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- Publisher
- Wiley
- Copyright
- Copyright © 2013 Wiley Periodicals, Inc.
- ISSN
- 0148-639X
- eISSN
- 1097-4598
- DOI
- 10.1002/mus.23796
- pmid
- 23532972
- Publisher site
- See Article on Publisher Site
Abstract
A 30‐year‐old man presented with a 2‐year history of painless involuntary muscle “twitches” affecting the instep of his right foot. There was no causative trigger nor any consequent functional deficit. He was not taking regular medications and did not smoke or drink excess alcohol. There was no family history of neuromuscular disease. Neurological examination was normal except for conspicuous spontaneous, tonic, continuous, and irregular muscle activity in the instep of his right foot with wrinkling of overlying skin and repetitive flexion of his right great toe (see video online). This movement was not distractible nor entrainable. The clinical impression was that of a hitherto unreported flexor hallucis brevis (FHB) muscle spasm; a condition that would be analogous to palmaris brevis spasm syndrome in the hand. Routine blood tests were unremarkable. The absence of structural pathology in the distribution of the medial plantar neurovascular bundle (which supplies the FHB muscle) was confirmed by normal ankle and foot radiographs plus an MRI scan. Electromyography showed high‐frequency motor unit potential discharges with normal duration, amplitude, and morphology. These were transient, spontaneous, and irregularly recursive. They exclusively affected the right FHB muscle. Other lower limb muscles sampled (including gastrocnemius and tibialis anterior) were electrically silent during the spasmodic episodes. Motor and sensory nerve conduction studies were normal, specifically in the tibial nerve, and F‐wave latencies were normal. Peripheral nerve electrophysiology thus excluded the possibility of an underlying entrapment neuropathy (tarsal tunnel syndrome). To exclude the remote possibility of focal motor seizures we performed electroencephalography, which was normal. We concluded that this condition was hitherto unreported FHB spasm. DISCUSSION The FHB muscle arises from the medial aspect of the cuboid bone, the third cuneiform, and the prolongation of the tibialis posterior tendon. It divides into 2 portions, which insert into the medial and lateral sides of the base of the first phalanx of the great toe. FHB is innervated by the medial plantar nerve, which is the larger of 2 terminal divisions of the tibial nerve. The condition we describe may result from entrapment of the first branch of the medial plantar nerve where it pierces the plantar fascia on the way to FHB. It likely resembles other focal muscular hyperactivity syndromes, including palmaris brevis syndrome, focal dystonia–blepharospasm, and hemifacial spasm. Typically, these are benign conditions involving spontaneous tonic contractions of a single muscle group causing “dimpling” in the skin superficial to the affected muscle. There are usually no specific triggers. The spasms are not under voluntary control, but they are exacerbated by stress and alleviated by rest. The extent to which motor unit potential size or recruitment pattern determine susceptibility to develop these conditions has yet to be established. We propose that this spectrum of disorders includes blepharospasm and hemifacial spasm, hence providing some rationale for using botulinum toxin therapeutically. In our patient, FHB could be targeted if the symptoms progress to become functionally incapacitating. Rickie Patani, MRCP, PhD 1,2,3 Nizar Muhammed, FRCP, MD 1 Abhijit Chaudhuri, FRCP, PhD 1 1 Essex Centre for Neurological Sciences, Queen's Hospital, Essex, UK 2 Anne Mclaren Laboratory for Regenerative Medicine, University of Cambridge, Cambridge, UK 3 Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
Journal
Muscle and Nerve – Wiley
Published: Jun 1, 2013
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