Talk:Spatial disorientation

People with spatial-related phobias experience deficits which is evidence for higher order cognitive processes involved in orientation

"The control of spatial orientation during navigational tasks and locomotion requires a dynamic updating of the representation of the relations between the body and the environment. This depends upon central integration of current multisensory information but also on the comparison of sensory signals with planned trajectories, the body schema and past memories. Three main sensory modalities are involved in these processes: vision, the vestibular system and proprioception. In addition, efferent copies from motor signals also contribute to the updating of spatial representations during navigation."

"Recently, brain imaging techniques have improved the anatomical identification of the projection areas of vestibular, visual and kinaesthetic signals to the multimodal integration areas of the cerebral cortex involved in spatial orientation and memory in humans [5•,6], and in the determination and perception of the mid-sagittal egocentric body reference [7•]. These data, together with the data obtained in the primate cortex concerning the cortical systems dealing with head-in-space movement (see [8••]), contribute to the knowledge of the neural structures involved in space perception but they provide little information concerning the neural processes involved. Novel psychophysical methods in humans, however, have allowed the study of both canal and otolith organs during tasks involving the perception and memory of bi-dimensional motion during navigation [9]. Mobile robots can be used to passively displace human subjects while visual stimuli can be provided by virtual reality techniques. Together, these recent developments have given rise to new tools for the study of visual—vestibular interactions during combined rotations and translations. They have also allowed the experimental testing of new hypotheses concerning the type of information that is stored in spatial memory during navigation. Such experiments have suggested that the brain stores dynamic patterns of motion, rather than just position on cartesian-like cognitive maps [10]. These, together with observations of deficits in vestibular memory in patients with cortical lesions, and positron emisson tomography (PET) studies of the brain areas involved in the memory of travelled routes, have led to the formulation of the concept of ‘topokinetic memory’ [11], (i.e. the dynamic memory of the movements and associated landmarks and views during locomotion)."

"Evidence of dysfunction of spatial orientation has been found in agoraphobics [17]. During navigation in a complex environment, panic–agoraphobic patients became lost more often and utilised fewer navigation points. Moreover, the maps drawn afterwards by these patients were inaccurate [18]."^[1]

Additional possible reference suggesting multisensory approach

"In order to register our position, motion, and attitude within this fi xed frame of reference, we require a number of sensory inputs and perceptual mechanisms for the identification and interpretation of our orientation. Within this multiloop control system, the individual sensory components are mutually interactive and partially redundant because their functional ranges overlap. To the extent that their functional ranges do not overlap, the individual components compensate for each other’s deficiencies ( 10 ). The neural processing of these sensory inputs requires integration, interpretation, and critical comparison with the internal model that was established based on our past experience and training. Benson ( 4 ) suggested that the etiology of SD can be attributed to input and central errors that are not mutually exclusive of each other. Input error occurs when inadequate and/or erroneous sensory inputs regarding orientation are presented to the CNS; central error occurs when inadequate and/or erroneous perception of correct sensory inputs are presented by the CNS. Unlike other aerospace medical phenomena such as G-induced loss of consciousness or hypoxia, SD occurs in less well-defined environments, it can be unrecognized, and can be incapacitating. Therefore, SD involves the complexity of multiple, interactive sensory, perceptual, and central processing that in turn are influenced by the operational flying environment. The complexity of SD necessitates a multipronged countermeasure."^[2]

Spatial disorientation is related to the disruption of hippocampal pathways in remembering locations

"Spatial orientation of an individual is a complex cognitive task which includes topographic learning, perception of environmental features, and capacity to represent the spatial relationships between the objects and him/herself. All these components may be affected in AD, resulting in severe difficulties to find the path within the locomotor environment [2, 4, 10, 13, 18, 20–24, 44]. Several studies in individuals with focal neurological diseases, as well as functional brain imaging studies, have revealed a network of brain areas that subserve spatial orientation, including the hippocampus and parahippocampal gyrus [1, 2, 10, 13, 21, 22, 24], occipito-parietal association areas [10, 19, 32, 44] and ventral occipito-temporal cortex [2, 14, 18, 25]. It has been postulated that the hippocampus and parahippocampal gyrus are in a position to combine spatial relationships represented in the occipito-parietal association areas and landmark features represented in the ventral occipito-temporal areas. The integrated spatial representation which results may be the basis of spatial learning and may depend on the integrity of hippocampal circuits [2]."

"The present study shows that spatial disorientation in AD is related to NFT pathology in areas 7, 23, and the CA1 field of the hippocampus. These relationships are not due to the increased clinical severity of AD cases with spatial or temporal disorientation, since the GDS score was not associated with the presence of either type of disorientation in this series. In a recent review of cortical representations of environmental space, Aguirre et al. [2] have distinguished two main types of spatial disorientation: exocentric disorientation which may be due to a deficit of topographic learning or to an inability to recognize previously familiar landmarks (landmark agnosia) and egocentric disorientation which refers to a deficit in the representation of spatial relationship between objects and the subject in the presence of intact recognition of environmental landmarks. Deficits of topographic learning are related to damage in the hippocampus and parahippocampal gyrus, whereas landmark agnosia is associated with lesions of the right ventral occipito-temporal cortex. Conversely, egocentric disorientation may result from lesions confined to the right parietal cortex. The absence of visual agnosia and, in particular, prosopoagnosia in all of the present AD cases suggests that landmark agnosia was not a prominent feature of our patients [2]. This is consistent with the absence of relationship between NFT densities in area 19 and spatial disorientation in this study. However, deficits in both topographic learning and egocentric orientation may contribute to spatial disorientation in our AD cases. In particular, the present data imply that even mild NFT formation in area 7 is associated with substantial impairment of spatial orientation abilities, and point to the importance of egocentric disorientation in AD.

This study also indicates a specific relationship between NFT densities in area 23 and spatial disorientation in AD. Previous studies have shown that selective topographic disorientation is caused by focal hemorrhages in the right retrosplenial region [38], and is also associated with hypoperfusion of the right cingulate cortex in cases with multi-infarct dementia [16]. In addition, several animal studies point toward a possible role for this area in spatial orientation abilities [31, 37, 39, 41]. In particular, studies in rats have identified in area 23 a subtype of neurons referred to as head direction cells which respond to the maintenance of a heading within the environment [39]. In conjunction with these data and in agreement with a recent report showing decreased regional glucose metabolic rate in the right posterior cingulate cortex in AD cases with spatial disorientation [11], our results indicate that area 23 may also play a key role in spatial orientation deficits in AD. Importantly, early metabolic deficits and NFT formation are present in this area in the course of the degenerative process, and it has been postulated that this would account for the early manifestation of disorientation in AD [27, 42]. The link between the damage to the posterior cingulate cortex and spatial disorientation in AD is still poorly understood, but it could reside in the directional abilities subserved by this area. In fact, a few cases with heading disorientation and lesions confined to area 23 were recently described [2]. Both exocentric and egocentric orientation were preserved but these patients failed to derive directional information from landmarks they recognize."

"The present results go beyond these observations, and reveal that both temporal and spatial disorientation in AD are associated with the disruption of the same pathways linking the hippocampus with the superior parietal and posterior cingulate cortex in the right hemisphere. In agreement with this viewpoint, place cells in the right human hippocampus have been shown to fire in specific locations of an environment and store the time of visits to particular locations, suggesting the presence of a unified neural network capable of describing both temporal discrimination and spatial learning [30, 34]."^[3]

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