Article Text

Hemifacial spasm
  1. PETER J JANNETTA,
  2. AMIN KASSAM
  1. Department of Neurological Surgery, School of Medicine, University of Pittsburgh, PA, USA
    1. R PEGO REIGOSA

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      We have looked with interest at the scan of a patient with hemifacial spasm by Reigosa and Rios.1 Indeed, this is a very nice MRI which shows an arterial loop and the internal auditory meatus. However, this loop is not the cause of hemifacial spasm.

      Typical hemifacial spasm, which begins in the orbicularis oculi and gradually progresses down the face, is caused by a blood vessel on the non-fascicular portion of the facial nerve on the caudal or anterior aspect, including the intrapontine nerve. Atypical hemifacial spasm, which starts in the buccal muscles and progresses up the face, is caused by a blood vessel on the posterior or rostral side of the nerve. This is much less common. The compression is also at the brainstem. A distal artery, as shown in the scan, does not cause hemifacial spasm. The syllogism that Reigosa and Rios bring out—namely, that botulinum toxin helped and that this picture showed the pathology, is inadequate. They do not have a completed explanation.

      This patient’s spasm will recur because the cause has not been treated. The spasm has an excellent chance of responding to a microvascular decompression of the facial nerve performed by a neurosurgeon who has experience in the nuances of the operative procedure.

      Nevertheless, Reigosa and Rios have shown a beautiful scan.

      References

      Pego Reigosa replies:

      We thank Jannetta and Kassam for their interest in our article.1-1 We think that the vascular loop that appears in the MR image is indeed the cause of the hemifacial spasm of our patient, as it is the only abnormal finding of the neuroimaging studies performed. Furthermore, we did not find compression of the nerve at other levels where it is more often encountered, as is the caudal aspect of the VII cranial nerve next to the pons.

      Moreover, it is evident that the hemifacial spasm will reappear or recur. For this reason, the patient is receiving local botulinum toxin, with an excellent response. This treatment was chosen because its secondary effects are scarce and limited in time, and it is beneficial for a great proportion of patients. Also, systemic complications have not been described.1-2 Undoubtly, it is a symptomatic treatment based on the blockade of neuromuscular transmision. With respect to surgery, microvascular decompression is an excellent treatment when it is performed by an experienced team,1-3although it poses potential complications and sequelae. Many patients, as in our case, are not willing to undergo such risks. For these reasons, we think that the treatment of choice in our patient is local injection of botulinum toxin.

      References

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