Diabetic Neuropathy – Diabetics can develop neuropathy which is classified into symmetrical and asymmetrical forms. Neuropathy in diabetics occurs in those with long standing disease with poor control of hypeiglycemia and is related to severity of diabetes. Diabetic neuropathy can be classified as:
1. Diffuse distal primarily sensory polyneuropathy
2. Autonomic neuropathy
3. Chronically evolving proximal motor neuropathy
1. Acute or subacute proximal motor neuropathy
2. Mono neuritis or mononeuritis multiplex
3. Cranial mononeuropathy
4. Entrapment neuropathy
(c) Diabetic amyotrophy
Clinical Features of Diabetic Neuropathy
Diffuse distal and symmetrical sensorimotor neumpathy
Diabetic Neuropathy is the commonest neuropathy seen in diabetes. Its incidence is variable ranging from 10-90%. It may develop in known diabetic or may be the presenting feature in a previously undiagnosed diabetic. Onset of symptoms may have no definite correlation with severity, duration and control of diabetes.
It may be first noticed in third or fourth decade in patients with juvenile onset diabetes and after the age of 50 in adult onset diabetes. The initial symptoms are in the form of parasthesiae especially tingling, numbness and burning sensation mostly in the lower limbs. The symptoms are worse at night.
Earliest signs of Diabetic Neuropathy are loss of vibration and position sense with absent ankle jerks. Impairment of touch, pain and temperature and glove and stocking type of sensory loss are present. Because of loss of all sensory modalities patient has areflexia and sensory ataxia. These patients later on develop neuropathic arthropathy and perforating ulcer on the sole of the foot. Electrophysiological studies show slowing of conduction velocity in the involved nerves.
Cases of symmetrical motor neuropathy may show minimal sensory involvement though motor weakness and wasting of distal muscles occurs at a late stage.
Asymetric proximal motor neuropathy
It includes diabetic femoral neuropathy where femoral and obturator nerve innerved muscles like quardriceps femoris, iliopsoas, and adductor magnus are predominantly involved. Patient complains of pain in the hip and anterior thigh followed by wasting and marked weakness.
There is history of falls and difficulty in getting up from sitting position. Sensory loss which may be minimal is present confined to the anterior aspect of thigh and medial aspect of the leg upto medial malleolus. There is loss of knee jerk on the side affected.
There is important correlation of Diabetic Neuropathy to the control of diabetes since it manifests itself when diabetic status is poor.
It may present in varied forms and mainly involves GI tract and genito urinary systems. One of its most distressing features is diarrhea which is usually watery and occurs mostly at night. It may be intermittent and alternate with constipation.
Genito urinary symptom includes a neurogenic bladder where there are longer interval between voiding leading to straining and post micturition dribbling. Cystometric examination shows a large atonic bladder. Impotence in men is an important feature.
Other features of autonomic Diabetic Neuropathy include postural Hypotension which may be severe enough to cause syncope. Disturbances of sweating and pupillary abnormalities ofArgyll-Robertson type are other manifestations.
Diabetic cranial neuropathy
The most common cranial nerve involved is occulomotor nerve though isolated involvement of 4th, 6th and 7th cranial nerves may occur. The onset is usually sudden and may start with pain and then nerve weakness.
Cranial nerve palsies are usually seen in elderly diabetics.
Mono neuritis and mono-neuritis multiplex
This group includes both cranial and peripheral nerves. The aetiology of mononeuritis multiplex is considered to be ischemic in nature. The peripheral nerves involved include peroneal, femoral, median, radial and ulnar nerves. Pain in the distribution of nerve is the initial symptom.
Diabetic Neuropathy mainly occurs in elderly diabetics and patient presents with pain in the thighs more marked at night. The picture is like that of femoral neuropathy and is accompanied by weakness and wasting of the muscles of the lower limb (iiopsoas, Quadriceps and occasionally muscles of the antero lateral compartment of the leg). The lesion is probably at the cord and anterior horn cell level.
CSF. Shows increased levels of proteins and high sugar content without any rise in cell count. Recovery is gradual but occurs with good diabetic control.
Diabetics are more prone to suffer pressure palsies because of inflammation. Features of meralgia paraesthetica (entrapment of femoral cutaneous nerve) are common in diabetics due to compression of the nerve. This type of neuropathy in diabetics is amenable to surgical decompression procedures.
The mechanism of diabetic neuropathy is either vascular or metabolic. Vascular factor operates by occlusion of vasa nervosum. Though there is poor correlation between occlusive vascular disease and diabetic neuropathy yet there is no doubt that in asymmetric neuropathies whether cranial or peripheral nerves, the primary factor responsible is ischemia.
Metabolic derangement is an important factor underlying chronic sensory motor neuropathy and is related to sorbital pathway and myoinosital deficiency. Sorbitol glucose and fructose are all increased in diabetic nerves. Conversion of glucose to fructose via sorbitol may contribute to diabetic neuropathy. The selective involvement of autonomic and sensory fibers mimics system degeneration and favors metabolic theory.
The main pathology in the nerves is extensive segmental demyelination and remyelination. Axonal changes appear in long standing and severe cases and are in the form of irregular thickening followed by swelling, beading, splitting and fragmentation with complete disappearance of axons. There is considerable loss of myelinated fibers as compared to axonal loss which is seen in peripheral nerves especially in chronic cases.
Conduction studies show that there is diminished conduction velocity in the peripheral nerves of patients of diabetic neuropathy. Electro-myographic studies of involved muscles show a peripheral neurogenic type of lesion.
Adeqate control of diabetes should be the primary aim. In patients with severe form of neuropathy insulin should be given instead of oral hypoglycemic drugs. Blood sugar should not be reduced suddenly since there are chances of aggravating the neuropathy.
Pain in the legs at night is a troublesome feature. Drugs like Diphenylhydantoin (100 mg thrice a day) or Carbamazepine (100-200 mg twice a day) are useful.
Symptoms due to autonomic dysfunction are difficult to manage Diarrhoea may respond to Codeine Phosphate (30 mg twice a day). Impotency does not respond to any drug therapy. For postural hypo-tension patient be instructed to get up slowly from the bed.
Use of heavy doses of vit B1, B6 & B12 is often recommended though their value is doubtful but giving these supplements does help and keeps the moral of the Diabetic Neuropathy patient high.