was held. Assoc. Prof. Daniela Lyubenova, a specialist in kinesitherapy and Vice-dean of the National Sports Academy “Vasil Levski” – Sofia presented the basic principles of physical rehabilitation and demonstrated a specialized program for individual home rehabilitation adapted for use by patients with diabetes mellitus. Participants in the event were given the
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Scientific Practical Workshop“Diabetic Neuropathy”
Scientific Practical Workshop“Diabetic Neuropathy”
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17. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

lf the optic nerve is affected by compression, clinical sigs of optic neuropathy may occur, such as reduced visual acuity, abnormal color vision, and relative afferent papillary defect [1, 2].
Patients with SOVT may complain of facial and orbital pain and swelling, double and decreasedblurred vision. Сlinical findings depend on the specific etiology and may include proptosis, chemosis, ophthalmoplegia, and ptosis. lf the optic nerve is affected by compression, clinical sigs of optic neuropathy may occur, such as reduced visual acuity, abnormal color vision, and relative afferent papillary defect [1, 2]. ln this case, the patient presented with clinical features consistent with an orbital process. Before additional diagnostics, we suspected Tolosa-Hunt syndrome, but after the MRl we diverted the examination to SOVT. MRl is sensitive even in early stages of the disease, and is recommended when there is a suspicion of SOVT or cavernous sinus thrombosis. MRl may demonstrate a dilated SOV, and extraocular muscle enlargement [2, 9]. ln our case, orbital MR examination was of crucial importance for the diagnosis.
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18. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 2 , , ,

Home-based Neurorehabilitation in Diabetic Neuropathy
Home-based Neurorehabilitation in Diabetic Neuropathy
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Home-based Neurorehabilitation in Diabetic Neuropathy.
Home-based Neurorehabilitation in Diabetic Neuropathy.
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He was deeply involved in clinical research regarding the pathophysiology of Familial Dysautonomia, also known as Riley-Day syndrome or Hereditary Sensory and Autonomic Neuropathy Type III, and in studies of Fabry disease that led to the approval of enzyme replacement therapy in the USA.
Since June 2015, he is Professor of Neurology at the University of ErlangenNuremberg in Erlangen, Germany. He is also Adjunct Professor of Neurology at Icahn School of Medicine at Mount Sinai, New York, NY, USA. Form September 1, 2016 to August 31, 2017, he was the Chair in Autonomic Neurology, and Director of the Clinical Department of Autonomic Neurology at the University College London, Institute of Neurology, Queen Square, London, UK. He was Professor of Neurology in Medicine and Psychiatry at the New York University, New York, NY (1992–2013). He also served as the Associate Director of the NYU Dysautonomia Evaluation and Treatment Center (until 2007). He was deeply involved in clinical research regarding the pathophysiology of Familial Dysautonomia, also known as Riley-Day syndrome or Hereditary Sensory and Autonomic Neuropathy Type III, and in studies of Fabry disease that led to the approval of enzyme replacement therapy in the USA.
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He co-authored the guidelines of the German Neurological Society on syncope, the guidelines on erectile dysfunction and the guidelines of the German Diabetes Society on diabetic neuropathy.
Professor Hilz is a member of 16 national and international scientific societies and is on the board of several autonomic nervous system societies. He currently co-chairs the Autonomic Nervous System Subspecialty Panel of the European Academy of Neurology, EAN. He also is PastPresident of the German Autonomic Society, Past-President of the European Federation of Autonomic Societies, and Past-Chair of the Autonomic Section of the American Academy of Neurology. He is ad hoc reviewer for more than 25 international scientific journals, a member of the editorial board of Clinical Autonomic Research, and Associate Clinical Editor of Autonomic Neuroscience: Basic and Clinical. He co-authored the guidelines of the German Neurological Society on syncope, the guidelines on erectile dysfunction and the guidelines of the German Diabetes Society on diabetic neuropathy. He has published more than 300 original and review articles in peer-reviewed journals and chapters in textbooks and presented his work at several hundred scientific conferences.
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kinesiotherapy, neurorehabilitation, gait, stroke, diabetic neuropathy, cardiologic and pulmonary rehabilitation, ets.
kinesiotherapy, neurorehabilitation, gait, stroke, diabetic neuropathy, cardiologic and pulmonary rehabilitation, ets.
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Ultrasound in the diagnosis of peripheral neuropathy: structure meets function in the neuromuscular clinic.
Gallardo E, Noto Y, Simon NG. Ultrasound in the diagnosis of peripheral neuropathy: structure meets function in the neuromuscular clinic.
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Diabetic neuropathy (DN).
Diabetic neuropathy (DN).
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It is a common late complication of diabetes, often manifested as a symmetric sensorimotor and autonomic neuropathy.
It is a common late complication of diabetes, often manifested as a symmetric sensorimotor and autonomic neuropathy. Histological studies show neurogenic muscular atrophy with signs of chronic denervation and reinervation – angular small muscle fibers, muscle fibers type “target”, grouping of muscle fibers in the form of bundle atrophy. The neurogenic damage of calf muscles are proved by different methods – clinical, neurophysiologic, neuroimaging, etc. [17]. The simultaneous usage of EMG and myosonography helps for evaluation of the severity of peripheral nerves damage and the changes in cross-striated muscles that could contribute to distinguish primary from secondary myogenic lesions in peripheral neuropathy [8]. Myosonographic patterns in low extremity neuropathy demonstrate bundle atrophy with mild to severe involvement of both lateral heads of triceps surae muscle, which correlates with the
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The simultaneous usage of EMG and myosonography helps for evaluation of the severity of peripheral nerves damage and the changes in cross-striated muscles that could contribute to distinguish primary from secondary myogenic lesions in peripheral neuropathy [8].
It is a common late complication of diabetes, often manifested as a symmetric sensorimotor and autonomic neuropathy. Histological studies show neurogenic muscular atrophy with signs of chronic denervation and reinervation – angular small muscle fibers, muscle fibers type “target”, grouping of muscle fibers in the form of bundle atrophy. The neurogenic damage of calf muscles are proved by different methods – clinical, neurophysiologic, neuroimaging, etc. [17]. The simultaneous usage of EMG and myosonography helps for evaluation of the severity of peripheral nerves damage and the changes in cross-striated muscles that could contribute to distinguish primary from secondary myogenic lesions in peripheral neuropathy [8]. Myosonographic patterns in low extremity neuropathy demonstrate bundle atrophy with mild to severe involvement of both lateral heads of triceps surae muscle, which correlates with the
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Myosonographic patterns in low extremity neuropathy demonstrate bundle atrophy with mild to severe involvement of both lateral heads of triceps surae muscle, which correlates with the
It is a common late complication of diabetes, often manifested as a symmetric sensorimotor and autonomic neuropathy. Histological studies show neurogenic muscular atrophy with signs of chronic denervation and reinervation – angular small muscle fibers, muscle fibers type “target”, grouping of muscle fibers in the form of bundle atrophy. The neurogenic damage of calf muscles are proved by different methods – clinical, neurophysiologic, neuroimaging, etc. [17]. The simultaneous usage of EMG and myosonography helps for evaluation of the severity of peripheral nerves damage and the changes in cross-striated muscles that could contribute to distinguish primary from secondary myogenic lesions in peripheral neuropathy [8]. Myosonographic patterns in low extremity neuropathy demonstrate bundle atrophy with mild to severe involvement of both lateral heads of triceps surae muscle, which correlates with the
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Triceps surae muscle myosonograms in diabetic neuropathy.
Triceps surae muscle myosonograms in diabetic neuropathy.
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Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy.
Chamova T, Titianova E, Tournev I, Dimova R. Myosonographic Assessment of Triceps Surae Muscle in Metabolic Neuropathy.
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Ultrasound in the diagnosis of peripheral neuropathy: structure meets function in the neuromuscular clinic.
Gallardo E, Noto, Y-I, Simon NG. Ultrasound in the diagnosis of peripheral neuropathy: structure meets function in the neuromuscular clinic.
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According to this theory, certain individuals labeled as supertasters (mainly females) due to the high density of fungiform papilla present on the anterior aspect of tongue, are at risk of developing burning pain; 2) Sensory dysfunction associated with small and/or large fiber neuropathy; 3)
The possible theories behind the cause of BMS are [2-9]: 1) Abnormal interaction between the sensory functions of facial and trigeminal nerves. According to this theory, certain individuals labeled as supertasters (mainly females) due to the high density of fungiform papilla present on the anterior aspect of tongue, are at risk of developing burning pain; 2) Sensory dysfunction associated with small and/or large fiber neuropathy; 3)
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This new evidence, in increasingly larger groups of BMS subjects, suggests a common background of neuropathy in the pathogenesis of this syndrome.
such a group of pathologies. Burning pain without mucosal or skin lesions, however, represents the typical symptom of chronic neuropathic pain conditions resulting from nerve damage, and in recent years a neuropathic basis of BMS has been better identified through the use of more sensitive diagnostic techniques [18]. This new evidence, in increasingly larger groups of BMS subjects, suggests a common background of neuropathy in the pathogenesis of this syndrome. As a result, it seems more appropriate to recognize two clinical forms of BMS:
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BMS) are associated with established organic/therapeutic-related etiologies (e.g., oral cavity disorders, including oral local neuropathy, systemic disorders, nutritional deficiencies, drug-induced, neurological and psychiatric abnormalities) [19].
BMS) are associated with established organic/therapeutic-related etiologies (e.g., oral cavity disorders, including oral local neuropathy, systemic disorders, nutritional deficiencies, drug-induced, neurological and psychiatric abnormalities) [19].
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Trigeminal small-fiber sensory neuropathy causes burning mouth syndrome.
Lauria G, Majorana A, Borgna M, et al. Trigeminal small-fiber sensory neuropathy causes burning mouth syndrome.
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Home-based Neurorehabilitation in Diabetic Neuropathy
Home-based Neurorehabilitation in Diabetic Neuropathy
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diabetes mellitus, diabetic neuropathy, neurorehabilitation,
diabetes mellitus, diabetic neuropathy, neurorehabilitation,
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Diabetic neuropathy (DN) is one of the most common complications in patients with diabetes mellitus type 2.
Diabetic neuropathy (DN) is one of the most common complications in patients with diabetes mellitus type 2. It affects from 22.5% to 28.5% of all diabetic patients worldwide; on national scale the morbidity reaches 50-70% of the affected patients.
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For this reason, we offer diabetic neuropathy patients the possibility of metabolic control, symptom reduction and orthostatic improvement through systemic self-fulfillment of purposeful physical exercises.
Neurorehabilitation is one of the main therapeutic approaches in the whole algorithm of treatment of DN. The ability to perform long-term, specialized physical therapy at home is essential for patients with chronic neurological deficits. For this reason, we offer diabetic neuropathy patients the possibility of metabolic control, symptom reduction and orthostatic improvement through systemic self-fulfillment of purposeful physical exercises. Increasing their daily motor activity will improve their self-esteem and quality of life.
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The disease is associated with an increased relative risk for ischemic stroke, ischemic cardiac disease, chronic insufficiency of the lower extremities and chronic microvascular complications as retinopathy, nephropathy and neuropathy [19].
Diabetes mellitus is the fourth leading cause of global death by disease. More than 246 million people suffer from diabetes worldwide with a tendency this incidence to rise to 380 million by 2025. The disease is associated with an increased relative risk for ischemic stroke, ischemic cardiac disease, chronic insufficiency of the lower extremities and chronic microvascular complications as retinopathy, nephropathy and neuropathy [19].
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Diabetic neuropathy (DN) is the most frequent complication.
Diabetic neuropathy (DN) is the most frequent complication. It affects 22,5% то 28,5% of all diabetic patients worldwide, and on national scale the morbidity reaches 50-70% of the affected patients [14]. Тhe feet and legs are often affected first, followed by hands and arms. Signs and symptoms of peripheral neuropathy are often worse at night, and may include: numbness or reduced ability to feel pain or temperature changes; a tingling or burning sensation; sharp pains or cramps; increased sensitivity to touch for some people, even the weight of a bed sheet can be agonizing; muscle weakness; loss of reflexes, especially Achilles’; loss of balance and coordination; serious foot problems, such as ulcers, infections, deformities, and bone and joint pain [12].
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Signs and symptoms of peripheral neuropathy are often worse at night, and may include: numbness or reduced ability to feel pain or temperature changes; a tingling or burning sensation; sharp pains or cramps; increased sensitivity to touch for some people, even the weight of a bed sheet can be agonizing; muscle weakness; loss of reflexes, especially Achilles’; loss of balance and coordination; serious foot problems, such as ulcers, infections, deformities, and bone and joint pain [12].
Diabetic neuropathy (DN) is the most frequent complication. It affects 22,5% то 28,5% of all diabetic patients worldwide, and on national scale the morbidity reaches 50-70% of the affected patients [14]. Тhe feet and legs are often affected first, followed by hands and arms. Signs and symptoms of peripheral neuropathy are often worse at night, and may include: numbness or reduced ability to feel pain or temperature changes; a tingling or burning sensation; sharp pains or cramps; increased sensitivity to touch for some people, even the weight of a bed sheet can be agonizing; muscle weakness; loss of reflexes, especially Achilles’; loss of balance and coordination; serious foot problems, such as ulcers, infections, deformities, and bone and joint pain [12].
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A study on the strength of extensors and flexors of the knee and ankle joints found that muscle weakness was linked to the severity of neuropathy and disturbed the pattern of walking of the patients [29].
A major problem with patients with DN is the motor dysfunction. A study on the strength of extensors and flexors of the knee and ankle joints found that muscle weakness was linked to the severity of neuropathy and disturbed the pattern of walking of the patients [29]. To improve
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Based on the indicated static balance disturbances, the principal recommendations for PT effect on sensory ataxia in neuropathy are aimed at improving proprioreception by excluding or destabilizing the visual analyzer when the patient is standing on a solid basis [9].
In patients with DN, balance is impaired as a result of sensory disturbances that are largely offset by the visual analyzer and impaired biomechanical balance factors (center of gravity, line of gravity, weight-bearing area and stability limits), due to muscle weakness in the distal parts of the lower limbs, decreased movement of the ankle joint and pain [17]. Based on the indicated static balance disturbances, the principal recommendations for PT effect on sensory ataxia in neuropathy are aimed at improving proprioreception by excluding or destabilizing the visual analyzer when the patient is standing on a solid basis [9].
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To objectify its effect we have studied 124 patients suffering from diabetic neuropathy and
To objectify its effect we have studied 124 patients suffering from diabetic neuropathy and
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The effect of exercise on neuropathic symptoms, nerve function, and cutaneous innervation in people with diabetic peripheral neuropathy.
Rucker J, Sharma N, Wright D. The effect of exercise on neuropathic symptoms, nerve function, and cutaneous innervation in people with diabetic peripheral neuropathy.
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Generalized Peripheral Neuropathy.
Kowalske K. Neuromuscular rehabilitation and electrodiagnosis. Generalized Peripheral Neuropathy.
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Fall and balance outcomes after an intervention to promote leg strength, balance, and walking in people with diabetic peripheral neuropathy: "feet first" randomized controlled trial.
Kruse R, Lemaster J, Madsen R. Fall and balance outcomes after an intervention to promote leg strength, balance, and walking in people with diabetic peripheral neuropathy: "feet first" randomized controlled trial.
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Diabetic peripheral neuropathy and depressive symptoms.
Loretta V, Jeffrey S, Richard R, Adam G, Peter R, Andrew J. Diabetic peripheral neuropathy and depressive symptoms.
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Didactic tools for self-performed specialized physical therapy in diabetic neuropathy.
Lubenova D. Didactic tools for self-performed specialized physical therapy in diabetic neuropathy. In: Self-directed didactic tools for physical therapy in diabetic neuropathy. Sofia, 2010, 7-23. Project number 502217-LLP-1-2009-1PT-GRUNDTVIG-GMP (www.projectpaladin.eu).
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In: Self-directed didactic tools for physical therapy in diabetic neuropathy.
Lubenova D. Didactic tools for self-performed specialized physical therapy in diabetic neuropathy. In: Self-directed didactic tools for physical therapy in diabetic neuropathy. Sofia, 2010, 7-23. Project number 502217-LLP-1-2009-1PT-GRUNDTVIG-GMP (www.projectpaladin.eu).
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A moderate-intensity weightbearing exercise program for a person with type 2 diabetes and peripheral neuropathy.
Tuttle L, Hastings M, Mueller M. A moderate-intensity weightbearing exercise program for a person with type 2 diabetes and peripheral neuropathy.
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Lower physical activity is associated with higher intermuscular adipose tissue in people with Type 2 diabetes and peripheral neuropathy.
Tuttle L, Sinacore D, Cade W, Michael J. Lower physical activity is associated with higher intermuscular adipose tissue in people with Type 2 diabetes and peripheral neuropathy.
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Vinik A. Neuropathy.
Vinik A. Neuropathy. In: Ruderman N, Devlin J (ads). The health professional’s guide to diabetes and exercise. Alexandria.
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Minimizing risks in patients who have neuropathy.
Ward S. Diabetes, exercise, and foot care. Minimizing risks in patients who have neuropathy.
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19. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 1 , , ,

Daniela Lubenova (Bulgaria) concluded the session with a program for home-based Neurorehabilitation in diabetic neuropathy.
(Serbia) made an overview on the recent concept of the Burning Mouth syndrome. Prof. Max Hiltz (Germany) spoke about differential diagnosis of syncope and seizure. Prof. Daniela Lubenova (Bulgaria) concluded the session with a program for home-based Neurorehabilitation in diabetic neuropathy.
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20. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 2 , , ,

Cubital Tunnel Syndrome: Compressive Neuropathy of the Ulnar Nerve –
Cubital Tunnel Syndrome: Compressive Neuropathy of the Ulnar Nerve –
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CUBITAL TUNNEL SYNDROME: COMPRESSIVE NEUROPATHY OF THE ULNAR NERVE – A CASE REPORT
CUBITAL TUNNEL SYNDROME: COMPRESSIVE NEUROPATHY OF THE ULNAR NERVE – A CASE REPORT
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Cubital tunnel syndrome (CTS) is the second most common neuropathy after the carpal tunnel syndrome.
Cubital tunnel syndrome (CTS) is the second most common neuropathy after the carpal tunnel syndrome. People with diabetes, cysts and swelling of the elbow joint, arthritis and repetitive, prolonged activity requiring permanently flicked and deflected elbow are more susceptible.
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Bulgarian participants presented two plenary reports, dedicated to the effect of six-month home-based neurorehabilitation on muscle pump efficacy in diabetic neuropathy (E. Titianova,
Bulgarian participants presented two plenary reports, dedicated to the effect of six-month home-based neurorehabilitation on muscle pump efficacy in diabetic neuropathy (E. Titianova,
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21. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 15, 2019, No. 1 , , ,

Often complications are the first manifestation of carbohydrate metabolism changes: cardiovascular or cerebrovascular events, retinopathy, neuropathy, extremity vascular disease and others.
life expectancy, urbanization, and increased obesity and physical inactivity [31]. Most of the patients (up to 50% in some regions) remain undiagnosed [3]. Often complications are the first manifestation of carbohydrate metabolism changes: cardiovascular or cerebrovascular events, retinopathy, neuropathy, extremity vascular disease and others. All this requires search of a reliable method for screening and early detection of diabetes and prediabetes. This will give the opportunity for prophylaxis and delay of early and late complications and their consequences, and for regulation of health care expenses [7].
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