Speaker: Marsel Mesulam, M.D., Northwestern University
Chair: Jeffrey Binder, Medical College of Wisconsin

Friday, October 16, 9:00 – 10:00 am, Grand Ballroom

Marsel Mesulam is Ruth Dunbar Davee Professor of Neuroscience and Director of the multidepartmental Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University’s Feinberg School of Medicine in Chicago. His research has addressed the neural connectivity of the monkey brain, the organization of human cholinergic pathways, the representation of cognitive functions by large-scale neurocognitive networks, and the neurobiology of dementias.

He has received the Potamkin Prize for Research in Pick’s, Alzheimer’s, and Related Diseases from the American Academy of Neurology, the Javits Award from the National Institute of Neurological Disease and Stroke, the Director’s Award from the McKnight Foundation, the Lishman Award from the International Neuropsychiatry Association and the Bengt Winblad Life Achievement Award from the Alzheimer’s Association. His current research focuses on the functional imaging of neurocognitive networks and on the pathophysiology of focal dementias..

Revisiting Wernicke’s Area

Wernicke’s aphasia is characterized by severe word and sentence comprehension impairments. The location of the underlying lesion site, known as Wernicke’s area, remains controversial. Questions related to this controversy were addressed in patients with primary progressive aphasia. Clinicoanatomical correlations were explored at the individual and group levels. These analyses showed that neuronal loss in temporoparietal areas traditionally included within Wernicke’s area leave single word comprehension intact and cause inconsistent impairments of sentence comprehension. The most severe sentence comprehension impairments were associated with a heterogeneous set of cortical atrophy sites variably encompassing temporoparietal components of Wernicke’s area, Broca’s area, and dorsal premotor cortex. Severe comprehension impairments for single words, on the other hand, were invariably associated with peak atrophy sites in the left temporal pole and adjacent anterior temporal cortex, a pattern of atrophy that left sentence comprehension intact. These results show that the neural substrates of word and sentence comprehension are dissociable and that a circumscribed cortical area equally critical for word and sentence comprehension is unlikely to exist anywhere in the cerebral cortex. Reports of combined word and sentence comprehension impairments in Wernicke’s aphasia come almost exclusively from patients with cerebrovascular accidents where brain damage extends into subcortical white matter. The syndrome of Wernicke’s aphasia is thus likely to reflect damage not only to the cerebral cortex but also to underlying axonal pathways, leading to strategic cortico-cortical disconnections within the language network. The results of this investigation further reinforce the conclusion that the left anterior temporal lobe, a region ignored by classic aphasiology, needs to be inserted into the language network with a critical role in the multisynaptic hierarchy underlying word comprehension and object naming.