Spectrum Of Diabetic Neuropathy Research Articles

Spectrum of Diabetic Neuropathy: New Insights in Diagnosis and Treatment.

Diabetic neuropathy is a highly prevalent complication of diabetes. It consists of a broad range of neuropathic conditions, such as distal symmetric polyneuropathy and various forms of autonomic neuropathies involving the cardiovascular, gastrointestinal, and urogenital systems. Prevention or diagnosis in early stages of disease is crucial to prevent symptomatic onset and progression, particularly in the absence of current disease-modifying therapies. In this review, we describe the four main types of diabetic neuropathy. We review current understanding with respect to diagnosis and treatment while highlighting knowledge gaps and future directions.

Treatment induced neuritis in diabetes (TIND) – Terra incognita in the spectrum of diabetic neuropathies

Treatment-induced neuropathy in diabetes (TIND), better known as insulin neuritis, is an uncommon, iatrogenic, small fibre neuropathy occurring with an abrupt betterment in glycaemic control in patients of chronic hyperglycaemia. TIND, as such, is a less reported entity often missed by clinicians on initial presentation, but is an important consideration in patients with rapid correction of their hyperglycaemic status. TIND is characterised by an acute onset length dependent or generalised neuropathic pain often accompanied by autonomic symptoms and signs. This mostly occur after 2-8 weeks of initiating glycaemic control with insulin and is associated with a decline in glycosylated haemoglobin (HbA1c) by ≥2% points over 3 months. In fact, these patients on presentation, have reasonably satisfactory glycosylated haemoglobin profiles, as this condition is seen with acute control of glycaemic status. We herein discuss details of this entity as a review of literature with an overview of its pathophysiology, clinical features, and management.

Spectrum of diabetic neuropathies.

The diabetic state results in neuropathy. The main causative mechanism is hyperglycemia, although microvascular involvement, hypertriglyceridemia, as well as genetic and immune mechanisms may be contributory. There is a growing spectrum of types of diabetic neuropathies that differ based on the type of fibers involved (e.g. myelinated, unmyelinated, autonomic, somatic), distribution of nerves involved, and mechanisms of neuropathy. The most common type is distal sensory neuropathy (DSN), which affects the distal ends of large myelinated fibers, more often sensory than motor, and is often asymptomatic. The next-most common is distal small fiber neuropathy (DSFN), which largely affects the unmyelinated fibers and carries the phenotype of burning feet syndrome. Diabetic autonomic neuropathy (DAN) occurs when widespread involvement of autonomic unmyelinated fibers occurs, and patients can be incapacitated with orthostatic hypotension as well as neurogenic bladder and bowel involvement. Radiculoplexus diabetic neuropathy causes proximal weakness and pain, usually in the lower extremity, and has a combination of immune, inflammatory, and vascular mechanisms. The nerve roots and plexus are involved. These patients present with proximal weakness of a subacute onset, often with severe pain and some autonomic failure. Finally, rapid and sustained reduction of blood glucose can result in treatment-induced diabetic neuropathy (TIND), which largely affects the sensory and autonomic fibers. This occurs if HbA1c is rapidly reduced within 3 months, and the likelihood is proportional to the original A1c and the size of the reduction.

Rare Case of Simultaneous Diabetic Oculomotor and Trochlear Nerve Neuropathy: Case Report

INTRODUCTION: Diabetic cranial neuropathy is a spectrum of diabetic neuropathy. Isolated cranial nerve involvement is common as the manifestation of diabetic cranial neuropathy. The cranial nerve that frequently involved are abducens and oculomotor nerve, trochlear nerve is the least involved. Simultaneous cranial nerve involvement is not common and need further investigation for other possible etiology. CASE REPORT: We reported a 52-year-old, diabetic and hypertensive male, presented with acute onset, first ever, severe temporal headache with left eye ptosis, diplopia and opthalmoplegia. Neurologic examination revealed left oculomotor and trochlear nerve palsy with sparring of pupillary function. Examination of blood D-dimer and C-reactive were normal. Head contrast MRI and MR Angiography revealed no lesion. He was diagnosed with diabetic cranial neuropathy after exclusion of other possible etiology. CONCLUSION: Simultaneous involvement of two or more cranial nerve neuropathy in diabetic patient is not common and need further investigation. Exclusion of the other possible diagnosis is important to diagnose diabetic cranial neuropathy.

Asymptomatic Neuropathy in Recently Diagnosed Diabetic Patients: Electrophysiological Evaluation

Aim & background: As significant electrophysiological changes are found in asymptomatic neuropathy in diabetes mellitus and electrophysiological studies of nerve conduction velocity are our most sensitive tools to quantify early abnormalities, therefore, we tried to find out status of asymptomatic peripheral nerve dysfunction in recently diagnosed diabetic patients in Bangladesh perspective. Method :This study was carried out at BSMMU and BIRDEM during November 2005 and April 2006. The study included 60 subjects, 30 recently diagnosed diabetic subjects (14 male, 16 female). None had neuropathic symptoms or signs. All cases were selected randomly diagnosed by ADA criteria accepted by WHO. Thirty healthy controls with mean age comparable to that of diabetic subject were selected from the friends of the subjects and patients attending neurology outdoor of BSMMU. Result:Findings (mean±SD) were (case and control, respectively): Tibial nerve, DML 4.05±0.81 and 3.84±0.70 msec (P>0.10), CMAP 16.90±5.14 and 19.49±4.73 mV (P<0.05), MCV 45.43±4.55 and 48.24±4.72 m/ s (P<0.05), and F latency 45.09±12.43 and 42.50±8.93 msec (P>0.10); peroneal nerve, DML 4.12±1.10 and 4.03±0.67 msec (P>0.50), CMAP 5.80±2.89 and 6.97±1.79 mV (P>0.05), MCV 43.10±8.89 and 48.27±3.56 m/s (P<0.01), and F latency 50.27±10.81 and 41.32±3.05 msec (P<0.001); median nerve, DML 3.57±0.46 and 3.55±0.52 msec (P>0.50), CMAP 16.33±4.24 and 17.84±3.73 mV (P>0.10) and MCV 55.16±5.33 and 57.70±4.33 m/s (P<0.05), and F latency 25.08±5.28 and 24.39±4.83 msec (P>0.50); and ulnar nerve DML 2.57±0.33 an 3.17±0.61 msec (P<0.001), CMAP 14.65±3.32 and 17.29±6.83 mV (P>0.05), MCV 55.74±5.00 and 58.50±5.13 m/s (P<0.05), F latency 25.09±5.35 and 25.82±3.33 msec (P>0.50); sural nerve, DSL 2.46±0.68 and 3.12±0.45 msec (P<0.001), SNAP 19.44±10.25 and 25.32±7.88 ìV (P<0.05), SCV 49.95±10.22 and 52.46±3.96 m/s (P>0.10); median nerve, DSL 2.52±0.39 and 2.77±0.49 msec (P<0.05), SNAP 30.23±12.79 and 31.69±11.02 ìV (P>0.50), and SCV 56.90±6.77 and 57.41±5.85 m/s (P>0.50); and ulnar nerve, DSL 2.03±0.39 and 2.48±0.49 msec (P<0.001), SNAP 29.30±14.36 and 30.72±10.76 ìV (P>0.50), and SCV 60.96±8.38 and 57.93±7.15 m/s (P>0.10). Mean (±SD) HbA1c was significantly high (P<0.001) in case group (7.10±0.80%) compared to control (5.51±0.65%). Mean (±SD) SGPT showed no significant difference between case (36.10±13.02 u/L) and control (36.20±7.94 u/L). Similarly, mean (±SD) total cholesterol also showed no significant difference between case (201.57±37.56 mg/dl) and control (191.00±17.17 mg/dl).
 Conclusion: Motor nerve conduction parameters are affected more than sensory nerves and F-wave latencies are more frequently and early involved in these subjects. Abnormalities on nerve conduction was started in the feet rather than the hands.Clinical spectrum of diabetic neuropathy is variable and may be asymptomatic, but once established as polyneuropathy, it is irreversible and may finally be disabling. Early detection of diabetic neuropathy is one of the major goals in the management of diabetes since timely intervention may substantially reduce mortality and morbidity.
 Bangladesh Journal of Neuroscience 2014; Vol. 30 (1): 16-22

What's in the Literature?

Abstract We review 2 recent studies of the frequency of the C9ORF72 mutation in sporadic cases of amyotrophic lateral sclerosis (ALS). There is an incidence of 11% in Greece, 3.7% from mainland Italy, and 6.8% from Sardinia. We also review other reports of overlapping pathological features in familial ALS and mutations in sequestosome 1 and profilin genes. There is also a report of serotonergic pathways being affected in ALS and leading to spasticity and opening a new therapeutic avenue. Treatment for Dok-7 congenital myasthenic syndrome is discussed as well as the possible role of vitamin D deficiency in autoimmune myasthenia gravis. New serological potentially diagnostic autoantibody markers for inclusion body myositis are reviewed. Finally, a report of cervical radiculoplexus neuropathy in diabetics formally places this entity within the spectrum of diabetic neuropathies.

Electrophysiological Changes in Diabetic Neuropathy: From Subclinical Alterations to Disabling Abnormalities

Clinical spectrum of diabetic neuropathy is variable; it may be asymptomatic, but once established as polyneuropathy, it is irreversible and may finally be disabling. To estimate the prevalence of subclinical diabetic polyneuropathy in the UAE, we undertook a pilot study by means of nerve conduction study (NCS) of peroneal motor and sural sensory studies in 60 diabetics with no symptoms of neuropathy. Neurological examination revealed clinical abnormalities suggesting polyneuropathy in 26 patients, 43% of the patients. NCS revealed abnormal values in 63% of the whole patients. Abnormal NCS was confirmed in 88% of the positive sign group. As to the negative sign group 44% had abnormalities in NCS. Prolonged F-wave latency was seen in 29% in no sign group and in 66% of the patients with positive signs. We found close association between neurological deficit score and abnormalities in NCS. Among various parameter of systemic nerve conduction study in subclinical patients, prolonged F-wave latency seems the commonest abnormality suggesting morphological changes in subclinical diabetic nerve. Decrease in amplitude of compound sensory action potential of sural nerve is another earlier abnormality, which is, then, accompanied by a fall in motor amplitude of peroneal nerve in advanced patients. Recently, our own group of Hirosaki has demonstrated that somatosensory central conduction time (CCT) between the spinal cord entry time and the arrival time to the sensory cortex is prolonged in diabetics. This abnormality might be partly responsible for the irreversible sensory deficits of diabetic neuropathy.