De geschiedenis van diabetische neuropathie

De geschiedenis van diabetische neuropathie is ouder dan we denken. Tegenwoordig lijkt het soms of de autonome stoornissen, de Dunne Vezel Neuropathie, een vrij nieuw verschijnsel is.

Een voorbeeld van Charcot voeten met ernstige zweren, zoals deze bij diabetische neuropathie graad 3 vaak gezien worden. Maar we vinden al inzicht op het gebied van autonome stoornissen bij diabetische neuropathie meer dan een halve eeuw geleden.pixabay-609676-INP-Instituut-voor-Neuropathische-Pijn diabetische neuropathie

Namen van neurologen die zich bezig hielden met diabetische neuropathie waren o.a. Bouchard, 1884; Pavy, 1885; Auche, 1890, Williamson, 1907.

We kijken hier o.a. naar de analyse van dr. F.W. Pavy uit 1885, via de ogen van een neuroloog uit 1950. In een tekst uit 1950 vinden we:[1]

Analyse van Pavy (1885)

  • The neurologic complications of diabetes mellitus remain • a matter of perennial interest. Although there is little really new to present at this time, a “present-status” report with particular attention to some of the contributions during the last 5 years may be useful. Some particular aspects of diabetic neuropathy, its relationship to other diabetic complications, the prominence in it of autonomic nerve disease, etc. can well be re-emphasized. 

Citaat uit 1885, uit the Lancet, ook van dr. Pavy:

  • “I am perfectly satisfied that certain symptoms of disordered nerve action are very apt to accompany diabetes. A lady aged 48, whom I saw for the first time in I87 I, and who had then been diabetic for ten years, presented no symptoms of nerve disorder till February, I88o. She then began to complain of pains in her limbs, and by April of that year she was decidedly ataxic. The usual account given by these patients of their condition is that they cannot feel properly in their legs, that their feet are numb, that their legs seem too heavy. Darting or ‘lightning’ pains are often complained of. Or there may be hyperaesthesia, so that a mere pinching up of the skin gives rise to great pain; or, it might be, the patiënt is unable to bear the contact of the seam of a dress against the skin on account of the suffering it causes.

    Not unfrequently there is deep-seated pain, located, as the patiënt describes it, in the marrow of the bones, which are tender on being grasped; and I have noticed that these pains are generally worse at night. With this there is the usual loss or impairment of the patellar tendon reflex. “Sometimes pains and manifestations of perverted sensibility are  noticed without ataxia. It is not always the legs that are affected; the arms may suffer. A gentleman I have seen has had nerve troubles in one arm. His skin and flesh were tender and the bone was pain- ful; there was, moreover, some wasting of the limb.”
    Pavy, F. W. Introductory address to the discussion on the clinical aspect of glycosuria, Lancet, 1885, 2:1085.

Complicaties beschreven anno 1950

  • diab-neuro-INP-Instituut-voor-Neuropathische-Pijn.jpgA high incidence of other diabetic complications was found in patients with neuropathy. In the scale of diabetic complications, peripheral nerve disease occurred as one of a middle group that we can call sub-acute. Susceptibility to infection was common and an unstable and often severe diabetes the rule. A third of our group had diabetic retinal disease and more than a quarter hepatomegaly. 

En ook autonome verschijnselen werden al in de geschiedenis van diabetische neuropathie beschreven. Waaronder de lage bloeddruk, spijsverteringsstoornissen (gasteroparese, diarree, obstipatie), impotentie en incontinentie, evenals zweetvermindering:

  • Orthostatic hypotension was one of the striking results of autonomic nerve disease observed in more than a dozen patients. Another manifestation of autonomic nerve disease in patients with diabetic neuropathy was disturbance in the motor function of the gastro-intestinal tract. About 1 in 4 of our patients with diabetic nerve disease developed genito-urinary and sphincter disturbances. Most of them had gastro-intestinal disturbances as well. The major complaints in the male were impotence, symptoms mimicking prostatism and, in both sekses, urinary and fecal incontinence. 

De pijn bij diabetische neuropathie

Zweettest: Een oude methode om met jodiumzouten de huid zichtbaar te maken waar een duidelijke afwijkend zweetpatroon is. Over de pijn werd 3 jaar later, in 1953 in het BMJ opgemerkt.[2]  

  • Pain is the most important manifestation of active diabetic neuropathy. We have been able to confirm the descriptions of its characteristic nature-cramp-like, twitching, or buming, and almost invariably worse at night but uninfluenced by posture. The intensity may be extreme and the response to analgesics poor. The colour and temperature of an affected limb and the local pulses are unaltered during an attack.

    Abnormal sensory signs are commonly present in association, and are the most frequent objective evidence of diabetic neuropathy. The most frequent abnormality is loss of vibra- tion sense in the legs. Sensorychange may occur in single or multiple areas, or it may be distal or limited to the area of distribution of one or more peripheral nerves. In one of our cases sensory loss was present in the zones of both ulnar nerves and one external popliteal nerve. There were paraesthesiae, and the small muscles of the hands were wasted. In six months of excellent diabetic control one arm improved, one was unchanged, and the foot lesion deteriorated.

Kortom, een interessante inzage in de geschiedenis van diabetische neuropathie.

Versie Oktober 2009; Drs David J. Kopsky, artsen
‘De geschiedenis van diabetische neuropathie’

Charles Féré schrijver van ‘Les epilepsies’

Bekijk hier video’s van onze patiënten over pijnstillende crèmes.

Diabetes pijn in Gambia Afrika verhelpen
Pycnogenol remt diabetische retinopathie
Ziekte van Fabry en neuropathische pijn


Referentielijst

[1] RUNDLES RW. | Diabetic neuropathy. | Bull N Y Acad Med. | 1950 Sep;26(9):598-616.

[2] HIRSON C, FEINMANN EL, WADE HJ. | Diabetic neuropathy. | Br Med J. | 1953 Jun 27;1(4825):1408-13.

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