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1. SPG11-related parkinsonism: Clinical profile, molecular imaging and <scp>l</scp> -dopa response

Author

Celso Dario Ramos, Ingrid Faber, Joseph H. Friedman, Charles Marques Lourenço, Juliana Pasquotto Souza, Wilson Marques, Orlando Graziani Povoas Barsottini, Celeste Montecchiani, Bárbara Juarez Amorim, Carlos Roberto Martins, José Luiz Pedroso, Marcondes C. França, Maidane Luise Maia, Iscia Lopes-Cendes, Alberto R. M. Martinez, and Antonio Orlacchio

Subjects
0301 basic medicine, medicine.medical_specialty, Hereditary spastic paraplegia, Degeneration (medical), Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Postsynaptic potential, Internal medicine, medicine, Dopamine transporter, medicine.diagnostic_test, biology, business.industry, Parkinsonism, Dopaminergic, medicine.disease, nervous system diseases, 030104 developmental biology, medicine.anatomical_structure, Neurology, Dopaminergic pathways, biology.protein, Neurology (clinical), business, 030217 neurology & neurosurgery, Emission computed tomography
Abstract

Background Molecular imaging has proven to be a powerful tool to elucidate degenerated paths in a wide variety of neurological diseases and has not been systematically studied in hereditary spastic paraplegias. Objectives To investigate dopaminergic degeneration in a cohort of 22 patients with hereditary spastic paraplegia attributed to SPG11 mutations and evaluate treatment response to l-dopa. Methods Patients and controls underwent single-photon emission computed tomography imaging utilizing 99m Tc-TRODAT-1 tracer. A single-blind trial with 600 mg of l-dopa was performed comparing UPDRS scores. Results Reduced dopamine transporter density was universal among patients. Nigral degeneration was symmetrical and correlated with disease duration and motor and cognitive handicap. No statistically significant benefit could be demonstrated with l-dopa intake during the trial. Conclusion Disruption of presynaptic dopaminergic pathways is a widespread phenomenon in patients with SPG11 mutations, even in the absence of parkinsonism. Unresponsiveness to treatment could be related to postsynaptic damage that needs to be further investigated.

Published
2018
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2. SPG11-related parkinsonism: Clinical profile, molecular imaging and l-dopa response

Author

Ingrid, Faber, Alberto Rolim Muro, Martinez, Carlos Roberto, Martins, Maidane Luise, Maia, Juliana Pasquotto, Souza, Charles Marques, Lourenço, Wilson, Marques, Celeste, Montecchiani, Antonio, Orlacchio, Jose Luiz, Pedroso, Orlando Graziani Povoas, Barsottini, Celso Darío, Ramos, Íscia, Lopes-Cendes, Joseph H, Friedman, Bárbara Juarez, Amorim, and Marcondes Cavalcante, França

Subjects
Adult, Male, Tomography Scanners, X-Ray Computed, Neuropsychological Tests, Statistics, Nonparametric, Antiparkinson Agents, Cohort Studies, Levodopa, Young Adult, Parkinsonian Disorders, Humans, Single-Blind Method, hereditary spastic paraplegia, dopamine transporter, parkinsonism, Tomography, Emission-Computed, Single-Photon, Dopamine Plasma Membrane Transport Proteins, SPG11 mutations, Mental Disorders, Brain, Proteins, Organotechnetium Compounds, Middle Aged, Mutation, Female, Cognition Disorders, Tropanes
Abstract

Molecular imaging has proven to be a powerful tool to elucidate degenerated paths in a wide variety of neurological diseases and has not been systematically studied in hereditary spastic paraplegias.To investigate dopaminergic degeneration in a cohort of 22 patients with hereditary spastic paraplegia attributed to SPG11 mutations and evaluate treatment response to l-dopa.Patients and controls underwent single-photon emission computed tomography imaging utilizingReduced dopamine transporter density was universal among patients. Nigral degeneration was symmetrical and correlated with disease duration and motor and cognitive handicap. No statistically significant benefit could be demonstrated with l-dopa intake during the trial.Disruption of presynaptic dopaminergic pathways is a widespread phenomenon in patients with SPG11 mutations, even in the absence of parkinsonism. Unresponsiveness to treatment could be related to postsynaptic damage that needs to be further investigated.

Published
2018

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