Neurological diabetic foot is a complication related to diabetic neuropathy, affecting nearly one in two patients after 20 years of diabetes. Microangiopathy results in the alteration of the microvessels of the epineurium and endoneurium of the nerve. At the level of Schwann cells, the transformation of excess glucose into sorbitol leads to an alteration of the cell membrane, therefore of the myelin sheath, ultimately leading to nerve degeneration.
Clinical signs of neurological diabetic foot
Damage to the nerve fibers contained within the nerves is called multiple neuritis or, more commonly, diabetic polyneuritis, due to the symmetry of the disorders. This condition constitutes the clinical picture in more than 90% of cases.
I – Autonomic (or vegetative) neuropathy
1 - Damage to the fibers of the autonomic or vegetative nervous system, and in particular the sympathetic fibers of the nerves, leads to poor distribution of blood flow in the structures of the foot.
At the skin level, the neurological foot is characterized by relative warmth, sometimes bounding pulses, thick and dry skin due to hyposweating, hyperkeratosis at the support points (i.e. under the head of the metatarsals, at the styloid of the 5th metatarsal and under the heel), as well as fissures serving as entry points for infections.
2 - At the bone level, there is a vascularization disorder that results in demineralization of the skeleton, a source of destruction of its architecture, associated with an anarchic reconstruction. All this is a source of deformations of the skeleton, and consequently of the joints that are integral to it. These anomalies are grouped under the term osteopathy, arthropathy or even Charcot diabetic osteoarthropathy.
II – Sensorimotor neuropathy
Damage to the nerve fibers of the nervous system, i.e. the sensory and motor fibers of the nerves, is called sensorimotor neuropathy.
1) Damage to motor fibers rarely results in paralysis (which is then peripheral), despite the name diabetic polyneuritis mentioned above.
– Involvement of the extrinsic muscles of the foot predominates over the muscles of the antero-external compartment and results in a decrease in the muscle strength of the foot lifters. The Achilles reflex is abolished, as is often the patellar reflex. Amyotrophy is rarely significant.
– Damage to the intrinsic muscles of the foot results in hammer toes and claw toes at the lumbrical and interosseous levels, which, through their subluxation, expose the metatarsal heads to excessive pressure and the back of the proximal interphalangeal joints, as well as the pulp of the toes, to conflict with the shoe.
2) Damage to sensory fibers:
– Superficial sensitivity disorders:
Subjective disorders manifest as symmetrical and distal paresthesias, progressively evolving upwards, with sometimes lightning-like pain, particularly in the calves, often at night. This results at most in a picture of painful polyneuritis, a form of neuropathy characterized by disabling pain that is difficult to treat. In this form, the signs are daytime and nighttime burning, often occurring at rest and relieved by walking. These pains, sometimes like cutting, grinding, or deep crushing of the legs, often cause insomnia, forcing the patient to get up at night and walk to relieve them.
– Objective disorders consist of anesthesia of the foot “in a sock” to touch, pain, heat and cold (thermoalgesic sensitivity).
Deep sensitivity disorders result in a loss of pressure sensitivity and vibration sensitivity (the first affected in diabetic neuropathy), detected using a tuning fork applied to the bony reliefs (malleoli, dorsum of the foot, anterior tibial crest and tuberosity).
Complications of neurological diabetic foot
I - Plantar perforating ulcer (MPP)
1 – The mechanism:
The loss of superficial sensitivity to pain, heat and cold (thermoalgesic sensitivity), as well as deep sensitivity to pressure, makes the foot insensitive to the harmful effects of the constraints to which it is exposed. These constraints are due to deformations linked to motor impairment, aggravated by those linked to the deformations of a possible arthropathy.
The non-perception of the pressure of the Semmes-Weinstein (MSW) monofilament (5.07 and 10g) applied to the skin is a good test to assess the risk of developing a wound or skin ulcer. The skin areas thus subjected to excessive pressure, continuous or intermittent (running, jumping, trauma), source of ischemic necrosis, will be the site of wounds, ulcerations or hyperkeratosis under which a phlyctenular detachment will lead to the ulceration characteristic of plantar perforating ulcer (PPE).
2 – The signs:
Under hyperkeratosis, a blister due to underlying detachment will cause an ulceration constituting the MPP. This ulceration is characteristic, deep, with clear edges which are themselves hyperkeratotic, and with a base covered with a purulent coating. It is located at the level of the hyper-pressure points, either physiological (heads of the 1st and 5th metatarsals and heel), or pathological, linked to changes in the statics of the foot secondary to the deformations.
3 – The treatment:
General treatment is based on parenteral insulin therapy for type I diabetes, and a hypocaloric diet with possible replacement by oral hypoglycemic agents in type II diabetes. Tetanus vaccination is necessary because of the frequency of wounds in this context, especially if there has been contact with soil (gardening). If tetanus vaccination is not up to date, an injection of tetaglobulins should be associated with vaccination.
Prevention of the onset of MPP is based on the advice of the podiatrist concerning the examination of the foot in search of an incipient lesion, the washing and hygiene of the feet, walking, socks and shoes. Podiatry care focuses particularly on areas of hyperkeratosis. Orthoplasties and plantar orthoses adapted to the various anomalies of the foot are also recommended.
Treatment of confirmed MPP includes MPP-specific care with offloading to ensure healing, as well as measures to prevent recurrence of healed MPP within one year. Surgery is rarely necessary. It aims to correct or reduce deformities that non-surgical means are not sufficient to treat adequately.
II - Diabetic arthropathy
It is actually an osteoarthropathy.
1 – The mechanism:
It is a complication of neuropathy that causes bone resorption by degeneration of neurovegetative fibers, leading to the opening of arteriovenous shunts of the dermis. Indeed, the diversion of blood flow to the benefit of the cutaneous territories, to the detriment of the bone, causes osteoporosis, leading to destruction of the skeleton accompanied by an anarchic bone reconstruction process, which results in bone and joint deformations of the foot.
Consequences: These deformations of the foot will be the cause of pathological supports or conflicts with the shoe, which, thanks to the cutaneous anesthesia linked to the neuropathy, will lead to skin lesions, the most typical and most serious of which is plantar perforating ulcer (PPE).
2 – Clinical signs:
The picture of pseudo-inflammatory arthritis is rare. It is an acute attack with swelling, redness and heat of the joint, but without pain, which will evolve over about two months. The picture of progressive disorders is the most frequent. More often, it is insidious, painless, leading to a progressive destruction of the joint and the skeleton of the foot. The attacks affect the 1st and 5th heads of the metatarsals, the metatarsophalangeal joint of the big toe, the Lisfranc joint and the tarsal bones. These anomalies result in joint ankylosis and especially in deformations of the foot, affecting the toes (which are curled or hammer-shaped), the forefoot (which is round or convex), and the arch which collapses, achieving at most the "elephant foot" or "blotting pad foot" or Charcot's cubic foot.
3 – Radiological signs:
Bone destruction (osteolysis) is characterized by geodes, areas of localized demineralization, pathological fractures of metatarsals coexisting with images of anarchic construction (osteophytosis). Bone scintigraphy of the foot skeleton can be very useful to specify an area of bone pain (hyperfixation) not detected by clinical examination and guide the creation of plantar orthoses intended to relieve excessive support points and thus prevent the appearance of MPP. These anomalies are located at the level of the 1st and 5th metatarsophalangeal joints, the navicular bone, the cuboid and the calcaneus.
In summary, the neurological diabetic foot illustrates the importance of prevention and proactive management in diabetes management. This complication, although common, can lead to serious consequences such as joint deformities, chronic ulcerations and, in the most severe cases, amputations. The clinical signs, although sometimes discreet, must be detected and treated quickly to avoid progression to more severe forms. Preventive approaches, including regular foot inspection, rigorous hygiene, and the use of suitable orthoses, play a crucial role in protecting against these complications. Similarly, patient education and close collaboration with specialized health professionals are essential for comprehensive and effective management.
This topic is vast and deserves continued attention, as it can affect the quality of life of people with diabetes. We encourage you to share your experiences, ask questions or give your opinions in the comments section below. Your contributions will enrich this discussion and help other readers facing similar situations.
