RESUMEN
The dorsolateral prefrontal cortex (DLPFC) is involved in the preparation of saccadic eye movements. Lesion studies and functional magnetic resonance imaging (fMRI) studies suggest that the human DLPFC is located in area 46 of Brodmann. The DLPFC has direct connections with the main cortical ocular motor areas, that is with the frontal eye field (FEF) and the supplementary eye field (SEF) in the frontal lobe; with several (associative, attentional, and motor) areas in the posterior parietal cortex (PPC), including the parietal eye field (PEF); with the cingulate eye field in the anterior cingulate cortex; and directly downstream with the superior colliculus in the brainstem. Lesion and fMRI studies using the antisaccade paradigm have shown that the DLPFC is involved in the inhibition of unwanted reflexive saccades (triggered toward the target by the PEF), whereas the triggering of correct intentional antisaccades (made in the direction opposite to the target) may depend mainly upon the FEF. The DLPFC also controls short-term spatial working memory involved in memory-guided saccades, as shown by lesion and transcranial magnetic stimulation (TMS) studies. By contrast, medium-term spatial memory (after 25 s) may be controlled by the medial temporal cortex (MTC). Recently, TMS studies have suggested that the transmission of memorized information from the integrative parietal areas (PPC) to the MTC is performed via both an indirect pathway comprising the DLPFC (i.e., transmission in series) and a direct pathway bypassing the DLPFC (i.e., transmission in parallel). Furthermore, the DLPFC is involved in the preparation of predictive saccades (i.e., saccades made before the appearance of an expected target) and saccade sequences, and, therefore, also controls some aspects of temporal working memory. Lastly, the involvement of the DLPFC has recently been reported in tasks comprising a target selection or a directional decision to make for the forthcoming saccade. These different functions suggest that the DLPFC plays a major role in the decisional processes governing ocular motor behavior.
Asunto(s)
Nervio Oculomotor/fisiología , Corteza Prefrontal/fisiología , Movimientos Sacádicos/fisiología , Percepción Visual/fisiología , Animales , Mapeo Encefálico , Lateralidad Funcional , Haplorrinos , Humanos , Memoria , Estimulación Luminosa , Corteza Prefrontal/anatomía & histologíaRESUMEN
Exploration of ocular motricity can be helpful for diagnosis in certain parkinsonian syndromes. Oculomotricity is perturbed in Parkinson's disease (PD) and in multiple system atrophy (MSA). The minimal anomalies, sometimes observed in these conditions, both clinically and on oculomotor recordings, cannot contribute significantly to diagnosis. In corticobasal degeneration (CBD), infraclinical oculomotor anomalies can be identified on oculomotor recordings and are relatively specific to atypical parkinsonian syndrome: particularly long latency of ocular saccades related to posterior parietal involvement. The most significant contribution is observed for progressive supanuclear palsy (PSP) where the oculomotor anomalies are evident at clinical examination and are even the cardinal signs of the condition: particularly paralysis of vertical ocular saccades (downbeat and upbeat) or downbeat saccades, ocular pursuit also being perturbed but not reflex movements (preservation of oculocephalic reflexes). This dissociation between palsy of saccade and pursuit movements and preservation of oculocephalic reflexes is the sign of the supranuclear origin of the oculomotor disorder in PSP. In early stage PSP before clinical expression, requiring oculomotor recordings to be recognized, it is relatively specific in the context of degenerative parkinsonian degeneration. PSP also involves other less specific anomalies such as a perturbation of the antisaccade movements (related to a frontal syndrome), anomalous ocular pursuit (becoming saccadic) and presence of square wave. A rigorous clinical examination of oculomotor function at a more advanced stage of PSP, or oculomotor recordings at an early stage of PSP or CBD, can thus contribute significantly to the diagnosis of both conditions.
Asunto(s)
Trastornos de la Motilidad Ocular/diagnóstico , Trastornos Parkinsonianos/etiología , Ganglios Basales/patología , Corteza Cerebral/patología , Diagnóstico Diferencial , Electrooculografía/métodos , Humanos , Degeneración Nerviosa/patología , Trastornos de la Motilidad Ocular/fisiopatología , Trastornos Parkinsonianos/patología , Trastornos Parkinsonianos/fisiopatología , Movimientos Sacádicos/fisiología , Parálisis Supranuclear Progresiva/diagnóstico , Parálisis Supranuclear Progresiva/patología , Parálisis Supranuclear Progresiva/fisiopatologíaRESUMEN
Our knowledge of the cortical control of saccadic eye movements (saccades) in humans has recently progressed mainly because of lesion and transcranial magnetic stimulation (TMS) studies, but also because of functional imaging. It is now well known that the frontal eye field is involved in the control of intentional saccades, the parietal eye field in that of reflexive saccades, the supplementary eye field (SEF) in the initiation of motor programs comprising saccades, the pre-SEF in the learning of these programs, and the dorsolateral prefrontal cortex (DLPFC) in saccade inhibition, prediction and spatial working memory. Saccades may also be used as a convenient model of motricity to study general cognitive processes such as motivation and spatial memory. Thus, it has been shown that the posterior part of the anterior cingulate cortex, called the cingulate eye field, is involved in motivation and the preparation of all intentional saccades, but not in reflexive saccades. Recently, our understanding of the cortical control of spatial memory has noticeably progressed by using the simple visuo-oculomotor model represented by the memory-guide saccade paradigm, in which a single saccade is made to the remembered position of a unique visual item presented a while before. Transcranial magnetic stimulation studies have determined that after a brief stage of spatial integration in the posterior parietal cortex (inferior to 300 ms), short-term spatial memory (i.e., up to 15-20 seconds) is controlled by the DLPFC. Behavioral and lesion studies have shown that medium-term spatial memory (between 15 and 20 seconds and a few minutes) is specifically controlled by the parahippocampal cortex, before long-term memorization (i.e., after a few minutes) in the hippocampal formation. These different but complementary study methods used in humans have thus contributed to a better understanding of both eye movement physiology and general cognitive processes preparing motricity as whole.