| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Chang Jin Shin, Myeongho Rho, Yu Sam Won, Si On Ki. Rapid Visual Deterioration Caused by Posterior Fossa Arachnoid Cyst. Journal of Korean Neurosurgical Society. vol 59. issue 3. 2016-05-26. PMID:27226868. |
although arachnoid cysts are benign and asymptomatic lesions, patients with posterior fossa arachnoid cysts often complain of headaches, gait disturbance, and ataxia due to the local mass effects on the cerebellum. |
2016-05-26 |
2023-08-13 |
Not clear |
| S Kaja, A J Payne, E Ø Nielsen, C L Thompson, A M J M van den Maagdenberg, P Koulen, T P Snutc. Differential cerebellar GABAA receptor expression in mice with mutations in CaV2.1 (P/Q-type) calcium channels. Neuroscience. vol 304. 2016-05-24. PMID:26208839. |
ataxia is the predominant clinical manifestation of cerebellar dysfunction. |
2016-05-24 |
2023-08-13 |
mouse |
| J W Koehler, B W Newcomer, M Holland, J M Caldwel. A Novel Inherited Cerebellar Abiotrophy in a Cohort of Related Goats. Journal of comparative pathology. vol 153. issue 2-3. 2016-05-23. PMID:26184806. |
heritable cerebellar ataxias have been reported in many domestic animal species, but not, to the authors' knowledge, as a heritable condition in goats. |
2016-05-23 |
2023-08-13 |
Not clear |
| Hazael Flores-Cantu, Carlos R Camara-Lemarroy, Hector J Calderon-Hernandez, Maria A Zapata-Rivera, Jesus Z Villareal-Perez, Hector J Villareal-Velazque. Anti-GAD Antibody, Seizures, Cerebellar Ataxias and Vitiligo: A Diagnostic Challenge. Cerebellum (London, England). vol 14. issue 3. 2016-05-02. PMID:25575726. |
anti-gad antibody, seizures, cerebellar ataxias and vitiligo: a diagnostic challenge. |
2016-05-02 |
2023-08-13 |
Not clear |
| Hélio A G Teive, Walter O Arruda, Adriana Moro, Mariana Moscovich, Renato P Munho. Differential diagnosis of sporadic adult-onset ataxia: The role of REM sleep behavior disorder. Parkinsonism & related disorders. vol 21. issue 6. 2016-05-02. PMID:25899546. |
sporadic adult-onset ataxia encompasses a group of degenerative, non-hereditary disorders, including idiopathic adult-onset ataxia and the cerebellar form of multiple system atrophy. |
2016-05-02 |
2023-08-13 |
Not clear |
| Ângela Zanatta, Carolina Maso Viegas, Fernanda Hermes Hickmann, Wagner de Oliveira Monteiro, Angela Sitta, Daniela de Moura Coelho, Carmen Regla Vargas, Guilhian Leipnitz, Moacir Wajne. Ornithine In Vivo Administration Disrupts Redox Homeostasis and Decreases Synaptic Na(+), K (+)-ATPase Activity in Cerebellum of Adolescent Rats: Implications for the Pathogenesis of Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome. Cellular and molecular neurobiology. vol 35. issue 6. 2016-04-20. PMID:25772141. |
it is presumed that these pathomechanisms may contribute at least partly to explain the neuropathology of cerebellum abnormalities and the ataxia observed in patients with hhh syndrome. |
2016-04-20 |
2023-08-13 |
rat |
| Simone Carreiro Vieira Karuta, Salmo Raskin, Arnolfo de Carvalho Neto, Emerson Leandro Gasparetto, Thomas Doring, Helio Afonso Ghizoni Teiv. Diffusion tensor imaging and tract-based spatial statistics analysis in Friedreich's ataxia patients. Parkinsonism & related disorders. vol 21. issue 5. 2016-04-18. PMID:25801908. |
friedreich's ataxia (frda) is the most common hereditary ataxia and thinning of the cervical spinal cord is a consistent observation in magnetic resonance imaging (mri), although neuropathological examination in frda reveals neuronal loss in gray matter (gm) nuclei and degeneration of white matter (wm) tracts in the spinal cord, brainstem and cerebellum. |
2016-04-18 |
2023-08-13 |
Not clear |
| Sarah M Ronnebaum, Cam Patterson, Jonathan C Schisle. Emerging evidence of coding mutations in the ubiquitin-proteasome system associated with cerebellar ataxias. Human genome variation. vol 1. 2016-04-15. PMID:27081508. |
emerging evidence of coding mutations in the ubiquitin-proteasome system associated with cerebellar ataxias. |
2016-04-15 |
2023-08-13 |
human |
| Jan Cendeli. Experimental neurotransplantation treatment for hereditary cerebellar ataxias. Cerebellum & ataxias. vol 3. 2016-04-06. PMID:27047666. |
experimental neurotransplantation treatment for hereditary cerebellar ataxias. |
2016-04-06 |
2023-08-13 |
mouse |
| Jan Cendeli. Experimental neurotransplantation treatment for hereditary cerebellar ataxias. Cerebellum & ataxias. vol 3. 2016-04-06. PMID:27047666. |
there are several therapies that have been shown to affect the pathogenetic process and thereby to delay the progress of the disease in mouse models of cerebellar ataxias. |
2016-04-06 |
2023-08-13 |
mouse |
| Jan Cendeli. Experimental neurotransplantation treatment for hereditary cerebellar ataxias. Cerebellum & ataxias. vol 3. 2016-04-06. PMID:27047666. |
the second experimental therapeutic approach for hereditary cerebellar ataxias is neurotransplantation. |
2016-04-06 |
2023-08-13 |
mouse |
| M Marek, S Paus, N Allert, B Mädler, T Klockgether, H Urbach, V A Coene. Ataxia and tremor due to lesions involving cerebellar projection pathways: a DTI tractographic study in six patients. Journal of neurology. vol 262. issue 1. 2016-04-04. PMID:25287016. |
ataxia and tremor due to lesions involving cerebellar projection pathways: a dti tractographic study in six patients. |
2016-04-04 |
2023-08-13 |
human |
| M Marek, S Paus, N Allert, B Mädler, T Klockgether, H Urbach, V A Coene. Ataxia and tremor due to lesions involving cerebellar projection pathways: a DTI tractographic study in six patients. Journal of neurology. vol 262. issue 1. 2016-04-04. PMID:25287016. |
it is suspected that ataxia in these cases is due to damage of efferent or afferent pathways of the cerebellum. |
2016-04-04 |
2023-08-13 |
human |
| M Marek, S Paus, N Allert, B Mädler, T Klockgether, H Urbach, V A Coene. Ataxia and tremor due to lesions involving cerebellar projection pathways: a DTI tractographic study in six patients. Journal of neurology. vol 262. issue 1. 2016-04-04. PMID:25287016. |
we used deterministic diffusion tensor magnetic resonance imaging (dti) tractography to study the anatomical relationship between lesions causing ataxia and efferent cerebellar pathways. |
2016-04-04 |
2023-08-13 |
human |
| Wladimir Bocca Vieira de Rezende Pinto, José Luiz Pedroso, Paulo Victor Sgobbi de Souza, Marcus Vinícius Cristino de Albuquerque, Orlando Graziani Povoas Barsottin. Non-progressive cerebellar ataxia and previous undetermined acute cerebellar injury: a mysterious clinical condition. Arquivos de neuro-psiquiatria. vol 73. issue 10. 2016-03-22. PMID:26291991. |
cerebellar ataxias represent a wide group of neurological diseases secondary to dysfunctions of cerebellum or its associated pathways, rarely coursing with acute-onset acquired etiologies and chronic non-progressive presentation. |
2016-03-22 |
2023-08-13 |
Not clear |
| Wolfgang M Schmidt, S Lane Rutledge, Rebecca Schüle, Benjamin Mayerhofer, Stephan Züchner, Eugen Boltshauser, Reginald E Bittne. Disruptive SCYL1 Mutations Underlie a Syndrome Characterized by Recurrent Episodes of Liver Failure, Peripheral Neuropathy, Cerebellar Atrophy, and Ataxia. American journal of human genetics. vol 97. issue 6. 2016-03-22. PMID:26581903. |
disruptive scyl1 mutations underlie a syndrome characterized by recurrent episodes of liver failure, peripheral neuropathy, cerebellar atrophy, and ataxia. |
2016-03-22 |
2023-08-13 |
mouse |
| Wolfgang M Schmidt, S Lane Rutledge, Rebecca Schüle, Benjamin Mayerhofer, Stephan Züchner, Eugen Boltshauser, Reginald E Bittne. Disruptive SCYL1 Mutations Underlie a Syndrome Characterized by Recurrent Episodes of Liver Failure, Peripheral Neuropathy, Cerebellar Atrophy, and Ataxia. American journal of human genetics. vol 97. issue 6. 2016-03-22. PMID:26581903. |
hereditary ataxias comprise a group of genetically heterogeneous disorders characterized by clinically variable cerebellar dysfunction and accompanied by involvement of other organ systems. |
2016-03-22 |
2023-08-13 |
mouse |
| Jessica M Y Ng, Daniel Martinez, Eric D Marsh, Zhe Zhang, Eric Rappaport, Mariarita Santi, Tom Curra. Generation of a mouse model of atypical teratoid/rhabdoid tumor of the central nervous system through combined deletion of Snf5 and p53. Cancer research. vol 75. issue 21. 2016-02-25. PMID:26363008. |
notably, these double mutants exhibited at/rt development, associated with an earlier failure in granule neuron migration in the cerebellum, reduced neuronal projections in the hippocampus, degeneration of the corpus callosum, and ataxia and seizures. |
2016-02-25 |
2023-08-13 |
mouse |
| Marie Coutelier, Iulia Blesneac, Arnaud Monteil, Marie-Lorraine Monin, Kunie Ando, Emeline Mundwiller, Alfredo Brusco, Isabelle Le Ber, Mathieu Anheim, Anna Castrioto, Charles Duyckaerts, Alexis Brice, Alexandra Durr, Philippe Lory, Giovanni Stevani. A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia. American journal of human genetics. vol 97. issue 5. 2016-02-25. PMID:26456284. |
hereditary cerebellar ataxias (cas) are neurodegenerative disorders clinically characterized by a cerebellar syndrome, often accompanied by other neurological or non-neurological signs. |
2016-02-25 |
2023-08-13 |
human |
| Myriam Srour, Fadi F Hamdan, Dianalee McKnight, Erica Davis, Hanna Mandel, Jeremy Schwartzentruber, Brissa Martin, Lysanne Patry, Christina Nassif, Alexandre Dionne-Laporte, Luis H Ospina, Emmanuelle Lemyre, Christine Massicotte, Rachel Laframboise, Bruno Maranda, Damian Labuda, Jean-Claude Décarie, Françoise Rypens, Dorith Goldsher, Catherine Fallet-Bianco, Jean-François Soucy, Anne-Marie Laberge, Catalina Maftei, Kym Boycott, Bernard Brais, Renée-Myriam Boucher, Guy A Rouleau, Nicholas Katsanis, Jacek Majewski, Orly Elpeleg, Mary K Kukolich, Stavit Shalev, Jacques L Michau. Joubert Syndrome in French Canadians and Identification of Mutations in CEP104. American journal of human genetics. vol 97. issue 5. 2016-02-25. PMID:26477546. |
joubert syndrome (jbts) is a primarily autosomal-recessive disorder characterized by a distinctive mid-hindbrain and cerebellar malformation, oculomotor apraxia, irregular breathing, developmental delay, and ataxia. |
2016-02-25 |
2023-08-13 |
human |