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.
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.
Authors: Scott D Z Eggers; Anja K E Horn; Sigrun Roeber; Wolfgang Härtig; Govind Nair; Daniel S Reich; R John Leigh Journal: Ann N Y Acad Sci Date: 2015-02-26 Impact factor: 5.691
Authors: Scott D Z Eggers; Anja K E Horn; Sigrun Roeber; Wolfgang Härtig; Govind Nair; Daniel S Reich; R John Leigh Journal: PLoS One Date: 2015-07-02 Impact factor: 3.240