Mirror Movements and Myelomeningocele: Report of A Single Case and Review of Literature

How to Cite This Article: IIbtihel Rébai I, Benrhouma H, Kraoua I, Drissi C, Ben Hammouda M, Gouider-khouja N. Mirror Movements and Myelomeningocele: Report of A Single Case and Review of Literature. Iran J Child Neurol. 2013 Summer;7(3):58-61. ObjectiveMirror movements (MM) have been described in several pathological conditions. Their association with neural tube defects is rare, and only 5 cases have been reported in literature to date. We report on a case of MM associated with cervical myelomeningocele, and we discuss the diffusion tensor imaging findings and the underlying mechanism. References1. Cohen LG, Meer J, Tarkka I, Bierner S, Leiderman DB,Dubinsky RM, et al. Congenital Mirror Movements. Abnormal organization of motor pathways in two patients. Brain 1991;114(Pt 1B):381-403.2. Rasmussen P. Persistent mirror movements: a clinicalstudy of 17 children, adolescents and young adults. DevMed Child Neurol 1993;35(8):699-707.3. Forget R, Boghen D, Attig E, Lamarre Y. Electromyographicstudies of congenital mirror movements. Neurology 1986;36(10):1316-22.4. Erdincler P. Cervical cord tethering and congenital mirrormovements: is it an association rather than a coincidence?Br J Neurosurg 2002;16(5):519–22.5. Odabasi Z, Gökçil Z, Kütükçü Y, Vural O, Yardim M.Mirror movements associated with cervical meningocele:case report. Minim Invas Neurosurg 1998;41(2):99–100.6. Erol FS, Topsakal C, Ozveren MF, Akdemir I, CobanogluB. Meningocele with cervical dermoid sinus tract presenting with congenital mirror movement and recurrent meningitis. Yonsei Med J 2004;45(3):568–72.7. Andrabi Y, Nejat F, El Khashab, Ashrafi MR. Mirror movement associated with neural tube defects. Neuropsychiatr Dis Treat 2008;4(6):1273–76.8. Avery LW, Rentfro CC. The Klippel–Feil syndrome. A pathological report. Arch Neurol Psychiat 1936;36:1068- 76.9. Gunderson CH, Solitaire GB. Mirror movements in patients with Klippel–Feil syndrome. Arch Neurol 1968;18(6):675–9.10. Tuch DS, Reese TG, Wiegell MR, Makris N, Belliveau JW, Wedeen VJ. High angular resolution diffusion imaging reveals intravoxel white matter fiber heterogeneity. Magn Reson Med 2002;48(4):577-82.11. Mamata H, Mamata Y, Westin CF, Shenton ME, Kikinis R, Jolesz FA, et al. High-resolution line scan diffusion tensor MR imaging of white matter fiber tract anatomy. AJNR Am J Neuroradiol 2002;23(1):67-75.12. Galléa C, Popa T, Billot S, Méneret A, Depienne C, RozeE. Congenital mirror movements: a clue to understandingbimanual motor control. J Neurol 2011;258(11):1911-9.

Astrocytoma in the Third Ventricle and Hypothalamus Presenting with Parkinsonism

Parkinsonism secondary to intracranial mass lesions usually results from compression or distortion of the basal ganglia. Secondary parkinsonism due to midbrain infiltration or compression is rare and generally associated with other neurologic signs caused by pyramidal tract and/or cranial nerve involvement. We report a case of 30-year-old woman in whom mild parkinsonism was the major clinical manifestation of an astrocytoma in the anterior third ventricle and hypothalamus. She underwent surgical resection, ventriculoperitoneal shunt and radiation therapy. All symptoms of parkinsonism were completely recovered 3 months after the treatment. Brain tumors can be manifested only by the symptoms of parkinsonism. This case emphasizes the significance of neuroimaging in the evaluation of parkinsonism

Genetic Etiology of Parkinson Disease Associated with Mutations in the SNCA, PARK2, PINK1, PARK7, and LRRK2 Genes: A Mutation Update

To date, molecular genetic analyses have identified over 500 distinct DNA variants in five disease genes associated with familial Parkinson disease; α-synuclein (SNCA), parkin (PARK2), PTEN-induced putative kinase 1 (PINK1), DJ-1 (PARK7), and Leucine-rich repeat kinase 2 (LRRK2). These genetic variants include ∼82% simple mutations and ∼18% copy number variations. Some mutation subtypes are likely underestimated because only few studies reported extensive mutation analyses of all five genes, by both exonic sequencing and dosage analyses. Here we present an update of all mutations published to date in the literature, systematically organized in a novel mutation database (http://www.molgen.ua.ac.be/PDmutDB). In addition, we address the biological relevance of putative pathogenic mutations. This review emphasizes the need for comprehensive genetic screening of Parkinson patients followed by an insightful study of the functional relevance of observed genetic variants. Moreover, while capturing existing data from the literature it became apparent that several of the five Parkinson genes were also contributing to the genetic etiology of other Lewy Body Diseases and Parkinson-plus syndromes, indicating that mutation screening is recommendable in these patient groups. Hum Mutat 31:763–780, 2010. © 2010 Wiley-Liss, Inc