Intrinsic Minus Foot

The term intrinsic minus foot was first used by Heinz I. Lippman, MD, in 1976. The term refers to a higher arched foot (pes cavus) with wasting of the intrinsic muscles of the foot that can occur in those with diabetes mellitus and neuropthy.

The lumbrical muscles are typically those first affected by the neuropathy and as they begin to atrophy some characteristic changes are noted in the foot. These changes associated with the intrinsic minus foot are usually described as:

  • a clawing of the toes and an associated plantar flexion of the metatarsals giving the foot a higher arched appearance and a plantar prominence of the metatarsal heads. 30-40% of those with diabetes have been reported has having claw toes.
  • with the clawing of the toes, the protective plantar fad pad migrates forward exposing the metatarsal heads to increased pressure.
  • this clawing of the toes, plantarflexion of the metatarsals and that distal migration of the fat pad leads to increased pressure and the appearance of pressure lesions (eg plantar calluses and corns) on the plantar forefoot and on the apex and dorsum of the toes. Claw toes in diabetes is a documented risk factor for diabetic foot ulceration.
  • a loss of bulk in the arch from the atrophy of the muscles.
  • muscle strength testing typically shows a developing weakness and neurological assessment shows the neurological changes of the neuropathy.
  • the intrinsic minus foot also tens to be much stiffer due to the limited joint mobility (LJM) that develops in diabetes.

There is no definitive experimental data or any prospective study supporting this model or mechanism of the intrinsic minus foot.

A similar foot develops during the neurological changes that occur in Charcot-Marie-Tooth disease.

However, Bus et al (2009) showed using MRI on 20 neuropathic diabetic patients, 10 with claw toe deformity and 10 with normally aligned toes that there was no intrinsic muscle atrophy nor muscle imbalance difference between the two groups; thou they did confirm the existence of the muscle atrophy. This does question the above model of the intrinsic minus foot and the mechanism by which it may develop. They concluded:

In summary, our results suggest that the role of intrinsic muscle atrophy and muscle imbalance in explaining the presence of claw toe deformity in the diabetic foot may not be as straightforward as widely believed. These muscle factors may not be primary or solely responsible for the development of claw toe deformity in diabetes. Other (predisposing) internal or external factors may be (more) important contributors, either in causing toe deformity or in preventing the establishment of a clear relationship between muscle atrophy and toe deformity.

In contrast, Kimura et al (2020) reported that the group with concurrent neuropathy and claw toes did have a thicker mean plantar aponeurosis (p < 0.006) and may have had less mean intrinsic muscle volume (p = 0.083); concluding that:

Subjects with concurrent neuropathy and claw toe deformity were associated with the smallest intrinsic foot muscle volumes and the thickest plantar aponeuroses. Intrinsic muscle atrophy and plantar aponeurosis thickening may be related to the development of claw toes in the presence of neuropathy.

Taylor et al (1998) reported on a link between a rupture of the plantar fascia and clawing of the toes in diabetes which could be an alternative mechanism to explain the appearance that occurs in the intrinsic minus foot.


  • During the barefoot running fad of around 2009-2013 a lot of claims got made by fanatical supporters of barefoot running without any evidence that running shoes weaken muscles and lead to a flat or ‘overpronated‘ foot. The concept of the intrinsic minus foot would tend to indicate that if running shoes did weaken the muscles, then that would lead to a higher arch foot.
  • The term ‘intrinsic minus foot’ does not appear to be used much now; or at least used less often than previously.

Related Pages:
Muscle strength and arch height

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