Abstract
Objectives
Cerebellar tonsillectomy is often performed for relief of symptoms associated with Chiari type I malformation (CMI). Nonetheless, the idea of removing supposedly healthy central nervous tissue has been a source of concern for neurosurgeons. The aim of this paper is to determine the histological changes in the cerebellar tonsils of patients with a wide range of symptoms and conditions related to CMI.
Materials and methods
The cerebellar tonsils of 43 pediatric patients with CMI were sent to pathology for histological examination.
Conclusion
The cerebellar tonsils in a great majority of CMI patients can be abnormal. We suggest that the reported histological findings are secondary to injury and ischemia.
Similar content being viewed by others
References
Allen G, Chase T (2001) Induction of heat shock proteins and motor function deficits after focal cerebellar injury. Neuroscience 102:603–614
Fukuda K, Aihara N, Sagar S, Sharp F, Pitts L, Honkaniemi J (1996) Purkinje cell vulnerability to mild traumatic brain injury. J Neurotrauma 5:255–265
Genitori L, Peretta P, Nurisso C, Macinante L, Mussa F (2000) Chiari type I anomalies in children and adolescents: minimally invasive management in a series of 53 cases. Childs Nerv Syst 16:707–718
Guyotat J, Bret P, Jouanneau E, Ricci AC, Lapras C (1998) Syringomyelia associated with type I Chiari malformation. A 21-year retrospective study on 75 cases treated by foramen magnum decompression with a special emphasis on the value of tonsils resection. Acta Neurochir (Wien) 140:745–754
Koga H, Mukawa J, Nakata M, Ishikawa Y, Sakuta O, Hokama A, Terada Y (1995) Histopathological analysis of herniated cerebellar tonsils resected from the patients with Chiari type I malformation with syringomyelia (in Japanese). No To Shinkei 47:1075–1079
Lazareff J, Galarza M, Gravori T, Spinks T (2002) Tonsillectomy without craniectomy for the management of infantile Chiari I malformation. J Neurosurg 97:1018–1022
Martin LJ, Sieber FE, Traystman RJ (2000) Apoptosis and necrosis occur in separate neuronal populations in hippocampus and cerebellum after ischemia and are associated with differential alterations in metabotropic glutamate receptor signaling pathways. J Cereb Blood Flow Metab 20(1):153–167
Mautes A, Fukuda K, Noble L (1996) Cellular response in the cerebellum after midline traumatic brain injury in the rat. Neurosci Lett 214:95–98
Munshi I, Frim D, Stine-Reyes R, Weir B, Hekmatpanah J, Brown F (2000) Effects of posterior fossa decompression with and without duroplasty on Chiari Malformation-associated hydromyelia. Neurosurgery 46:1384–1390
Nishikawa M, Sakamoto H, Hakuba A, Nakanishi N, Inoue Y (1997) Pathogenesis of Chiari malformation: a morphometric study of the posterior cranial fossa. J Neurosurg 86:40–47
Norenberg M (1994) Astrocyte responses to CNS injury. J Neuropathol Exp Neurol 53:213–220
Sarna J, Hawkes R (2003) Patterned Purkinje cell death in the cerebellum. Prog Neurobiol 70:473–507
Welsh JP, Yuen G, Placantonakis DG, Vu TQ, Haiss F, O'Hearn E, Moliver ME, Aicher SA (2002) Why do Purkinje cells die so easily after global brain ischemia? Aldolase C, EAAT4, and the cerebellar contribution to posthypoxic myoclonus. Adv Neurol 89:331–359
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Pueyrredon, F., Spaho, N., Arroyave, I. et al. Histological findings in cerebellar tonsils of patients with Chiari type I malformation. Childs Nerv Syst 23, 427–429 (2007). https://doi.org/10.1007/s00381-006-0252-y
Received:
Revised:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00381-006-0252-y