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Clinical short communication| Volume 446, 120577, March 15, 2023

Secondary dystonia following parenchymal brain tumors

  • José Fidel Baizabal-Carvallo
    Correspondence
    Corresponding author at: Ave León 428, Jardines del Moral, León, Guanajuato 37320, Mexico.
    Affiliations
    Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA

    Department of Sciences and Engineering, University of Guanajuato, León, Mexico
    Search for articles by this author
  • Joseph Jankovic
    Affiliations
    Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA
    Search for articles by this author
Published:January 31, 2023DOI:https://doi.org/10.1016/j.jns.2023.120577

      Highlights

      • Secondary dystonia may follow in patients with parenchymal brain tumors.
      • Hemidystonia is the most common presentation in patients with brain tumors.
      • Dystonia developed in patients with slow growth tumors (WHO I or II).
      • Basal ganglia, thalamus and cortex were the most common sites of brain tumors with dystonia.
      • Dystonia may improve, persist, re-emerge or develop following treatment of brain tumors.

      Abstract

      Background

      Secondary dystonia has been associated with diverse etiologies. Dystonia associated with brain tumors has not been well characterized.

      Objectives

      To characterize dystonia and relationship with parenchymal brain tumors.

      Methods

      We present six patients (1.03%) with dystonia related to parenchymal brain tumors, among 580 screened cases.

      Results

      Contralateral hemidystonia was observed in four cases, followed by focal limb (n = 1) and cervical dystonia (n = 1). Dystonia presented during the phase of tumor growth in four cases, and following tumor treatment in two, one case had re-emergent dystonia. Tumors were low-grade (WHO I or II) and located in the basal ganglia (n = 3), cortical areas (n = 2), thalamus (n = 1) and cerebral peduncle (n = 1).

      Conclusions

      Secondary dystonia may be caused by brain tumors in diverse locations including basal ganglia, cortex and thalamus. It may be the presenting symptom of brain tumor or follow surgical resection combined with ancillary therapy.

      Keywords

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      References

        • Albanese A.
        • Bhatia K.
        • Bressman S.B.
        • et al.
        Phenomenology and classification of dystonia: a consensus update.
        Mov Disord. 2013; 28: 863-873
        • Krauss J.K.
        • Nobbe F.
        • Wakhloo A.K.
        • Mohadjer M.
        • Vach W.
        • Mundinger F.
        Movement disorders in astrocytomas of the basal ganglia and the thalamus.
        J Neurol Neurosurg Psychiatry. 1992; 55: 1162-1167
        • Chuang C.
        • Fahn S.
        • Frucht S.J.
        The natural history and treatment of acquired hemidystonia: report of 33 cases and review of the literature.
        J Neurol Neurosurg Psychiatry. 2002; 72: 59-67
        • Scott B.L.
        • Jankovic J.
        Delayed-onset progressive movement disorders after static brain lesions.
        Neurology. 1996; 46: 68-74
        • Krasovsky T.
        • Bar O.
        • Nachshon U.
        • Livny A.
        • Tsarfaty G.
        • Brezner A.
        • Landa J.
        Despite dystonia: natural history of delayed-onset pediatric secondary dystonia.
        Brain Inj. 2019; 33: 952-958
        • Przedborski S.
        • Kostic V.N.
        • Burke R.E.
        Delayed-onset dyskinesias.
        Neurology. 1996; 47: 1358-1359
        • Ruge D.
        • Liou L.M.
        • Hoad D.
        Improving the potential of neuroplasticity.
        J Neurosci. 2012; 32: 5705-5706
        • Brüggemann N.
        Contemporary functional neuroanatomy and pathophysiology of dystonia.
        J Neural Transm (Vienna). 2021; 128: 499-508
        • Jinnah H.A.
        • Neychev V.
        • Hess E.J.
        The anatomical basis for dystonia: the motor network model.
        Tremor Other Hyperkinet Mov (N Y). 2017; 7: 506
        • Corp D.T.
        • Joutsa J.
        • Darby R.R.
        • et al.
        Network localization of cervical dystonia based on causal brain lesions.
        Brain. 2019; 142: 1660-1674
        • Conte A.
        • Rocchi L.
        • Latorre A.
        • Belvisi D.
        • Rothwell J.C.
        • Berardelli A.
        Ten-year reflections on the neurophysiological abnormalities of focal dystonias in humans.
        Mov Disord. 2019; 34: 1616-1628
        • Mantel T.
        • Meindl T.
        • Li Y.
        • et al.
        Network-specific resting-state connectivity changes in the premotor-parietal axis in writer’s cramp.
        Neuroimage Clin. 2017; 17: 137-144
        • Shakkottai V.G.
        • Batla A.
        • Bhatia K.
        • et al.
        Current opinions and areas of consensus on the role of the cerebellum in dystonia.
        Cerebellum. 2017; 16: 577-594
        • Neychev V.K.
        • Fan X.
        • Mitev V.I.
        • Hess E.J.
        • Jinnah H.A.
        The basal ganglia and cerebellum interact in the expression of dystonic movement.
        Brain. 2008; 131: 2499-2509
        • Ceballos-Baumann A.O.
        • Passingham R.E.
        • Marsden C.D.
        • Brooks D.J.
        Motor reorganization in acquired hemidystonia.
        Ann Neurol. 1995; 37: 746-757
        • Wijemanne S.
        • Jankovic J.
        Hemidystonia-hemiatrophy syndrome.
        Mov Disord. 2009; 24: 583-589
        • Pettigrew L.C.
        • Jankovic J.
        Hemidystonia: a report of 22 patients and a review of the literature.
        J Neurol Neurosurg Psychiatry. 1985; 48: 650-657
        • Münchau A.
        • Mathen D.
        • Cox T.
        • Quinn N.P.
        • Marsden C.D.
        • Bhatia K.P.
        Unilateral lesions of the globus pallidus: report of four patients presenting with focal or segmental dystonia.
        J Neurol Neurosurg Psychiatry. 2000; 69: 494-498
        • Narbona J.
        • Obeso J.A.
        • Tuñon T.
        • Martinez-Lage J.M.
        • Marsden C.D.
        Hemi-dystonia secondary to localised basal ganglia tumour.
        J Neurol Neurosurg Psychiatry. 1984; 47: 704-709
        • LeDoux M.S.
        • Brady K.A.
        Secondary cervical dystonia associated with structural lesions of the central nervous system.
        Mov Disord. 2003; 18: 60-69
        • Pandey S.
        • Jain S.
        Secondary cervical dystonia and Titubatory head tremor.
        Mov Disord Clin Pract. 2018; 6: 179-180
        • Patel N.
        • Hanfelt J.
        • Marsh L.
        • Jankovic J.
        • Members of the Dystonia Coalition
        Alleviating manoeuvres (sensory tricks) in cervical dystonia.
        J Neurol Neurosurg Psychiatry. 2014; 85: 882-884
        • Berlot R.
        • Bhatia K.P.
        • Kojović M.
        Pseudodystonia: a new perspective on an old phenomenon.
        Parkinsonism Relat Disord. 2019; 62: 44-50
        • Krauss J.K.
        • Braus D.F.
        • Mohadjer M.
        • Nobbe F.
        • Mundinger F.
        Evaluation of the effect of treatment on movement disorders in astrocytomas of the basal ganglia and the thalamus.
        J Neurol Neurosurg Psychiatry. 1993; 56: 1113-1118