An autosomal dominant genetically heterogeneous variant of rolandic epilepsy and speech disorder. (57/188)

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Tool use, communicative gesture and cerebral asymmetries in the modern human brain. (58/188)

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Broca's aphemia: an illustrated account of its clinico-anatomic validity. (59/188)

OBJECTIVE: To present the case of a 54-year-old man with loss of speech, but with preservation of voluntary facio-lingual motility, language and other cognitive abilities (Broca's aphemia). METHOD: Observation of patient oral communicative abilities and general behavior, neuropsychological assessment and cranial computed tomography. RESULTS: Computed tomography showed a hyperdense lesion in the subcortex of the left precentral gyrus corresponding to Brodmann's area 6 and 44. Neuropsychological assessment confirmed that the major cognitive domains were intact. CONCLUSION: Our patient reiterates the validity of Broca's aphemia as a clinico-anatomic entity allowing us to portray it for the first time in pictures. From a neurobehavioral perspective, aphemia is related to apraxia rather than to aphasia, a fact that may have hampered the full grasp of its far-reaching implications for neurology and aphasiology.  (+info)

Parietal lobe deficits in frontotemporal lobar degeneration caused by a mutation in the progranulin gene. (60/188)

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Acquired ocular motor apraxia after aortic surgery. (61/188)

PURPOSE: To describe an unusual form of acquired ocular motor apraxia. METHODS: Case reports with electronic eye movement recordings. RESULTS: Three patients had surgery to repair aortic root or arch dissections or aneurysms. A few days after surgery, all had ophthalmoplegia. Neuro-ophthalmic examination found complete absence of horizontal and vertical volitional and reflex saccades in 1 patient and slow, hypometric saccades in 2 others. However, smooth pursuit, slow phases of optokinetic nystagmus, and the vestibulo-ocular response (VOR) were intact. Fast phases of the VOR were absent in 2 patients but were intact in the other. Video and electronic eye movement recordings documented the findings. Magnetic resonance imaging (MRI) in 1 patient showed small infarcts in a cerebellar hemisphere, pons, and cerebral hemispheres. The other patients' MRIs showed no significant lesions. CONCLUSIONS: Acquired ocular motor apraxia with profoundly impaired volitional saccades after aortic surgery is a distinctive syndrome, but its pathophysiology is unclear. Studies of neurologic damage in animals and patients undergoing similar surgical procedures provide conflicting data. However, knowledge about the complex neural pathways generating saccades from animal and human studies, and detailed clinical observations, as in the patients described here, can help to determine the location of lesions. Based on the 3 cases reported here, we propose that this syndrome might be due to damage to excitatory burst and/or omnipause neurons in the brainstem or by damage to pathways from the frontal eye fields to the brainstem.  (+info)

Visuomotor tracking abilities of speakers with apraxia of speech or conduction aphasia. (62/188)

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Concepts and categories: a cognitive neuropsychological perspective. (63/188)

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Update on blepharospasm: report from the BEBRF International Workshop. (64/188)

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