Lab test: CBC, CRP, HbA1c, LFT, RFT, VitB12, folate, thyroid function test, ECG, ECHO
Addition tests: Nerve conduction test(Gold standard)
EMG
Static Posturography test
Skin Biopsy
Nerve Biopsy
PAINFUL DIABETIC NEUROPATHY
Diabetic Peripheral Neuropathies (DPN) are the foremost common sort of neuropathies worldwide with up to 50% of individuals with type 2 diabetics eventually developing same degree of peripheral neuropathy. There has been significant progress in the understanding of the clinical aspects of those conditions, however many questions remain unanswered or difficult to answer in terms of causation, risk factors and genetic susceptibility, effective treatments, and restoration of nerve functions, and pain management.
Diabetic polyneuropathy is one among the foremost common sorts of neuropathy. it’s associated with the duration of diabetes and glycemic control of diabetes. Unfortunately and despite numerous drug trials, aside from strict glycemic control, which is usually difficult to take care of , there are not any other treatments to slow the progression or delay the event of DPN.
Pathophysiology:
Pathogenesis of painful symptoms remains unclear. In diabetic neuropathy variety of metabolic and vascular changes interconnect to cause damage to nerve cells with the first underlying factor being hyperglycemic .Changes includes increased oxidative stress, a buildup of glycation and products, increased activity of the polyol pathway, activation of pro-inflammatory mechanism and ischemia .These process have direct and indirect effect on the neurons and blood vessels that provide the nerves.
Hyper excitability of and aberrant spontaneous impulse generation by damaged first order sensory neurons and their peripheral axons are well established processes that strongly contribute to pain related to DPN.
Central neuropathic mechanisms also can contribute to pain experienced with diabetes. Severe studies have demonstrated that thalamic dysfunction occurs in patients with DM which is experimental models of this disease, neurons in ventral posterior-lateral thalamus can become hyperexcitable, firing at abnormally high frequencies and generating aberrant spontaneous activity.
It affects all kinds of nerve fibers.
Diagnosis:
History:
More than 80% of the patients with DM induced poly-neuropathy have distal, symmetric sort of this condition. The initial symptoms are the signs of diminished sensation, burning feet, which can occurs particularly during night and worsen when touched and therefore the sensation of tingling in feet. Attack of shooting pain also occurs.
Other examinations includes:
General inspection of Feet: For ulceration, callus, erythematous areas
Musculoskeletal assessment: For deformity Charcot neuro-osteoarthopathy(CNO)
Neurological assessment: Length dependent, non- dermatomal distribution of sensory loss(Gloves and stocking)
Vascular assessment: pulse and BP lying/sitting
Eye can also be a crucial site of diagnosis and monitoring of neuropathy. Corneal nerve morphology may be a promising marker of DPN occurring elsewhere within the body
Potential diagnostic role for retinal structure and visual functional marker in diagnostic and monitoring of DPNs.
Current technique:
Management:
Intensive Glycemic Control
Medications:
Anticonvulsants: Carbamazepine, Depokene , Gabapentin are traditionally used.
Efficacy of Gabapentin has enhanced when combined with opoids like morphine or sustained released oxycodine and highly effective when combined with nortriptylline.
2.Anti-Depressant:
3.Local Anesthetics:
Mexiletine –Oral
5% Lidocaine patch
4.NMDA :Dextromethorphan
5.Opoids:Tramadol
Others:
Alpha –Lipoic acid
Topical Clonidine in foot pain
Combined Treatment:
Combination of pharmacotherapy are often utilized in instances where but adequate response is obtained with monotherapy or when side effects limit further dose –up titration of single agent. A study demonstrates that combination of nortriptylline with Gabapentin at maximal tolerated dose was simpler than either of monotherapy.