Aurelio Campos-Romo
National Autonomous University of Mexico
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Publication
Featured researches published by Aurelio Campos-Romo.
Behavioral and Brain Functions | 2010
Pablo Moreno-Briseño; Rosalinda Díaz; Aurelio Campos-Romo; Juan Fernandez-Ruiz
Gender differences have been shown across many domains, and motor skills are no exception. One of the most robust findings is a significant sex difference in throwing accuracy, which reflects the advantage of men in targeting abilities. However, little is known about the basis of this difference. To try to dissect possible mechanisms involved in this difference, here we tested for gender variations in a prism adaptation throwing task. We tested 154 subjects in a visuomotor prism adaptation task that discriminates between motor performance, visuomotor adaptation and negative aftereffects. Our results corroborate mens significant better throwing accuracy, although there were no adaptation differences between genders. In contrast, women showed significant larger negative aftereffects, which could be explained by a larger contribution of spatial alignment. These results suggest that different learning mechanisms, like strategic calibration and spatial alignment, may have different contributions in men and women.
Journal of Neuroscience Methods | 2009
Aurelio Campos-Romo; Rafael Ojeda-Flores; Pablo Moreno-Briseño; Juan Fernandez-Ruiz
Parkinsons disease (PD) is a progressive neurodegenerative disorder. An experimental model of this disease is produced in nonhuman primates by the administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In this work, we put forward a new quantitative evaluation method that uses video recordings to measure the displacement, gate, gross and fine motor performance of freely moving subjects. Four Vervet monkeys (Cercopithecus aethiops) were trained in a behavioral observation hallway while being recorded with digital video cameras from four different angles. After MPTP intoxication the animals were tested without any drug and after 30 and 90 min of Levodopa/Carbidopa administration. Using a personal computer the following behaviors were measured and evaluated from the video recordings: displacement time across the hallway, reaching time towards rewards, ingestion time, number of attempts to obtain rewards, number of rewards obtained, and level of the highest shelf reached for rewards. Our results show that there was an overall behavioral deterioration after MPTP administration and an overall improvement after Levodopa/Carbidopa treatment. This demonstrates that the HALLWAY task is a sensitive and objective method that allows detailed behavioral evaluation of freely moving monkeys in the MPTP Parkinsons disease model.
Journal of the Neurological Sciences | 2014
Roberto E. Mercadillo; Victor Galvez; Rosalinda Díaz; Carlos Roberto Hernández-Castillo; Aurelio Campos-Romo; Marie-Catherine Boll; Erick H. Pasaye; Juan Fernandez-Ruiz
Spinocerebellar Ataxia Type 2 (SCA2) is a genetic disorder causing cerebellar degeneration that result in motor and cognitive alterations. Voxel-based morphometry (VBM) analyses have found neurodegenerative patterns associated to SCA2, but they show some discrepancies. Moreover, behavioral deficits related to non-cerebellar functions are scarcely discussed in those reports. In this work we use behavioral and cognitive tests and VBM to identify and confirm cognitive and gray matter alterations in SCA2 patients compared with control subjects. Also, we discuss the cerebellar and non-cerebellar functions affected by this disease. Our results confirmed gray matter reduction in the cerebellar vermis, pons, and insular, frontal, parietal and temporal cortices. However, our analysis also found unreported loss of gray matter in the parahippocampal gyrus bilaterally. Motor performance test ratings correlated with total gray and white matter reductions, but executive performance and clinical features such as CAG repetitions and disease progression did not show any correlation. This pattern of cerebellar and non-cerebellar morphological alterations associated with SCA2 has to be considered to fully understand the motor and non-motor deficits that include language production and comprehension and some social skill changes that occur in these patients.
World Neurosurgery | 2013
Rogelio Revuelta-Gutiérrez; Jaime Jesús Martínez-Anda; Juan Barges Coll; Aurelio Campos-Romo; Nadia Perez-Peña
OBJECTIVE Trigeminal neuralgia (TN) surgical treatment with microvascular decompression is highly effective and safe, but for a percentage of patients who undergo this procedure, no vascular compression is found. The purpose of this study was to evaluate the long-term efficacy with trigeminal root compression of the trigeminal nerve in patients with TN refractory to medical treatment who underwent neurosurgical management by a retrosigmoid approach of the cerebellopontine angle and were found to be negative for vascular compression. METHODS A prospective collection of clinical data on all patients with a diagnosis of idiopathic TN was conducted at our institution. A total of 277 patients with TN were treated by a keyhole retrosigmoid approach for exploration of the cerebellopontine angle between January of 2000 and August of 2010. A total of 44 patients were found to be negative for vascular compression of the trigeminal nerve; all of these patients underwent trigeminal root compression. RESULTS We found that all patients were pain free after the procedure. There was a 27% relapse in a mean time of 10 months, but 83% of these patients were adequately controlled by medical treatment, and only 17% needed a complementary procedure for pain relief. We also found that 63% of the patients complained of a partial loss of facial sensitivity, but only 1 patient presented with a corneal ulcer. There was a 6.7% rate of significant complications. CONCLUSIONS We concluded that trigeminal root compression is a safe and effective option for patients with primary TN without vascular compression.
European Journal of Neuroscience | 2013
Juan Manuel Gutierrez-Garralda; Pablo Moreno-Briseño; Marie-Catherine Boll; Consuelo Morgado-Valle; Aurelio Campos-Romo; Rosalinda Díaz; Juan Fernandez-Ruiz
Visuomotor adaptation is often driven by error‐based (EB) learning in which signed errors update motor commands. There are, however, visuomotor tasks where signed errors are unavailable or cannot be mapped onto appropriate motor command changes, rendering EB learning ineffective; and yet, healthy subjects can learn in these EB learning‐free conditions. While EB learning depends on cerebellar integrity, the neural bases of EB‐independent learning are poorly understood. As basal ganglia are involved in learning mechanisms that are independent of signed error feedback, here we tested whether patients with basal ganglia lesions, including those with Huntingtons disease and Parkinsons disease, would show impairments in a visuomotor learning task that prevents the use of EB learning. We employed two visuomotor throwing tasks that were similar, but were profoundly different in the resulting visual feedback. This difference was implemented through the introduction of either a lateral displacement of the visual field via a wedge prism (EB learning) or a horizontal reversal of the visual field via a dove prism (non‐EB learning). Our results show that patients with basal ganglia degeneration had normal EB learning in the wedge prism task, but were profoundly impaired in the reversing prism task that does not depend on the signed error signal feedback. These results represent the first evidence that human visuomotor learning in the absence of EB feedback depends on the integrity of the basal ganglia.
The Journal of Neuroscience | 2006
Juan Fernandez-Ruiz; Rosalinda Díaz; Pablo Moreno-Briseño; Aurelio Campos-Romo; Rafael Ojeda
Information about the world is often encoded in the brain as topographic maps. These internal representations are not always static but can have a dynamic nature, allowing for constant adjustments that depend on factors like experience or injury. Recently, it has been shown that areas involved in visuomotor transformations also show topographical organization. These findings suggest that it could be possible to observe plastic modifications in specific parts of the representation in response to a local perturbation that affects only a part of the space that is represented. Here, we tested this hypothesis using an adaptation paradigm with hemiprisms. Our results suggest that, initially, the system tries to modify the visuomotor transformation in the whole spatial representation; however, if feedback is available from both hemifields, the system can perform specific regional topographical realignments. The results also suggest that access to the rearranged visuomotor transformation is independent of eye position, in contrast with previous studies that found a kind of conditional learning. Also, whereas prism adaptation experiments using ballistic movements do not show intermanual transfer of learning, the topographical modification found here is available to both hands. These results provide strong evidence for rapid topographical plasticity that can modify space transformations between two different modalities.
PLOS ONE | 2015
Carlos R. Hernandez-Castillo; Victor Galvez; Roberto E. Mercadillo; Rosalinda Díaz; Aurelio Campos-Romo; Juan Fernandez-Ruiz
Background Previous studies of SCA2 have revealed significant degeneration of white matter tracts in cerebellar and cerebral regions. The motor deficit in these patients may be attributable to the degradation of projection fibers associated with the underlying neurodegenerative process. However, this relationship remains unclear. Statistical analysis of diffusion tensor imaging enables an unbiased whole-brain quantitative comparison of the diffusion proprieties of white matter tracts in vivo. Methods Fourteen genetically confirmed SCA2 patients and aged-matched healthy controls participated in the study. Tract-based spatial statistics were performed to analyze structural white matter damage using two different measurements: fractional anisotropy (FA) and mean diffusivity (MD). Significant diffusion differences were correlated with the patients ataxia impairment. Results Our analysis revealed decreased FA mainly in the inferior/middle/superior cerebellar peduncles, the bilateral posterior limb of the internal capsule and the bilateral superior corona radiata. Increases in MD were found mainly in cerebellar white matter, medial lemniscus, and middle cerebellar peduncle, among other regions. Clinical impairment measured with the SARA score correlated with FA in superior parietal white matter and bilateral anterior corona radiata. Correlations with MD were found in cerebellar white matter and the middle cerebellar peduncle. Conclusion Our findings show significant correlations between diffusion measurements in key areas affected in SCA2 and measures of motor impairment, suggesting a disruption of information flow between motor and sensory-integration areas. These findings result in a more comprehensive view of the clinical impact of the white matter degeneration in SCA2.
Journal of The International Neuropsychological Society | 2016
Carlos R. Hernandez-Castillo; Israel Vaca-Palomares; Galvez; Aurelio Campos-Romo; Rosalinda Díaz; Juan Fernandez-Ruiz
OBJECTIVES The aim of this study was to explore the relationship between cognitive and white matter deterioration in a group of participants with spinocerebellar ataxia type 2 (SCA2). METHODS Fourteen genetically confirmed participants with SCA2 and 14 aged-matched controls participated in the study. Diffusion tensor imaging tract-based spatial statistics were performed to analyze structural white matter integrity. Significant group differences in the mean diffusivity were correlated with SCA2 cognitive deficits. RESULTS Our analysis revealed higher mean diffusivity in the SCA2 group in cerebellar white matter, medial lemniscus, and middle cerebellar peduncle, among other regions. Cognitive scores correlated with white matter mean diffusivity in the parahippocampal area, inferior frontal and supramarginal gyri and the stria terminalis. CONCLUSIONS Our findings show significant correlations between white matter microstructural damage in key areas affected in SCA2 and cognitive deficits. These findings result in a more comprehensive understanding of the effect of the neurodegenerative process in people with SCA2.
Cerebellum & Ataxias | 2017
Carlos R. Hernandez-Castillo; Rosalinda Díaz; Aurelio Campos-Romo; Juan Fernandez-Ruiz
BackgroundSpinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD) is an autosomal dominant inherited neurodegenerative disorder. Several post-mortem and imaging studies have shown cerebellar and brainstem atrophy. A number of studies have used volumetric regional information to investigate the relationship between neurodegeneration and the ataxia severity. However, regional analysis can obscure the specific location in which the degenerative process is affecting the brain tissue, which can be crucial for the development of new target treatments for this disease.Here we explored the relationship between the gray matter degeneration and the ataxia severity on a cohort of SCA3 patients using a voxel-wise approach.MethodsSeventeen patients with molecular diagnose of SCA3 and 17 matched healthy controls participated in this study. Magnetic resonance imaging (MRI) brain images were acquired and voxel-based morphometry was used to obtain the grey matter volume of each participant. Ataxia severity in the patient group was evaluated using the scale for the assessment and rating of ataxia (SARA).ResultsGroup comparison revealed significant atrophy in SCA3 including bilateral cerebellum, vermis, brainstem, and occipital cortex. Significant negative correlations between gray matter volume and SARA scores were found in the cerebellum and the cingulate gyrus.ConclusionsThese findings highlight the specific contribution of the cerebellum and the cingulate cortex to the ataxia deficits among the other regions showing neurodegeneration in SCA3 patients.
NeuroImage: Clinical | 2017
Israel Vaca-Palomares; Brian C. Coe; Donald C. Brien; Aurelio Campos-Romo; Douglas P. Munoz; Juan Fernandez-Ruiz
The ability to inhibit automatic versus voluntary saccade commands in demanding situations can be impaired in neurodegenerative diseases such as Huntingtons disease (HD). These deficits could result from disruptions in the interaction between basal ganglia and the saccade control system. To investigate voluntary oculomotor control deficits related to the cortico-basal circuitry, we evaluated early HD patients using an interleaved pro- and anti-saccade task that requires flexible executive control to generate either an automatic response (look at a peripheral visual stimulus) or a voluntary response (look away from the stimulus in the opposite direction). The impairments of HD patients in this task are mainly attributed to degeneration in the striatal medium spiny neurons leading to an over-activation of the indirect-pathway thorough the basal ganglia. However, some studies have proposed that damage outside the indirect-pathway also contribute to executive and saccade deficits. We used the interleaved pro- and anti-saccade task to study voluntary saccade inhibition deficits, Voxel-based morphometry and Tract-based spatial statistic to map cortico-basal ganglia circuitry atrophy in HD. HD patients had voluntary saccade inhibition control deficits, including increased regular-latency anti-saccade errors and increased anticipatory saccades. These deficits correlated with white-matter atrophy in the inferior fronto-occipital fasciculus, anterior thalamic radiation, anterior corona radiata and superior longitudinal fasciculus. These findings suggest that cortico-basal ganglia white-matter atrophy in HD, disrupts the normal connectivity in a network controlling voluntary saccade inhibitory behavior beyond the indirect-pathway. This suggests that in vivo measures of white-matter atrophy can be a reliable marker of the progression of cognitive deficits in HD.