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Neurolosical Manifestations of Diabetes Mellitus

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Neurolosical Manifestations of Diabetes Mellitus 1954] MANIFESTATIONS OF DIABETES MELLITUS : VAISHNAVA 463 is the commonest lesion in diabetic neuropathy inal Articles but nerve trunks, spinal ganglia, posterior nerve Orig roots, posterior and lateral columns and ante- rior horn cells of the spinal cord or the motor nuclei of the brain stem, the autonomic ner- Neurological manifestations of vous system and the brain may also be affected. DIABETES MELLITUS The lower extremities appear to bear the greatest brunt of the disease. % HARI P. VAISHNAVA, m.b., b.s. (Lucknow), exact mechanism of these M.R.C.P. (Ed.) The neurological manifestations is not known. As this condi- Medical Registrar and Resident Medical Officer, tion is more common in elderly people, arterio- Victoria Hospital, Blackpool, England sclerosis is considered the most likely cause Neurological complications of diabetes though this theory does not account for its ^ellitug have baffled many physicians. There occurrence in younger people without signs of ]s an extensive American literature on this sub- arterio-sclerosis; moreover, so many elderly ject which is being increasingly recognised in subjects with arterio-sclerosis do not suffer ?ther countries. The incidence of diabetic neu- from neuropathy. r?Pathy varies with different authors, Jordan Martin (1953).states that the condition is a (1936) mentioning 67 per cent; Collens at al degenerative one in which non-myelinated (1952) 93 per cent ; Bonkalo (1950) 49.3 per small calibre fibres degenerate more extensively contrasting with Rundles (1945) 5 per cent. ^eilt, than the larger myelinated ones. The primary *he difference in these figures is mainly due to lesion, according to Martin, is a degeneration lriterpretation of the symptoms; if objective of axis cylinders and sheaths are re- ^gns must be taken into account with the myelin duced as a secondary effect. These parts of Objective symptoms, only low figures are the nervous system containing the most non- ?btained. The presence of subjective symptoms myelinated fibres are most affected. Lewis and a^?ne according to some authors does not Pochin (1938) hold the view that non-myeli- institute diabetic neuropathy. Jordan (1936) nated and thinly myelinated nerve fibres are neuropathies into hyperglycaemic, cjassifies more resistant to loss of their blood supply than Clrculatory, degenerative and neurotic types, the larger myelinated fibres but that the former ^binowitch (1952) adds the achlorohydric tend to be affected by noxious influences ^Pe in which diarrhoea and other intestinal long before the myelinated sensory and motor fibres. symptoms improve with the administration of Other authors consider that patchy de-myelina- hydrochloric acid. Hirson et al (1953) have tion is early and is mostly confined to the divided them into hyperglycaemic, active and. peripheral nerves but that it can be widespread Symptomatic neuropathies. Roots and Jordan and become continuous and that also, it can be ^aVe tried to separate them into degenerative reversed control of the diabetes. and vascular. by adequate The neuropathy may be permanent once the The writer has found the following anatomi- involvement of axis cylinder takes place. Cal classification of value : Autonomic disturbances and an.early difficulty in the perception of pain and of extremes of 1. Peripheral neuropathy including cranial temperature can be explained as due to early nerve palsies. involvement of non-myelinated nerve fibres. 2. Autonomic neuropathy. Ischaemic neuropathy,. which is due to defi- ciency of vascular supply, is progressive and 3. Involvement of central nervous system, shows itself as nocturnal and brain cord and paroxysmal pain including stem, spinal sometimes cerebellum. hyperaesthesia, anaesthesia, change in colour and gangrene which is extremely pain- 4. Combination of two or more. ful and it is mostly confined to the lower extremities. Symptoms in hyperglycaemic (or functional) **eUropathy improve with the treatment of hy- Post-treatment neuropathy has also been Psrglycaemia and restoration of electrolytes and mentioned for Rundles noticed in a few of his ^ater. Involvement of the peripheral nerves cases that pain and parasthesiae had sometimes 464 THE INDIAN MEDICAL GAZETTE [Aug., 1954 been brought about by Insulin treatment and extremities. The objective sensory signs include this condition has sometimes been termed anaesthesia, loss of vibration and position sense, "Insulin neuritis" and has reverted back on hypersensitivity of the skin to the extent of stopping the Insulin treatment or by administra- having difficulty in dressing and tolerating the tion of Aneurine. Vitamin B. Complex plays bedclothes. These sensory manifestations are an important role in the intermediate metabo- mostly marked in the lower extremities arH* lism of carbohydrate, deficiency of Vitamin Ba sometimes along the distribution of the femoral, causing excessive formation of pyruvic and sciatic, anterior tibial, ulnar and other main lactic acid. Insulin therapy, by utilising car- nerves. Tabes dorsalis may be simulated when bohydrate, necessary for the full operation and lightening pains occur particularly when these existence of Vitamin B, may make a latent are accompanied by sensory ataxia, hypotonia Vitamin B deficiency quite apparent. Even and pupillary changes. This condition is some- pellagra has been precipitated in this way. times called pseudotabes or tabes diabetica. Besides arterio-sclerosis of the vasovasorum Sensory symptoms have also been complained and Vitamin B deficiency, other factors which of on the face. Nocturnal pains are sometimes so severe that the cannot and have been said to play a part in some way or patient sleep other in the pathogenesis of diabetic neuropathy prefers walking to get relief; this condition include toxic effects of glucose, ketone bodies, has been mistaken for osteo-arthritis of the hips- infections, local deprivation of carbohydrates, Pains in the chest, may also simulate angina- lipoid disturbances and mal-nutrition. Collens All these symptoms may be mild, moderate or severe in et al and Rabinowitch have claimed great suc- and may disappear with treatment cess in the treatment of diabetic neuropathy by weeks, months or years respectively. mammalian liver extract. Cases giving pregnant Martin (1953) believes that the earliest of "diabetic cord bladder" and diabetic gross manifestations of diabetic neuropathy are have shown in a few neuropathies improvement diffuse pain, thermal pallesthesia, vaso-motor instead of the months and days years which disturbances, changes in the tendon reflexes these cases used to take with Vitamin Bx, B12, and alteration in pain sensibility in the distal Liver Extract and even B.A.L. (Dimercaprol). part of the lower extremities. Touch and also believe that such as They complications pressure sensibility are also altered. If the and sexual in retinopathy importance diabetes, disease progresses shooting pains develop and in future be treated may successfully. Though vibration sense is lost together with a sense of it is to other mechanisms involved early say, position and touch. Lastly motor power be- in these be found neuropathies may and, per- comes affected. Sometimes the only physical new fields in the metabolism of diabetes haps, sign may be the loss of reflexes, ankle jerks will be opened. being earliest to go. Bailey and Root (1942 and 1947) described Motor changes.?Certain groups of muscles neuropathies occurring between the age group of tend to be wasted. These are the 29 and 69. The duration of diabetes in these quadriceps; the anterior tibial group giving foot uni- cases had been from several weeks to several drop lateral or bilateral; scapulo-humeral muscles years but recently Hirson et al (1953) published causing resemblance to the myopathies. Weak- cases in which the neuropathy had preceded the ness of the pelvic muscles and even of diabetes mellitus. wasting the small muscles of the hand, with or without Peripheral NeuropcCthy sensory symptoms, have been mentioned. Sensory changes.?Subjective sensory symp- Cranial nerve changes.?Involvement of all toms are very common and more often occur the cranial nerves has been described but the without objective signs. Moreover, the patients 6th and 3rd are the most frequently affected. do not always volunteer their symptoms. Some Irregular pupils which react, sluggishly to light consider them to be part of their creeping old are quite common. Partial 6th and 3rd nerve age, especially when symptoms are slight. They palsy may be of fairly rapid onset and, as in may complain of tingling, numbness, nocturnal the writer's three cases, may revert completely cramps, formication, "pins and needles", diffuse to normal after treatment. There may be optic pains in the extremities, burning sensations in or retrobulbar neuritis?unilateral or bilateral- the toes and feet and sometimes stiffness in the Sensory changes on the face have been men- Kxjg., 1954] MANIFESTATIONS OF DIABETES MELLITUS : VAISHNAVA 465 tioned above. These cranial nerve lesions are afferent pain and proprioceptive impulses and c?nsidered to be due to small nuclear haemorr- with intact motor power, repeated minor trauma hages in the brain stem or in some way to peri- lead to destructive and proliferative lesions of pheral neuropathy. Arteriosclerosis in the the bone. Other joints of the body have also retina is a common feature in the old diabetics been involved. Charcot spine in this condition hut the writer has noticed it also in young has been described by Zucker and Marder Patients who have .suffered from this disease for (1952). Signs and symptoms of neuropathy ^any years. The youngest one in his series are usually severe. Bailey and Root collected Was a boy of 23 who suffered from diabetes for 17 cases (in their 2,000 diabetics) with joint ^ years. Discrete waxy exudates with red dots changes which were observed mostly in the scattered all over the retina due to micro- tarsus and matatarsal bones, unilateral or ai*eurisms or haemorrhages, are frequently seen bilateral, earliest changes being thickening of 111 elderly diabetics but it is well known that the trasal bones without any fluid, pain or signs they occur in younger diabetics with long- of inflammation.
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