Archives of neurology · 2010
Default mode network disruption secondary to a lesion in the anterior thalamus.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Jones David T, Mateen Farrah J, Lucchinetti Claudia F, Jack Clifford R, Welker Kirk M
Аннотация
OBJECTIVE: To describe the neuroanatomical correlations of an isolated lesion in the anterior thalamus using functional imaging in a 40-year-old man with multiple sclerosis.
DESIGN: Case report with 10 cognitively normal controls.
SETTING: Mayo Clinic, Rochester, Minnesota.
PATIENT: A 40-year-old man with a 2-week course of acute-onset amnesia, abulia, poor concentration, hypersomnolence, and reclusiveness.
INTERVENTION: Functional magnetic resonance imaging.
RESULTS: Magnetic resonance imaging demonstrated a large gadolinium-enhancing plaque in the left anterior thalamus and other demyelinating plaques in the subcortical and periventricular white matter, consistent with the diagnosis of multiple sclerosis. His symptoms persisted at the 7-month follow-up. The patient's resting state functional magnetic resonance image demonstrated an asymmetric disruption of the posterior cingulate portion of the default mode network ipsilateral to the left thalamic lesion.
CONCLUSIONS: A large multiple sclerosis plaque in the deep gray matter altered the resting state functional connectivity in a patient presenting with pure cognitive dysfunction. Such altered connectivity may underlie cognitive symptoms in neurologic disease. In addition, this case provides lesional evidence of default mode network circuitry involving the pathways of the circuit of Papez.
DESIGN: Case report with 10 cognitively normal controls.
SETTING: Mayo Clinic, Rochester, Minnesota.
PATIENT: A 40-year-old man with a 2-week course of acute-onset amnesia, abulia, poor concentration, hypersomnolence, and reclusiveness.
INTERVENTION: Functional magnetic resonance imaging.
RESULTS: Magnetic resonance imaging demonstrated a large gadolinium-enhancing plaque in the left anterior thalamus and other demyelinating plaques in the subcortical and periventricular white matter, consistent with the diagnosis of multiple sclerosis. His symptoms persisted at the 7-month follow-up. The patient's resting state functional magnetic resonance image demonstrated an asymmetric disruption of the posterior cingulate portion of the default mode network ipsilateral to the left thalamic lesion.
CONCLUSIONS: A large multiple sclerosis plaque in the deep gray matter altered the resting state functional connectivity in a patient presenting with pure cognitive dysfunction. Such altered connectivity may underlie cognitive symptoms in neurologic disease. In addition, this case provides lesional evidence of default mode network circuitry involving the pathways of the circuit of Papez.