Default mode network disruption secondary to a lesion in the anterior thalamus.
David T Jones, Farrah J Mateen, Claudia F Lucchinetti, Clifford R Jack, Kirk M Welker
Archives of Neurology October 11, 2010 DOI: 10.1001/archneurol.2010.259 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | A 40-year-old man with multiple sclerosis and acute-onset cognitive symptoms, compared with 10 cognitively normal controls |
| Duration | Symptoms persisted at 7-month follow-up |
| Topics | Default mode network |
| Keywords | Thalamus Neural pathways Humans Multiple sclerosis Amnesia Acute disease Diagnosis, differential Magnetic resonance imaging Brain mapping Attention Cognition disorders Adult Male |
| Key findings | The authors report that a large gadolinium-enhancing multiple sclerosis plaque in the left anterior thalamus was associated with asymmetric disruption of the posterior cingulate portion of the default mode network ipsilateral to the lesion in a patient with pure cognitive dysfunction. They propose that such altered resting-state connectivity may underlie cognitive symptoms in neurologic disease and provides lesional evidence of default mode network circuitry involving the circuit of Papez. |
Abstract
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.
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