Akinetic mutism after fourth ventricle choroid plexus papilloma: Treatment with a dopamine agonist


Caner H., Altinörs N., Benli S., ÇALIŞANELLER A. T., Albayrak A.

Surgical Neurology, cilt.51, sa.2, ss.181-184, 1999 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 51 Sayı: 2
  • Basım Tarihi: 1999
  • Doi Numarası: 10.1016/s0090-3019(98)00120-7
  • Dergi Adı: Surgical Neurology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.181-184
  • Anahtar Kelimeler: akinetic mutism, choroid plexus papilloma, dopamine agonists, posterior fossa
  • Sağlık Bilimleri Üniversitesi Adresli: Evet

Özet

BACKGROUND: Akinetic mutism is a behavioral state wherein a patient seems to be awake but does not move or speak. Several patients are reported to have developed mutism after posterior fossa surgery. We present a patient who developed akinetic mutism after total excision of a choroid plexus papilloma of the fourth ventricle, and who was treated with bromocriptine. CASE DESCRIPTION: An 18-year-old woman was admitted with akinetic mutism, which had developed 6 days after posterior fossa surgery. She had no neurologic deficit in the first 5 days after surgery and could communicate with her family. Despite antioedematous therapy and daily lumbar punctures to drain cerebrospinal fluid, there was no clinical improvement after she entered the akinetic mute state. Brain magnetic resonance revealed ventriculomegaly; brain single photon emission computed tomography revealed bilateral reduction of perfusion in the frontal region. Because daily lumbar drainage did not result in clinical improvement, shunt placement was not considered. Bromocriptine therapy was begun at a dose of 2 x 2.5 mg; 24 hours later, the patient started to speak and move her upper extremities. Further improvement occurred over the following week when the dose was increased to 3 x 2.5 mg. Bromocriptine was replaced with a placebo to determine whether the neurologic improvement was caused by the medicine. The patient's neurologic status deteriorated progressively; therefore, bromocriptine was restarted and she was discharged from the hospital. During the 6 months of follow-up, the patient has remained in good health. CONCLUSIONS: The etiology of akinetic mutism is not clear. Monoaminergic pathways, particularly dopaminergic cell groups, are most probably involved in this syndrome, because bromocriptine has a dramatic effect on these patients, as demonstrated in our case.