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Diabetic neuropathy (DN) is a descriptive term meaning a demonstrable disorder, either clinically evident or sub-clinical, that occurs in the setting of diabetes mellitus without other causes for peripheral neuropathy.
In this review, we have summarized the epidemiology, clinical features, pathogenesis, classification and diagnosis of diabetic neuropathy. The true prevalence is not known and depends on the criteria and methods used to define neuropathy. The acute onset symmetric neuropathies include diabetic neuropathic cachexia which is an uncommon painful sensory neuropathy occurring in type 1 diabetes in the setting of poor glucose control and weight loss. The asymmetric neuropathies can also be divided into those with acute onset and those with gradual onset. An easy and practical way to approach this conundrum of classifications is to classify diabetic neuropathy as typical and atypical. Diabetic neuropathy has a wide spectrum of clinical manifestations, the most common being distal symmetrical sensorimotor loss in the classical 'stocking-glove' distribution (DSPN). Diabetic sensorimotor polyneuropathy (DSPN) is a mixed neuropathy with small and large fibre sensory, motor and autonomic involvement in various combinations. Diabetic small fibre neuropathy (DSFN): Small fibre predominant neuropathy in diabetes is being increasingly recognised and is an early manifestation of peripheral nerve involvement. Diabetic autonomic neuropathy affects various organs of the body resulting in cardiovascular, gastrointestinal, urinary, sweating, pupils, and metabolic disturbances.
Diabetic lumbar radiculoplexopathy: Also known as Diabetic amyotrophy or proximal diabetic neuropathy, it presents with abrupt onset, often unilateral severe pain in the anterior thigh, buttock or lower back followed by weakness and wasting in the thigh. Diabetic truncal radiculoneuropathy: It presents with abrupt onset severe pain (burning, stabbing or belt like) with contact hyperesthesia in the thoracic spine, flank, rib cage or upper abdomen. Cranial neuropathy: The oculomotor nerves are most often affected (third, sixth, rarely fourth).
Patients with diabetes can also present with mononeuritis multiplex without an underlying rheumatological cause and are at increased risk of entrapment mononeuropathy. Chronic hyperglycaemia is an important contributing factor leading to diabetic complications. It is generally agreed that diabetic neuropathy should not be diagnosed on the basis of one symptom, sign, or test alone. Traditionally, nerve conduction studies (NCSs) have been the most frequently used diagnostic tool for DSPN. Pathologically, DSFN is characterized by degeneration of distal terminations of small-diameter sensory fibres, observed as low IENF density (IENFD) on histological analysis of tissue from patients with the condition.
Over the past decade, the non-invasive technique of in vivo confocal microscopy of the cornea has been developed, mainly for use in patients with diabetic neuropathy. Microneurography has made recording of single Ad-fibre and C fibre activity possible, and provides a direct method for measuring sympathetic activity. To conclude, diabetes is associated with a variety of chronic and acute neuropathies, the commonest form being distal symmetric polyneuropathy.
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Of patients attending a diabetes clinic, 25% volunteered symptoms, but 50% were found to have neuropathy after a simple clinical test such as eliciting the ankle reflex or vibration perception test.
Insulin neuritis, which is again a painful neuropathy is seen with initiation of insulin treatment.
Diabetic truncal radiculoneuropathy, radiculoplexopathy or diabetic amyotrophy, cranial neuropathies (third or sixth nerves) and mononeuritis multiplex constitute the acute onset group. It presents with pain and dyesthesias in the feet and is difficult to diagnose, as the clinical examination and nerve conduction studies may be normal.
Orthostatic hypotension, resting tachycardia, and heart rate unresponsiveness to respiration are a hallmark of diabetic autonomic neuropathy. Diabetic third nerve palsy presents with abrupt onset retro-orbital pain, followed by double vision, unilateral ptosis, restriction of medial and upgaze and sparing of the pupil.
As with most other axonal neuropathies, the central feature of DSPN is reduced distal lower extremity sensory nerve action potential amplitudes.14 But over the years it has been realised that diagnosis of DSFN (Ad-fibres and C fibres) is challenging as the clinical picture can be difficult to interpret and results from nerve conduction studies are often normal.
For the evaluation of small nerve fibre dysfunction, only temperature thresholds are measured. In the nerve axon reflex, C nociceptive fibres are stimulated by acetylcholine iontophoresis producing vasodilatation which can be quantitatively measured and serves as a measure of small fibre function.22 The laser Doppler imaging flare test evaluates 44°C heat-induced vasodilation and is reduced in subjects with IGT and type 2 diabetic patients with and without neuropathy. Performing an annual screening through a good neurological history and clinical examination and using a sensitive screening tool can facilitate an early diagnosis. Pop-Busui R, Evans GW, Gerstein HC, Fonseca V, Fleg JL, Hoogwerf BJ, et al; Action to Control Cardiovascular Risk in Diabetes Study Group.
It is mostly prevalent in young children and teens, who must take multiple insulin injections daily to replace the insulin the body is not making.when glucose levels rise (hyperglycemia) the pancreas responds by releasing the hormone insulin to convert the excess glucose into energy for the cells to use as fuel. The symptoms start as numbness, tingling, burning or pricking sensation in the feet and spread proximally in a length dependent fashion (stocking glove pattern).
Aneurysm must be excluded by neuroimaging in atypical cases (pupillary involvement or absence of pain). The other common parameter measured by QST in clinical practice, reflecting large fiber involvement is vibration sensation. More sensitive and quantitative measures of detecting early peripheral nerve injury including skin biopsy for intra-epidermal and dermal nerve fiber density and confocal corneal microscopy, hold promise to identify neuropathy patients early in their disease course.
The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study. Prevalence of microvascular complications in newly diagnosed patients with type 2 diabetes. Frequency of cardiac autonomic neuropathy in patients with type 2 diabetes mellitus reporting at a teaching hospital of Sindh. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments.


Corneal confocal microscopy: a non-invasive surrogate of nerve fibre damage and repair in diabetic patients. On the relationship between nociceptive evoked potentials and intraepidermal nerve fiber density in painful sensory polyneuropathies.
The LDI flare: a novel test of C-fiber function demonstrates early neuropathy in type 2 diabetes. Clinical examination versus neurophysiological examination in the diagnosis of diabetic polyneuropathy. A practical two-step quantitative clinical and electrophysiological assessment for the diagnosis and staging of diabetic neuropathy. Effects of cardiac autonomic dysfunction on mortality risk in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. In Type 1 diabetes there is no insulin production, thus depriving the cells of the fuel they need for proper functioning. Pathological assessment reveals evidence of ischaemic injury and microvasculitis and prognosis is favourable. Report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society. If blood sugar levels are not brought under control, complications can occur and cause damage to the major organs of the body. This is due to damage of the vagus nerve, which is responsible for moving food through the digestive tract.Persons who have been diagnosed with diabetes require specialized care to to stay in the most optimal health.
It is important to monitor daily blood glucose levels to keep them within normal limits to prevent the many complications that can occur. There is extra work involved as diabetics must do for their bodies what their bodies can't do. When the body ceases to make insulin, or the insulin being produced is not being used effectively, one must take over that job by closely monitoring their glucose levels and administering to the body the insulin that is lacking. Be mindful of your salt intake as too much sodium in the diet can raise the blood pressure. Consistently high blood pressure causes damage to the major organs of the body leading to added complications of diabetes.Make regular visits with your health care provider to catch any potential problems in their early stages when they are most easily treated. This is why the condition is sometimes called a€?juvenile diabetes.a€? The most common age of diagnosis is between 11 and 14 years old. People with type 1 diabetes regularly measure their blood sugar to figure out how much insulin they need.
Diet and Exercise People with type 1 diabetes should eat regular meals and snacks to keep blood sugar stable.



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Comments

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    22.02.2016

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    22.02.2016

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    22.02.2016