A recent article in Diabetes Care (1) reminded me that I have never seen in publication a full list of the clinical signs of the so-called “diabetic” or “intrinsic minus foot” that can be discerned on physical examination. It is the purpose of this letter to describe these signs, most of which are present in severe cases.
The term “intrinsic minus foot” was first coined by my long-term teacher and colleague, Heinz I. Lippman, MD, in 1976 (2). The longest motor nerves are those that activate the intrinsic muscles of the foot (lumbricals). Since diabetic neuropathies progress from distal to proximal, the lumbricals are the first muscles to be affected by neuropathy. The characteristics of the intrinsic minus foot that can be discerned on simple physical examination are described below.
Hammer toes: the lumbricals wrap around the toes in such a fashion that they extend the interphalangeal (i-p) joints and flex the metacarpal-phalangeal (m-p) joints. When they are denervated, the opposing muscles will cause flexion of the i-p joints and extension of the m-p joints with the resultant hammer toes.
Prominent plantar metatarsal heads: extension of the m-p joints causes the appearance of visible and palpable bony prominences on the bottom of the foot, at the base of each toe. At first, these prominences are found only at the bases of the first and fifth toes, but as neuropathy progresses, all of the toes are affected and calluses can be palpated under each metatarsal head.
Wasting of lumbricals: the lumbricals originate on the distal metatarsal bones on one side of each toe, wrap around the toe, and insert in the opposite side of each metatarsal. When sufficiently wasted by denervation, visible channels appear on the dorsum of the foot between the metatarsals. Contrary to the results of the referenced study (1), observations in our clinic of hundreds of patients with wasted interossei have shown that hammer toes are inevitably apparent when visible atrophy is present.
Upward rotation of the forefoot: extension of the m-p joints eventually leads to upward rotation of the entire forefoot. This can be quantified and tracked over time by placing a rigid ruler against the forefoot under the second toe so that it extends below the heel. The distance from the heel to the ruler can then be measured with a second ruler, perpendicular to the first.
Distal migration of the plantar metatarsal fat pads: normally these fat pads are thick enough under the metatarsal heads that they can be pinched by the examiner. Over time, weight bearing at these prominent sites will cause distal migration of fat so that it can no longer be pinched over the metatarsal heads but instead can be pinched more distally.
Weak extension of the hallux longus (great toe): normally the strengths upon extension and flexion of the toe are approximately equal (balanced). When the lumbricals are weakened, extension from the rest position may weaken because the toe is already fully extended. Weak flexion is also possible. This can be readily discerned by offering passive resistance to both directions of motion and estimating the force of each.
Cock-up deformity of the hallux longus with prominent extensor tendon: the impaired flexion at rest can cause the distal end of this toe to be visibly higher than the other toes. When this occurs, the extensor tendon of this toe is usually visibly prominent.
High arch: this feature is common in patients with intrinsic minus feet but cannot be attributed directly to atrophy of interossei. It clearly relates to tightening of the plantar fascia. The fascia then acts like a bowstring to flex the bones of the longitudinal arch. The fascia may be stretched by the upward rotation of the forefoot. It may also be shortened by glycation, as found in the palmer tendons of Duputreyn’s Contracture.
Xerotic skin: inevitably seen in individuals with the intrinsic minus deformity. Dry skin is secondary to another condition, sympathetic neuropathy.
The above complex of visible and palpable signs is based on the observation of many patients over >20 years at a university-affiliated clinic devoted to foot pathology in a major New York City hospital.
References
Address correspondence to Richard K. Bernstein, MD, FACE, FACN, CWS, New York Diabetes Center, 1160 Greacen Point Rd., Mamaroneck, NY 10543-4606. E-mail: [email protected].
