diabetes and dizziness vomiting

🔥+ diabetes and dizziness vomiting 05 Jul 2020 Complications of diabetes Microvascular complications include damage to eyes (retinopathy) leading to blindness, to kidneys (nephropathy) leading to renal failure and to nerves (neuropathy) leading to impotence and diabetic foot disorders (which include severe infections leading to amputation).

diabetes and dizziness vomiting The answer is yes. In addition to the noticeable symptoms of diabetes, this condition can also cause different long-term effects on the body. Since ...

what can happen if diabetes is left untreated Skip to Main content
ScienceDirect
RegisterSign in

Neurologic Aspects of Systemic Disease Part II

Gerald Charnogursky, ... Norma Lopez, in Handbook of Clinical Neurology, 2014

Pathophysiology

Diabetic neuropathy occurs when there is an imbalance between nerve fiber damage and repair. The nerve damaging process preferentially affects autonomic and distal sensory fibers, leading to the progressive loss of sensation. Besides metabolic factors listed above, ischemic factors and inflammation also contribute to the development of diabetic neuropathies. Metabolic factors seem to prevail in length-dependent diabetic polyneuropathy, whereas inflammation superimposed on ischemic nerve lesions is found in severe forms of focal neuropathies. The thickening and hyalinization of the walls of small blood vessels due to the reduplication of the basal lamina around endothelial cells suggests a role for nerve ischemia in diabetic neuropathy. There is also a reduction in endoneurial oxygen tension in the sural nerves of diabetic patients with advanced polyneuropathy (Newrick, 1986).

Possible mechanisms for neuropathy development include oxidative stress, nonenzymatic glycation, the polyol pathway, the hexosamine pathway, protein kinase C pathway, poly (ADP-ribose) polymerase and the reduction of neurotrophic factors (Table 51.1). These various pathogenetic factors may act synergistically to cause DPN

Table 51.1. Pathogenetic mechanisms of neuropathy

Oxidative stress with nitric oxide depletion
Advanced glycosylated end products
Activation of the polyol pathway
Activation of the hexosamine pathway
Excessive protein kinase C activity
Activation of poly(ADP-ribose) polymerase
Diminished neurotrophic peptide factors

Oxidative stress

Elevated glucoses can increase oxidative stress by glucose auto-oxidation and production of advanced glycosylation end products and activation of the polyol pathway. Oxidative stress can also lead to activation of cytokoines, vascular adhesion molecules, endothelium-1 and procoagulant tissue factor . Oxidative stress also reduces endothelial production of nitric oxide which leads to impairment of endothelial function and reduced capillary vasodilation. This ultimately contributes to nerve hypoxia.

The AGE pathway

Advanced glycosylation end products (AGEs) from chronic hyperglycemia play an important role in diabetic neuropathy and microvascular complications (Thornalley, 2002; Sugimoto et al., 2008). Excess glucose combines with amino acids on circulating or tissue proteins to form AGEs. AGEs do not resolve when hyperglycemia is corrected. These AGE peptides cross-link strongly with collagen in vitro, damaging nerve fibers. AGEs also bind to and activate the cell surface receptor called RAGE(Receptor for Advanced Glycation Endproducts). RAGE proteins are proinflammatory and expressed on endothelial cells, fibroblasts, mesangial cells, and macrophages. Endothelial cells with RAGE internalize AGEs into subepithelium enhancing permeability and endothelium-dependent coagulant activity which can contribute to vascular injury and endoneural hypoxia (Singh et al., 2001).

The polyol pathway

Excess glucose is shunted into the polyol pathway and converted to sorbitol by aldose reductase and then to fructose by sorbitol dehydrogenase. Increased activity of this metabolic pathway depletes the nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) needed to regenerate the antioxidant glutathione. Without adequate glutathione, nerves are less able to scavenge reactive oxygen species, thus promoting oxidative stress in the nerve. The excess fructose and sorbitol also decrease expression of the sodium/myoinositol cotransporter, leading to a reduction in cellular uptake of myoinositol. Decreased levels of intracellular myoinositol subsequently lower the levels of its metabolite phosphoinositide. Consequently, the phosphoinositide signaling pathway is impaired, interfering with activation of the transmembrane sodium pump and decreasing nerve sodium/potassium ATPase activity. This results in slowed nerve conduction and with chronic exposure neuronal membrane breakdown ensues.

The hexosamine pathway

The glycolytic intermediates of excess glucose are also shunted into the hexosamine pathway. Fructose-6-phosphate is converted to N-acetylglucosamine-6-phosphate by glutamine: fructose-6-phosphate amidotransferase (GFAT). N-Acetylglucosamine-6-phosphate is then converted to N-acetylglucosamine-1,6-phosphate and to uridine diphosphate-N-acetyl glucosamine (UD-PGlcNAc). UD-PGlcNAc modifies gene expression and protein production essential for normal cell function. Many of the proteins produced in this pathway are inflammatory intermediates that promote neuropathy and include plasminogen-activator inhibitor, which inhibits normal blood clotting and increases vascular complications (Brownlee, 2001).

Protein kinase C (PKC) pathway and poly (ADP-ribose) polymerase (PARP)

Protein kinase C (PKC) is involved in controlling the function of proteins through the phosphorylation of hydroxyl groups of serine and threonine amino acid residues on these proteins. PKC is responsible for the activation of essential proteins and lipids in cells that are needed for cell survival (Vincent et al., 2004). Nevertheless, excessive PKC can be harmful to the nervous system. Its contribution to diabetic neuropathy is likely through effects on vascular blood flow and microvascular disease rather than directly on neuronal cells. Glucose is converted to diacylglycerol which activates PKC. PKC then activates the mitogen-activated protein kinases (MAPK) which phosphorylate transcription of stress genes such as heat shock proteins and c-Jun kinases that can lead to cell apoptosis or vascular atherosclerosis ( the 1 last update 05 Jul 2020 Tomlinson, 1999Tomlinson, 1999). The inhibition of PKC reduces oxidative stress and normalizes blood flow and nerve conduction deficits in diabetic rats (Ishii et al., 1998; Cameron and cotter, 2002). Poly (ADP-ribose) polymerase (PARP) is activated in response to hyperglycemia. Overactivation of PARP results in increased free radical formation, enhanced protein kinase C activity, and AGE formation (diabetes and dizziness vomiting korean (🔥 juvenile) | diabetes and dizziness vomiting zero carbhow to diabetes and dizziness vomiting for Pacher et al., 2005). Each promotes nerve damage through the metabolic pathways described above.

diabetes and dizziness vomiting treatment home remedies (☑ epidemiology) | diabetes and dizziness vomiting and exercisehow to diabetes and dizziness vomiting for Neurotrophic factors and nerve repair

The neurotrophic factors comprise a group of endogenous proteins essential to the health and survival of certain populations of neurons. These neurotrophic peptides include nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, the insulin-like growth factors (IGF), and vascular endothelial growth factors. They are important for the maintenance of nerve structure and function as well as repair following injury. Impaired peripheral nerve repair in diabetes may be due to diabetes-induced loss of these peptides (Kennedy, 2000, 2005). Insulin also functions as a neurotrophic factor to peripheral neurons, and thus loss of insulin in diabetics may compromise nerve viability and repair. Intrathecal delivery of low-dose insulin has reversed the slowing of motor and sensory nerve conduction velocity. Insulin and IGF-1 have also been shown to reverse atrophy in myelinated sensory axons in the sural nerve (diabetes and dizziness vomiting urine test (🔴 symptoms in children) | diabetes and dizziness vomiting virushow to diabetes and dizziness vomiting for Brussee et al., 2004).

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780702040870000516

Peripheral Nerve Disorders

Gérard Said, in Handbook of Clinical Neurology, 2013

Preventive treatment

diabetes and dizziness vomiting teens (🔥 nurse teaching) | diabetes and dizziness vomiting by racehow to diabetes and dizziness vomiting for Prevention of diabetic neuropathy and of its complications remains the best treatment. Tight diabetic control diminishes the risk of developing a disabling peripheral neuropathy, but it is not often achievable, because it carries a higher risk of hypoglycemia. Prevention of complications of diabetic neuropathy includes prevention of trophic changes in the feet. Diabetics need advice about foot care and footware and about protection of hyposensitive areas and pressure points, to prevent the occurrence of painless ulcers and decrease the risk of bone infection. Prevention and treatment of the diabetic foot are at best given in specialized foot clinics. Diabetics with sensory loss also need advice about painless burns and injuries. Pancreatic transplantation is not routinely performed yet. Although it may stabilize the neuropathy it does not seem to improve it (Kennedy et al., 1990).

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780444529022000333

Diabetic Neuropathy

H.C. Powell, A.P. Mizisin, in Encyclopedia of Neuroscience, 2009

Somatic and autonomic peripheral nervous system manifestations

The most common diabetic neuropathy is a symmetric, predominately sensory, neuropathy that affects the distal regions of the lower limbs for 1 last update 05 Jul 2020 first, gradually spreads proximally, and later similarly affects the upper limbs. Symptoms include paresthesias, numbness, and, in some patients, burning and lancinating pain in the lower limbs. Once established, sensory diabetic neuropathy is persistent even if hyperglycemia is controlled.The most common diabetic neuropathy is a symmetric, predominately sensory, neuropathy that affects the distal regions of the lower limbs first, gradually spreads proximally, and later similarly affects the upper limbs. Symptoms include paresthesias, numbness, and, in some patients, burning and lancinating pain in the lower limbs. Once established, sensory diabetic neuropathy is persistent even if hyperglycemia is controlled.

Acute painful diabetic neuropathy is an infrequent syndrome that often follows precipitous weight loss. Patients with this neuropathy experience unremitting, burning pain in the lower limbs. Cutaneous hyperesthesia that results from contact with clothing or sheets is especially troublesome to these patients. Their symptoms often resolve over the course of a few months, after weight gain accompanying diabetic control.

Severe autonomic neuropathy is rare in diabetic patients, and symptoms usually occur in conjunction with a distal symmetric sensory neuropathy in insulin-dependent diabetes mellitus. A wide variety of symptoms affecting all aspects of autonomic function can be present, including heart rate abnormalities and postural hypotension; distal anhidrosis and gustatory sweating; diabetic diarrhea and gastric, duodenal, and colonic atony; bladder atony and impotence; disturbances of respiratory control; and unawareness of hypoglycemia. Once established, autonomic neuropathy is usually irreversible.

A poorly reversible symmetric lower limb motor neuropathy is sometimes present in older diabetic patients, often accompanied by a distal sensory neuropathy. Proximal lower limb neuropathy can have the natural history of an acute or chronic inflammatory polyradiculoneuropathy. The disorder tends to be painless and may represent inflammatory neuropathy concurrent with diabetes.

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780080450469006550

Diabetic Neuropathy

Asa the 1 last update 05 Jul 2020 J. Wilbourn, Bashar Katirji, in Office Practice of Neurology (Second Edition), 2003Asa J. Wilbourn, Bashar Katirji, in Office Practice of Neurology (Second Edition), 2003

DIABETIC POLYRADICULOPATHY

GSMP-DM constitutes approximately 75% of all diabetic neuropathies. The other 25% consist of a variety of entities; the one often responsible for the most disabling symptoms is diabetic polyradiculopathy.

Diabetic polyradiculopathy, similar to diabetic neuropathy, is an umbrella title; it includes several diabetic-induced clinical disorders that affect predominantly the proximal PNS limb and trunk fibers, often in an asymmetrical fashion. Included under this group designation are what some investigators formerly considered independent syndromes (e.g., diabetic amyotrophy and diabetic thoracic radiculopathy), certain neuropathic processes responsible at times for the lower extremity weaknesses associated with DM (e.g., diabetic foot drop) and some more diffuse disorders. Various subgroups of diabetic polyradiculopathy often appear in classifications of diabetic neuropathy under such terms as diabetic amyotrophy, asymmetrical or symmetrical proximal motor neuropathy, diabetic lumbosacral radiculoplexus neuropathy, and diabetic thoracoabdominal neuropathy.

Although diabetic amyotrophy, the most common subgroup of diabetic polyradiculopathy, was well described by Garland and Taverner in 1953, it was not until 1981 that Bastron and Thomas proposed a unifying concept linking all the subgroups. They suggested that several of the non-GSMP-DM types of diabetic neuropathy have a common, underlying basis: injury, often sequential, of various lumbar, thoracic, and occasionally cervical roots, caused by DM. This hypothesis has not been universally accepted, primarily because there is controversy regarding the exact site of nerve fiber damage (e.g., roots, plexus, peripheral nerves) in diabetic amyotrophy. For example, Dyck contends that this debilitating PNS disorder is caused by microvasculitis simultaneously involving the roots (primarily L2–L4), the plexus (primarily lumbar), and the peripheral nerves (femoral and obturator, at least initially) in a multifocal manner, hence the cumbersome name diabetic lumbosacral radiculoplexus neuropathy (DLSRPN). Nonetheless, diabetic polyradiculopathy has great appeal because it permits what appears to be a number of independent neuropathic syndromes linked only by underlying DM to be viewed in a coherent manner, with regard to underlying pathophysiology, clinical features, and prognosis.

Diabetic polyradiculopathy affects the motor and sensory root fibers, causing axon degeneration, presumably from ischemia. Characteristically, it severely involves one root or two or more contiguous roots. Although the process may remain focal, it often spreads to additional roots, either contiguous ones ipsilaterally or, particularly, the corresponding contralateral roots. This "territorial extension" occurs in nearly 70% of patients. The L2, L3, and L4 roots are the ones most likely to be affected, producing the clinical syndrome called diabetic amyotrophy or DLSRPN. The next most common subgroup is the syndrome of diabetic thoracic radiculopathy, also called diabetic thoracoabdominal neuropathy or diabetic truncal radiculoneuropathy, in which one or more thoracic roots, usually the lower ones (e.g., T6–T12), are affected. GSMP-DM often coexists with diabetic polyradiculopathy. The simultaneous occurrence of these two independent diabetic PNS disorders can create confusion about the nature of the underlying pathophysiology. It probably also has been responsible for pathologic changes caused by GSMP-DM being attributed erroneously to diabetic polyradiculopathy, particularly the subgroup that involves the L2–L4 roots (i.e., diabetic amyotrophy or DLSRPN). This is because much neuropathologic research focused on L2–L4 diabetic polyradiculopathy has been based on biopsies of distal cutaneous nerves (sural, less often superficial peroneal sensory), which not only derive from sensory roots other than L2–L4 (i.e., from the S1 and L5 roots, respectively) but also are very likely to show abnormalities secondary to their involvement by GSMP-DM.

Diabetic polyradiculopathy involving the L2–L4 roots has a variable mode of onset and evolution. Typically, it occurs in patients over age 60 who have mild DM, often NIDDM. Most commonly, it begins unilaterally in the anterior aspect of the proximal lower extremity, with severe pain, followed by significant weakness and atrophy of the anterior thigh muscles. The pain typically subsides after several weeks, although it may last much longer. However, weakness persists and often is accompanied by an inexplicable weight loss, sometimes 10% of body weight or more. This constellation of symptoms often raises suspicion of an underlying malignancy.

diabetes and dizziness vomiting zero to finals (🔥 natural dressings) | diabetes and dizziness vomiting veganhow to diabetes and dizziness vomiting for Neurologic examination often discloses atrophy of the anterior thigh muscles and a reduced or absent patellar tendon reflex. Muscle testing usually reveals weakness of hip flexors, knee extensors, and thigh adductors. The presence of abnormalities in the distribution of both the femoral and obturator nerves suggests on clinical grounds that the responsible lesion involves the lumbar plexus or L2–L4 roots. Many patients (approximately 70%) also have clinical evidence of GSMP-DM of varying severity.

Diabetic polyradiculopathy affecting the L2–L4 roots may also present in a bilaterally symmetrical, painless fashion, with clinical features identical to the 1 last update 05 Jul 2020 those described earlier. Intermediate syndromes of bilateral but asymmetrical painless weakness, as well as other variations, also may occur.Diabetic polyradiculopathy affecting the L2–L4 roots may also present in a bilaterally symmetrical, painless fashion, with clinical features identical to those described earlier. Intermediate syndromes of bilateral but asymmetrical painless weakness, as well as other variations, also may occur.

The differential diagnosis of diabetic polyradiculopathy subgroup includes a lumbar intraspinal lesion causing L2–L4 root compression, a lumbar plexopathy, and a femoral mononeuropathy.

EDX studies usually are very helpful in documenting motor axon loss in the L2–L4 myotomes, including the thigh adductors, thereby excluding femoral mononeuropathy. The high or midlumbar paraspinal muscles typically show prominent active denervation, rendering a lumbar plexopathy less likely. It is usually necessary to perform imaging studies on the lumbar spine, either MRI scanning or CT myelogram, to exclude a compressive lesion in the lumbar intraspinal canal. In certain patients, CSF examination to exclude inflammatory lesions or infiltration of the subarachnoid space with malignant cells is also advisable. In patients with the painless symmetrical syndrome, EDX studies are helpful in excluding myopathy, as are serum creatine kinase and aldolase assays.

Diabetic polyradiculopathy may also involve the lower lumbar and sacral (L5–S2) roots, although this usually occurs in conjunction with higher lumbar (L2–L4) root involvement. One of the prominent clinical features of diabetic L5 radiculopathy is foot drop. Bilateral foot drop from bilateral diabetic L5 radiculopathy often is mistakenly attributed to severe GSMP-DM. Diabetic rather than compressive L5 radiculopathy should be suspected whenever a patient with DM develops substantial L5 myotomal weakness and pain that is not relieved by bed rest and is more severe at night.

Diabetic thoracic radiculopathy results when diabetic polyradiculopathy affects thoracic roots, either in isolation or by territorial extension from ipsilateral L2–L4 involvement. Usually, one or more of the T6–T12 roots is involved unilaterally or, less often, bilaterally. The characteristic symptom is severe, persistent pain in the middle or lower thoracic region, radiating to the upper or middle abdomen. A dermatomal sensory loss often is demonstrable. The thoracic motor, as well as sensory fibers are sometimes affected, but generally this is subclinical and discovered only upon needle electrode examination of the thoracic paraspinal or abdominal muscles. The symptoms of diabetic thoracic radiculopathy often are attributed to an intra-abdominal disorder. Many asymptomatic gall stones have been removed in an attempt to treat the pain caused by diabetic thoracic radiculopathy. Even when it is appreciated that the lesion is at the root level, other causes of thoracic radiculopathies must be excluded. Neuroimaging studies, and sometimes other tests as well, are indicated.

Rarely, diabetic polyradiculopathy may involve cervical roots. Typically, the midcervical roots, particularly C5–C7, are bilaterally affected. This usually occurs in combination with L2–L4 root involvement.

All the subgroups of diabetic polyradiculopathy have a favorable ultimate prognosis. Approximately three quarters of patients show satisfactory functional recovery after 1 year. Therapy for 1 last update 05 Jul 2020 consists primarily of pain management and an aggressive physical therapy program for gait training to prevent falls and injuries and eventually to assist during recovery. There are anecdotal reports of the benefits of intravenous immunoglobulin in the subacute forms of diabetic polyradiculopathy. Although this treatment is based on the presence of an inflammatory process in some of these neuropathies, there have been no controlled trials that support the use of IVIg in any diabetic neuropathies.All the subgroups of diabetic polyradiculopathy have a favorable ultimate prognosis. Approximately three quarters of patients show satisfactory functional recovery after 1 year. Therapy consists primarily of pain management and an aggressive physical therapy program for gait training to prevent falls and injuries and eventually to assist during recovery. There are anecdotal reports of the benefits of intravenous immunoglobulin in the subacute forms of diabetic polyradiculopathy. Although this treatment is based on the presence of an inflammatory process in some of these neuropathies, there have been no controlled trials that support the use of IVIg in any diabetic neuropathies.

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B0443065578500952

Controversies In Diabetic Neuropathy

N.J. Gardiner, O.J. Freeman, in International Review of Neurobiology, 2016

Abstract

diabetes and dizziness vomiting weight gain (🔥 exhaustion) | diabetes and dizziness vomiting insulin pumphow to diabetes and dizziness vomiting for Diabetic neuropathy is a common secondary complication of diabetes that impacts on patient's health and well-being. Distal axon degeneration is a key feature of diabetic neuropathy, but the pathological changes which underlie axonal die-back are incompletely understood; despite decades of research a treatment has not yet been identified. Basic research must focus on understanding the complex mechanisms underlying changes that occur in the nervous system during diabetes. To this end, tissue culture techniques are invaluable as they enable researchers to examine the intricate mechanistic responses of cells to high glucose or other factors in order to better understand the pathogenesis of nerve dysfunction. This chapter describes the use of in vitro models to study a wide range of specific cellular effects pertaining to diabetic neuropathy including apoptosis, neurite outgrowth, neurodegeneration, activity, and bioenergetics. We consider problems associated with in vitro modeling and future refinement such as use of induced pluripotent stem cells and microfluidic technology.

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/S0074774216300046

Diabetic Truncal Neuropathy

diabetes and dizziness vomiting urine test (👍 diagnostic procedures) | diabetes and dizziness vomiting pillshow to diabetes and dizziness vomiting for Steven D. Waldman MD, JD, in diabetes and dizziness vomiting kidney failure (⭐️ vitamin d) | diabetes and dizziness vomiting vbidhow to diabetes and dizziness vomiting for Atlas of Common Pain Syndromes (Fourth Edition), 2019

The Clinical Syndrome

Diabetic neuropathy is a term used by clinicians to describe a heterogeneous group of diseases that affect the autonomic and peripheral nervous systems of patients suffering from diabetes mellitus. Diabetic neuropathy is now thought to be the most common form of peripheral neuropathy that afflicts humankind, with an estimated 220 million people worldwide suffering from this malady.

One of the most commonly encountered forms of diabetic neuropathy is diabetic truncal neuropathy. In this condition, pain and motor dysfunction are often incorrectly attributed to intrathoracic or intraabdominal disorders and lead to extensive workups for appendicitis, cholecystitis, renal calculi, and so on. The onset of symptoms frequently coincides with periods of extreme hypoglycemia or hyperglycemia or with weight loss or gain. Patients who present with diabetic truncal neuropathy complain of severe dysesthetic pain with patchy sensory deficits in the distribution of the lower thoracic or upper thoracic dermatomes. The pain is often worse at night and causes significant sleep disturbance. The symptoms of diabetic truncal neuropathy often resolve spontaneously over 6 to 12 months. However, because of the severity of symptoms, aggressive treatment with pharmacotherapy and neural blockade is indicated.

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780323547314000645

Diabetic Neuropathic Pain Syndromes

Fatima Z. Syed MD, MSc, ... Nazish Ahmad MD, in Challenging Neuropathic Pain Syndromes, 2018

diabetes and dizziness vomiting insulin resistance (🔴 common complications) | diabetes and dizziness vomiting immune systemhow to diabetes and dizziness vomiting for Introduction

diabetes and dizziness vomiting with neuropathy (👍 vegan) | diabetes and dizziness vomiting too much insulinhow to diabetes and dizziness vomiting for Diabetic the 1 last update 05 Jul 2020 neuropathyDiabetic neuropathy is a common complication of diabetes. The goal of this chapter is to present the symptoms, understand the demographics, provide differential diagnosis and diagnostic criteria, explore treatment options, and understand disease prognosis. Diabetic amyotrophy is also discussed as a less frequent but potentially debilitating complication of diabetes. It refers to the weakness and pain, particularly along the lumbosacral plexus, which can be associated with diabetes. It can be idiopathic or related to diabetes. Diabetic amyotrophy is also known as Bruns-Garland syndrome, diabetic myelopathy, proximal diabetic neuropathy, diabetic lumbosacral plexopathy, or diabetic lumbosacral radiculoplexus neuropathy. It differs from peripheral neuropathy, which is commonly seen in diabetic patients, because it is specific to the proximal muscles. It can be associated with weakness and excruciating pain. Other causes can be idiopathic.1

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780323485661000103

Diabetes and the Nervous System

diabetes and dizziness vomiting glucose levels (👍 song) | diabetes and dizziness vomiting fruitshow to diabetes and dizziness vomiting for Anders A.F. Sima, Weixian for 1 last update 05 Jul 2020 Zhang, in Handbook of Clinical Neurology, 2014Anders A.F. Sima, Weixian Zhang, in Handbook of Clinical Neurology, 2014

Abstract

diabetes and dizziness vomiting food plan (🔴 symptoms in children) | diabetes and dizziness vomiting naturally with diethow to diabetes and dizziness vomiting for Diabetic neuropathy is the most common complication of diabetes. It shows a progressive development with sensory loss, pain and autonomic dysfunction as common symptoms. Pathologically it is characterized by a series of interrelated metabolic abnormalities with insulin deficiency and hyperglycemia as the initiating culprits. The neuropathy accompanying type 2DM (insulin resistance) and type 1DM (insulin deficiency) appears to differ as to their structural changes; the former showing a milder axonal involvement and segmental myelin breakdown, whereas the latter shows a more severe axonal atrophy and axonal loss. Based mainly on animal data we will describe the sequential neuropathologic changes and differences in the two types of diabetes. These differences are related to differences in a myriad of underlying sequential metabolic abnormalities, which will be dealt with in detail. How metabolic defects affect nerve function will be elaborated upon. The disorder does not only involve somatic peripheral nerves but also autonomic and central nerve tracts.

Today no successful therapy exists for diabetic neuropathy. During the last 30 years several experimental drugs targeting the polyol-pathway and oxidative stress have been tested, but with limited or no success. Instead therapies targeting the initiating and overriding pathogenetic abnormalities, such as insulin-deficiency and hyperglycemia need to be employed. One such agent is the insulinomimetic C-peptide which has demonstrated significant therapeutic and preventive effects in type 1 diabetic patients. Not surprisingly this has been particularly successful following early intervention. However diabetic neuropathy still remains a major medical problem affecting millions of patients.

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B978044453480400031X

diabetes and dizziness vomiting and insulin (🔴 blood sugar) | diabetes and dizziness vomiting woundshow to diabetes and dizziness vomiting for Analgesic and Neuroprotective Effects for 1 last update 05 Jul 2020 of B VitaminsAnalgesic and Neuroprotective Effects of B Vitamins

X.-J. Song, in Nutritional Modulators of Pain in the Aging Population, 2017

Analgesic Effect of B Vitamins on Painful Diabetic Neuropathy

Diabetic neuropathy is a prevalent and disabling disorder. Painful diabetic neuropathy, a common sequel of diabetic peripheral neuropathy, is severe and intractable, and affects 10–20% of the millions of patients with diabetes (Alge-Priglinger et al., 2011; DiBonaventura, Cappelleri, & Joshi, 2011; de Salas-Cansado et al., 2012; Sandercock, Cramer, Biton, & Cowles, 2012). Despite decades of studies and numerous processes that have been implicated, the specific cellular and molecular mechanisms underlying the pathogenesis of diabetic neuropathic pain remain elusive. The possible for 1 last update 05 Jul 2020 etiologies that underlie the pathogenesis of diabetic neuropathic pain may include the following: (1) hyperglycemia-induced damage to nerve cells, including the reduced conduction failure of the main axon of polymodal nociceptive C-fibers (Sun et al., 2012) and a decrease in neurovascular flow (Edwards, Vincent, Cheng, & Feldman, 2008); (2) production of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β, and interleukin-6; (3) perturbations in growth factors, such as insulin-like growth factor, nerve growth factor, and neurotrophin 3; (4) immune dysfunction; (5) diabetes-related oxidant stresses, such as mitochondrial oxidant stress, and other cellular stresses including endoplasmic reticulum stress; and (6) multifocal loss of myelinated and unmyelinated fibers (Obrosova et al., 2004; Brownlee, 2005; Obrosova, 2009). Because of the complexities of pathogenesis, painful diabetic neuropathy is still a common and challenging complication of diabetes mellitus, and the clinical approaches for its treatment are very limited. It is often resistant to treatment with the available modalities. Currently, the most effective treatment available to patients with diabetic neuropathy is likely pain management, in addition to critical glucose control. B vitamins, however, have been demonstrated to be effective in treating painful diabetic neuropathy.Diabetic neuropathy is a prevalent and disabling disorder. Painful diabetic neuropathy, a common sequel of diabetic peripheral neuropathy, is severe and intractable, and affects 10–20% of the millions of patients with diabetes (Alge-Priglinger et al., 2011; DiBonaventura, Cappelleri, & Joshi, 2011; de Salas-Cansado et al., 2012; Sandercock, Cramer, Biton, & Cowles, 2012). Despite decades of studies and numerous processes that have been implicated, the specific cellular and molecular mechanisms underlying the pathogenesis of diabetic neuropathic pain remain elusive. The possible etiologies that underlie the pathogenesis of diabetic neuropathic pain may include the following: (1) hyperglycemia-induced damage to nerve cells, including the reduced conduction failure of the main axon of polymodal nociceptive C-fibers (Sun et al., 2012) and a decrease in neurovascular flow (Edwards, Vincent, Cheng, & Feldman, 2008); (2) production of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β, and interleukin-6; (3) perturbations in growth factors, such as insulin-like growth factor, nerve growth factor, and neurotrophin 3; (4) immune dysfunction; (5) diabetes-related oxidant stresses, such as mitochondrial oxidant stress, and other cellular stresses including endoplasmic reticulum stress; and (6) multifocal loss of myelinated and unmyelinated fibers (Obrosova et al., 2004; Brownlee, 2005; Obrosova, 2009). Because of the complexities of pathogenesis, painful diabetic neuropathy is still a common and challenging complication of diabetes mellitus, and the clinical approaches for its treatment are very limited. It is often resistant to treatment with the available modalities. Currently, the most effective treatment available to patients with diabetic neuropathy is likely pain management, in addition to critical glucose control. B vitamins, however, have been demonstrated to be effective in treating painful diabetic neuropathy.

Several clinical trials and observations have shown the efficacy of B vitamins (B1 and B12) and its combination with analgesics, such as gabapentin in treating painful diabetic neuropathy. Benfotiamine, a lipid-soluble vitamin B1 prodrug with high bioavailability, may extend the treatment option for patients with diabetic polyneuropathy based on its influence on impaired glucose metabolism ( the 1 last update 05 Jul 2020 Stracke, Gaus, Achenbach, Federlin, & Bretzel, 2008Stracke, Gaus, Achenbach, Federlin, & Bretzel, 2008). It was observed that the most pronounced effect of benfotiamine was a reported decrease in pain, and no side effects were observed in patients with diabetic pain (Haupt, Ledermann, & Kopcke, 2005). A recent study shows that benfotiamine acts on μ-opioid receptor mediated antinociception in experimental diabetes (Nacitarhan, Minareci, & Sadan, 2014). This study determined the effects of benfotiamine on the antinociception produced by μ-opioid receptor agonist fentanyl in diabetic mice. It was found that μ-opioid agonist fentanyl in the benfotiamine-treated diabetic group caused more potent antinociceptive effects than in the diabetic group without benfotiamine treatment. A brief benfotiamine dietary supplement did not show an antinociceptive effect, but during the development of streptozotocin-induced diabetes, benfotiamine replacement increased the antinociceptive effect of fentanyl in mice based on the tail-flick test. This study suggests that benfotiamine replacement therapy may be useful in ameliorating the analgesic effect of μ-opioid agonists on neuropathic pain in diabetics.

Vitamin B12 has also been shown to be effective in treating diabetic neuropathy (Kuwabara et al., 1999). A very recent study shows that gabapentin plus the B1/B12 combination is as effective as gabapentin by itself. Moreover, the combination therapy reduced pain intensity with a gabapentin dose at 50% of the minimum dose required when gabapentin was used alone (800 vs. 1600 mg/day). Decreased occurrence of vertigo and dizziness was also observed with the combination treatment (Alvarado, 2016). These observations support an extended use of vitamins B1 and B12 for painful diabetic neuropathy in the clinic. In addition, deficiency of vitamins B1 and B6 was thought to contribute to the diabetic peripheral neuropathy in Dar es Salaam (Abbas & Swai, 1997).

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780128051863000229

Neuropathic Pain Syndromes

diabetes and dizziness vomiting fruits to eat (⭐️ health promotion) | diabetes and dizziness vomiting vomitinghow to diabetes and dizziness vomiting for Robert W. Hurley, ... Christopher L. Wu, in Practical Management of Pain (Fifth Edition), 2014

Pathophysiology

Diabetic for 1 last update 05 Jul 2020 neuropathyDiabetic neuropathy is theorized to occur by three mechanisms: the polyol pathway, microvascular damage, and glycosylation end-product theories. These three models most likely act simultaneously, but there may also be some overlap between them.diabetes and dizziness vomiting genetics nature (☑ food choices) | diabetes and dizziness vomiting questions and answershow to diabetes and dizziness vomiting for 110 Neurotrophic factors and neuronal membrane ion channel dysfunction may likewise play a role in DPN.

The polyol pathway theory proposes that increased blood glucose leads to elevated glucose concentrations within nerve endings. Through a series of reactions, the glucose is converted into sorbitol via the polyol pathway involving aldose reductase and elevation of the fructose level. The high sorbitol and fructose levels subsequently lead to a decrease in sodium-potassium adenosine triphosphatase (Na+,K+-ATPase) activity. Activation of the aldose reductase–depleting cofactor NADPH (reduced nicotinamide adenine dinucleotide phosphate) leads to decreased nitric oxide and glutathione, which inhibits the buffer against oxidative injury and vasodilation and results in chronic ischemia.110 In the microvascular damage theory, thickening of the capillary basement membrane along with endothelial cell hyperplasia leads to neuronal ischemia and infarction.110 The glycosylation end-product theory proposes that interference in axonal transport results in decreased nerve conduction velocity because of chronic hyperglycemia, which results in deposition of advanced glycosylation end products around peripheral nerves. These end products may also produce NADPH (which activates NADPH oxidase) and thereby contribute to the formation of hydrogen peroxide and increased oxidative stress. Nerve growth factors are important in the repair of nerve structure and function after an injury. Low levels of these neurotrophic factors correlate with diabetic neuropathy in animal models. Other factors associated with diabetic neuropathy are abnormal calcium channel activity contributing to cellular injury and death and sodium channel dysfunction playing a role in the genesis of painful neuropathy.111

Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780323083409000244