ncarbone's blog

This article is more of review and takes examples of previous studies and compiles them all into one document. The methods used to detect neuropathy are not explicitly states therefore it is difficult to determine how they decided what was minor and severe neuropathy. I think that using the Toronto clinical scoring system (TCSS) would be the best choice in determining minor or full onset neuropathy. With this system a score of 6-8 points would be considered mild neuropathy while a score of 12-19 would be considered severe neuropathy. This system also uses three different parts in order to come up with a neuropathy score, The three parts include a symptom score, a reflex score, and a sensory test score. Another scoring system that I think would be adequate would be the clinical neurological examination system (CNE). This system also classifies neuropathy in four different stages, none, mild, moderate, and severe.

Subjects will be broken up into three groups consisting of an aerobic exercise group, a resistance exercise group, and a control group. All subjects’ vitals will be taken at baseline and each week for the length of the study. If possible, A1C records will be taken at baseline and at the completion of the intervention. Both exercise groups will perform their respective similar caloric activities at 70% VO2 for 3 days a week for 30-minute sessions each for a total of 12-weeks. Blood glucose and nerve measurements (TBD) will also be taken at baseline and after each week. The aerobic group will participate in a 30-minute session of cycling/running on the treadmill (caloric expenditure of about 9.3k-cal/min). The resistance group meanwhile will perform a resistance band exercise for 30 mins involving the lower extremities. In order to ensure that all groups receive equal amount of face-to-face time the control group will also meet (or be sent via email) 3 times a week and be given an informational reading or videos related to exercise and diabetes for 30-minutes. 

This study focuses on the impact of exercise on nerve function in patients previously diagnosed with diabetic peripheral neuropathy. Both aerobic and resistance exercise methods were performed in a 10 week program consisting of 17 subjects ages 40-70 with DPN. The subjects blood glucose, blood pressure, heart rate, and rate of perceived exertion were all measured during each session. The sessions ran either 3 or 4 days a week and the workload was gradually increased each week. A1C and BMI were recorded before and after the intervention. The study found a significant improvement in pain but found no change in BMI or waist circumference. Pain was assessed using the MNSI system and the symptom score of “worst pain” decreased from 5.2 to 4.0. Pain was measured using an unmarked 100-mm visual analog scale to indicate the level of “current pain”, “usual pain over the past month”, and “worst pain over the past month.” A1C levels dropped from 7.8% to 7.1% following the intervention. Also following the study, an increase in the number of branches per fiber was found. Neuropathy scoring was assessed using the Michigan neuropathy screening instrument.

Nick Carbone & Liam Potter

http://www.sciencemag.org/

First indication of this source not being reliable is it comes up as a "Not Secure" website on the top of the bowser screen. However it is sponsored by AAAS (American Associastion for the Advancement of Science) which is a legitimate non-profit organization. They also have a list of sceince awards that they have won in the past. They also do have research articles that are cited and refrenced and it is inlcuded on the UMASS Amherst Library webpage. Overall I would say that it is a credible source of information.

The main focus of this article is to show an improvement in preventing the risk factors of diabetic foot after weeks of exercise therapy. The article focuses on multiple diabetic complications and the role of exercise therapy in terms of improving conditions.  Exercise therapy is known to improve blood glucose and insulin sensitivity as well as weight loss. These are theorized to be factors in reducing the chances of developing neuropathy. The subclinical onset of neuropathy is usually more peripheral rather than central. Sensory nerves are detected before motor and autonomic nerves. Detecting minor nerve damage before full onset neuropathy can be difficult due to the fact that nerve conduction velocities do not significantly change early on all the time.

Types of Diabetic Neuropathy

Diabetes can lead to many complications over time. One of the most common and relevant complications is neuropathy. Diabetic neuropathy, or nerve damage, is most commonly caused by elevated blood glucose levels (hyperglycemia) over long periods of time. There are four major types of diabetic neuropathy: peripheral, proximal, autonomic, and focal neuropathy. Peripheral neuropathy is the most common type of neuropathy in people with diabetes and can be either acute or chronic. Peripheral neuropathy affects the nerves that lead to the body’s extremities such as the feet, hands, arms, and legs. Proximal neuropathy, also known as amyotrophy, is a neuropathy found more often in type 2 diabetics. It can be caused by endoneural micro vessel disease and causes muscle weakness in the upper legs, buttocks, and hips. Autonomic neuropathy often co-exists with other complications such as peripheral neuropathy, but it can be isolated as well. Autonomic neuropathy is nerve damage to the central nervous system which can lead to complications such as: tachycardia (rapid heartbeat), orthostatic hypotension (low blood pressure), erectile dysfunction, sudomotor dysfunction, and impaired muscle control. Autonomic neuropathy can also affect many organ systems and lead to a serious complication known as cardiovascular autonomic neuropathy (CAN). CAN results from damage to nerves that innervate the heart and blood vessels. Lastly, focal neuropathy is specific to one single nerve and causes pain in that lone location. It is found commonly in older individuals and is also known to improve itself over time.

Cardiovascular disease is caused by a combination of all three factors, but lipid control is thought to be the most influential. Often, cardiovascular problems can arise from the development of atherosclerosis which is an increased risk in diabetics. Poor glucose control or resistance to insulin causes a lack of nitric oxide production which is important in maintaining vascular flow. The lack of sufficient nitric oxide leads to an increase in plaque formation within the blood vessels. Lastly, neuropathy is caused by a metabolic cascade resulting from a lack of glycemic control, a long duration of diabetes, and potentially vascular abnormalities as well. Hyperglycemia causes the polyol pathway to produce more sorbitol from glucose, but at the same time this process consumes NADPH which results in less cofactor available for glutathione reductase. This inhibits the cells’ ability to respond to oxidative stress. Oxidative stress is defined as an imbalance between antioxidants and free radicals in one’s body. Too many free radicals cause chemical chain reactions due to their high reactivity. Conversely, anti-oxidants have been proposed to prevent generation of free radicals (or reduce the impact of free radicals). Oxidative stress can alter nerve blood supply, nerve structure, and endoneural metabolism. High glucose levels also are found to be directly correlated with the production of advanced glycation end-products (AGE). AGE’s are produced by a chemical transformation of sugars binding amino acids or fats. High blood glucose levels and increased fat/lipid levels can lead to the production of AGE’s. When AGE interacts with receptors (RAGE) it can lead to oxidative stress. In rats RAGE is expressed in endothelial and Schwann cells. Incubation of these neuronal and Schwann cells with AGE’s leads to cell death. Vascular complications can also lead to neuropathy. A lack of glycemic control can cause microvascular blood vessels to narrow or harden due to plaque build-up known as atherosclerosis resulting in a restricted blood flow to the nerves. This lack of blood flow causes damage to the peripheral nervous system thus leading to complications such as neuropathy and foot ulcers.

Mechanisms of Diabetes

Diabetes can lead to major health complications such as nerve damage, kidney damage, and cardiovascular disease. The three mechanisms which influence these diabetic complications are: blood pressure, glucose control, and lipid control.

Nephropathy, a disease/damage to the kidneys, is characterized by the development of proteinuria and a decline in glomerular filtration rate. High glucose levels and high blood pressure are the main causes of nephropathy. The high levels of glucose in the blood cause an increase in glucose reabsorption which then leads to both hyperfiltration and increased intraglomerular. This extra pressure on nephrons over time weakens their ability to filter, ultimately leading to kidney damage and leakage of proteins into the urine.

Retinopathy, described as lesions within the retina, is also caused by high blood pressure and poor glycemic control. Hyperglycemia causes changes to the blood vessels in the retina by damaging or killing pericyte cells (The cells that line blood vessels and help regulate blood flow) which then alters the blood-retinal barrier and vascular permeability. Damage to the retinal blood vessels eventually results in ischemia. In response to ischemia, neovascularization takes place which is the formation of new blood vessels. The new fragile blood vessels that grow in the retina are prone to leaking blood into the back of the eye. The leaking of the fluid into the macula (Area responsible for clear central vision) causes the macula to swell, thus leading to vision loss.

The first thing that I notice about this organism is the segmented body it has. It is broken down into about 15 or so segments and each segment has one brown spot on each side of every individual segment. On one end of its body there is a dark brown head that does not appear to have eyes. The way it moves its head around makes it appear as if it is sensing its surroundings before moving. Perhaps it is blind or has poor vision, so it relies on sensing. When it does move it uses its segments to thrust forward and grabs on with it front legs. It has 6 front legs/feet and 8 mid feet that appear to be used for grip. The tail also has 2 grippers on the end. Despite these gripper feet it cannot seem to gain traction on the plastic container. It looks like a larvae of some sort, so perhaps it is only in it's inital life stage and could eventually morph into it's next life stage similar to a catipillar and a butterfly.