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Trastorno de la marcha del nivel superior como forma de presentación de una parálisis supranuclear progresiva: descripción de un vídeo caso

INTRODUCTION. Frontal gait disorder/gait apraxia is a higher-order motor deficit with various causes, characterized by difficulties with gait initiation, such as freezing or ignition failure. We aimed to report a patient who presented with progressive higher-level gait disorder and fall episodes as...

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Detalles Bibliográficos
Autores principales: Ghosh, Ritwik, León-Ruiz, Moisés, Dubey, Souvik, Chakraborty, Arkaprava, Benito-León, Julián
Formato: Online Artículo Texto
Lenguaje:English
Publicado: EVIDENZE 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662191/
http://dx.doi.org/10.33588/rn.7704.2022393
Descripción
Sumario:INTRODUCTION. Frontal gait disorder/gait apraxia is a higher-order motor deficit with various causes, characterized by difficulties with gait initiation, such as freezing or ignition failure. We aimed to report a patient who presented with progressive higher-level gait disorder and fall episodes as the initial manifestations of progressive supranuclear palsy (PSP). Patient data were obtained from medical records from the Department of General Medicine, Burdwan Medical College & Hospital (Burdwan, West Bengal, India). CASE REPORT. A 58-year-old previously healthy woman presented with a gait disorder and fall episodes. Detailed neurological examination highlighted characteristic facial appearance (wide-eyed staring, furrowing of the forehead with a frowning expression, and fixed expression of the lower face). She was hypokinetic-rigid with symmetrical signs and predominant axial rigidity with retrocolic trunk and neck posture. Gait examination revealed a higher-level gait pattern characterized by an exhibition of profound start hesitation requiring assistance from nearby objects/persons. Once walking was underway, steps became relatively better, but ineffective gait re-emerged when she attempted turning. She had short strides, freezing, broad stance base, disequilibrium, slow leg movement, shuffling, and loss of normal fluidity of trunk and limbs. Postural reflexes were impaired. Brain magnetic resonance imaging revealed atrophy of the midbrain, dilated aqueduct of Sylvius and third ventricle, atrophy of frontal lobes and typical hummingbird sign. Diagnosis of probable PSP was finally made. CONCLUSIONS. Several etiologies, including PSP, should be considered in appropriate clinical contexts if gait examination demonstrates a higher-order gait disorder.