Explore chapters and articles related to this topic
Diabetic Neuropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
To resolve autonomic neuropathy, the underlying cause must be treated. Patients should follow physician instructions about managing their diabetes – the blood glucose, BP, and cholesterol. This can stop the nerve damage from progressing. Measures used for treatment include more physical activity, increased salt in the diet if there is orthostatic hypotension, increasing hydrating fluids, raising the head of the bed, wearing elastic stockings to improve blood flow, rising up from sitting to standing slowly, and avoiding hypoglycemia. Medications may be prescribed to help the body retain salt, increase BP, and regulate the heart rate. Dietary changes may be needed, and some patients require OTC medications to treat constipation, diarrhea, and fecal incontinence. For bladder problems, prescription medications may be needed, such as antibiotics for bladder infections.
Autonomic Nervous System Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Chronic autonomic neuropathy: Cholinergic – chronic anhidrosis manifesting as heat intolerance or a chronic enteric neuropathy.Adrenergic – manifesting as orthostatic hypotension.Pandysautonomia.
Autonomic Neuropathy and the Heart in Diabetes
Published in Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla, Heart Dysfunction in Diabetes, 2019
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla
On the basis of NE uptake, storage, metabolism, and release, many investigators have implicated the involvement of the sympathetic nervous system in the pathophysiology of several heart diseases.73–75 While these results favor the view that the sympathetic nervous system is activated in diabetes, the significance of such a lesion in the development of diabetic cardiomyopathy and associated changes in the ultrastruucture and function of subcellular organelles64,76,77 remains to be investigated. In this regard, insulin plays a crucial role in the regulation of sympathetic activity because most of the changes of NE stores, synthesis, uptake, release, and metabolism observed in diabetes are reversible upon insulin treatment.53,58 It should be noted that there is a close correlation between the development of diabetic cardiomyopathy and the rise in cardiac NE level as both of these defects are shown to occur 4 weeks after the injection of streptozotocin.77 At any rate, it would appear that the sympathetic nervous system is activated during the early stages of experimental diabetes. Autonomic neuropathy is preceded by this increased activity of the sympathetic nervous system and this abnormality may play a crucial role in the cellular damage in cardiac muscle.
Cardiovascular involvement in patients affected by multiple myeloma: a comprehensive review of recent advances
Published in Expert Review of Hematology, 2021
Massimiliano Camilli, Giulia La Vecchia, Rosa Lillo, Giulia Iannaccone, Priscilla Lamendola, Rocco Antonio Montone, Stefan Hohaus, Nadia Aspromonte, Massimo Massetti, Gaetano Antonio Lanza, Filippo Crea, Francesca Graziani, Antonella Lombardo
Systemic manifestations may even precede cardiac involvement and represent ‘red flags’ that can point to the final diagnosis of AL amyloidosis [53]. Periorbital purpura (so-called ‘panda eyes’) [54] in a patient with HF of unknown origin is highly suspicious for AL amyloidosis, but even if pathognomonic, it is present in no more than 20% of cases and is a late finding in AL amyloidosis. It represents the expression of infiltration of small vessels and soft tissues, which also causes macroglossia (approximately 10% of patients, sometimes leading to dysphonia or dysgeusia), nail dystrophy (brittle and slow-growing nails), and submandibular gland enlargement. Hepatomegaly is frequent because of amyloid infiltration and also reflecting venous congestion. Neurological symptoms include peripheral and autonomic neuropathy, as well as carpal tunnel syndrome. Peripheral neuropathy is quite common, predominantly sensory, symmetric, and with a glove-and-stocking distribution. Autonomic nervous system dysfunction may manifest as significant orthostatic hypotension, expression also of reduced cardiac output and low peripheral tone [55]. Other autonomic neuropathy manifestations are erectile dysfunction and fluctuating changes of bowel habits [56]. In 7.5% of patients with AL amyloidosis a Factor X deficiency is found and could result from binding of the factor to the amyloid fibrils. This may cause serious bleedings, which are observed in up to 1% to 2% of individuals.
Possible roles of mitochondrial dysfunction in neuropathy
Published in International Journal of Neuroscience, 2021
Chutikorn Khuankaew, Passakorn Sawaddiruk, Poomarin Surinkaew, Nipon Chattipakorn, Siriporn C. Chattipakorn
Neuropathy is a pathological pain in which the function of the nervous system has been disturbed [1,2]. Neuropathy is commonly found with different underlying pathophysiological conditions, including trauma-induced neuropathy, chemotherapy-induced neuropathy, diabetes-induced neuropathy and HIV-associated sensory neuropathy. Neuropathy may affect the sensory, motor or autonomic nervous system which causes suffering in many patients [1,2]. Sensory neuropathy may present neuropathic pain with abnormal sensations such as numbness or changes in the ability to detect heat and cold, whereas muscle weakness, cramps or paralysis are found in patients with motor neuropathy [1]. In addition, autonomic neuropathy may result in abnormal feelings such as dizziness and fainting due to sudden changes in blood pressure, abnormal sweating, incontinence or impotence [2]. The exact pathophysiology of neuropathy is still unclear. Although currently neuropathy cannot be cured, symptomatic therapy has been used to relieve pain in these patients. It is expected that the underlying aetiology of neuropathy should be identified to be targeted for the future therapy.
Hereditary transthyretin amyloidosis: baseline characteristics of patients in the NEURO-TTR trial
Published in Amyloid, 2018
Marcia Waddington-Cruz, Elizabeth J. Ackermann, Michael Polydefkis, Stephen B. Heitner, Peter J. Dyck, Fabio A. Barroso, Annabel K. Wang, John L. Berk, P. James B. Dyck, Brett P. Monia, Steven G. Hughes, Li Tai, T. Jesse Kwoh, Shiangtung W. Jung, Teresa Coelho, Merrill D. Benson, Morie A. Gertz
Presence of autonomic neuropathy, as reported by patients, was consistent with the NSC results. Over 50% of patients had a history of gastrointestinal manifestations, which are generally attributed to deficits in the autonomic nervous system. GI amyloidosis or symptoms, such as recurring diarrhea, constipation, defecation urgency, GI mobility disorder, or GI hypomotility were reported in 80 (47%) patients; nausea, vomiting, or early satiety in 23 (13%) patients; and unintentional weight loss (abnormal loss of weight, weight decreased, cachexia, decreased appetite) in 31 (18%) patients. In addition, 61 (35%) patients reported a history of either orthostatic hypotension, sexual dysfunction, urinary tract infection (UTI), urinary retention/hesitation/incontinence or neurogenic bladder.