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[Sensory deprivation].

A review of sensory deprivation is presented. The history of the concept and the terminological problems are reviewed. The symptoms are subdivided into: perceptual, cognitive and affective and the physiological disturbances are reviewed. Various etiological theories are discussed. These include biological, psychodynamic and social psychological theories. Experimental variables related to the subject, the investigator and the design of the research are presented. A review of the clinical and practical implications of sensory deprivation is given. It is emphasized that sensory deprivation might contribute to development of symptomatology in numerous situations. Finally, the potential therapeutic effects of controlled sensory deprivation are discussed.

Humans↗

Sensory deprivation in geriatric patients.

Sensory deprivation speeds up the degenerative changes normally associated with aging and enhances the loss of functional cells in the central nervous system. Since it connotes reduction or absence of stimulation of the five senses, it involves the patient's physical activity, social relationships, intellectual status and overall "value system." Geriatric patients with various illnesses are particularly vulnerable to sensory deprivation, which becomes increasingly pronounced as physical or mental deterioration progresses. All cells require stimulation for continued growth and activity; lack of stimulation leads to atrophy, with secondary physical or psychosocial abnormalities. Depression acts as a negative reinforcement of stimuli, and anxiety acts as a blocking mechanism. The goal of rehabilitation is to maintain and strengthen the patient's social values and to preserve mental and physical motility. The recommended procedure involves assessment of medical, psychologic and social factors, and determination of whether organic disease is present. A specific treatment plan to meet the individualized needs of each patient is then established so as to minimize sensory deprivation and maximize physical and mental functioning. Re-evaluation (physical and psychologic) at regular intervals establishes a pattern not only for individual comparison but for comparison with results in untreated control groups.

Aged↗

Time course of recovery of the somatosensory map following hindpaw sensory deprivation in the rat.

Hindlimb sensory deprivation is known to induce a decrease in the cortical representation of hindpaw, and an increase in the size of the cutaneous receptive fields. The aim of the present study was to determine (i) the time-course of recovery when the rat retrieves a normal use of its limbs after a 14-day period of sensory disruption and (ii) whether a 1-day period of sensory deprivation is sufficient to induce a plasticity. Our results indicate that the remodelling of the cortical map was not observed after 1 day of sensory deprivation. On the other hand, the recovery was achieved after 6 h. These findings suggest that a procedure reducing sensory function resulted in reversible changes in the somatosensory cortex. The recovery was more rapid than the induction of plasticity.

Animals↗

Changes in mouse barrel synapses consequent to sensory deprivation from birth.

Neonatal sensory deprivation induced by whisker trimming affects significantly the functional organization of receptive fields in adult barrel cortex. In this study, the effects of deprivation on thalamocortical synapses and on asymmetrical and symmetrical synapses not of thalamic origin were examined. Thalamocortical synapses were labeled by lesion-induced degeneration in adult (postnatal day 60) mice subjected to whisker trimming from birth, other synaptic types were unlabeled. Brains were processed for electron microscopy, and numerical densities of synapses were evaluated by using stereologic approaches for whisker trimmed vs. control animals. Results demonstrated no change in nonthalamic, asymmetrical synapses; however, a decrease of 52% in the numerical density of symmetrical synapses (46.3 vs. 88.5 million per mm(3); Z = -2.121; P < 0.05) and a decrease of 43% in the numerical density of thalamocortical synapses (57.5 vs. 102.33 million per mm(3); Z = -2.121; P < 0.05) were observed after deprivation. Thus, experience-dependent plasticity of receptive fields in barrel cortex involves directly axons of both extrinsic and intracortical origin. The proportion of thalamocortical axospinous to axodendritic synapses was the same in control vs. deprived animals: in each instance, 80% of the synapses were axospinous (Z = 0.85; P = 0.2). These results suggest that neither excitatory neurons, whose thalamocortical synapses are primarily axospinous, nor inhibitory neurons, whose thalamocortical synapses are mainly axodendritic (White [1989] Cortical Circuits. Synaptic Organization of the Cerebral Cortex; Structure, Function, and Theory. 1989; Boston: Birkhauser), are affected preferentially by the deprivation-associated decrease in thalamocortical synapses.

Animals↗

Sensory deprivation and clinical psychiatry.

Sensory deprivation as a scientific procedure was conceived in the early 1950s, intensively studied in the early 1960s, and applied in a limited way in the 1970s. From a consideration of the data, it is clear that clinical psychiatry could benefit from its more general application in the 1980s.

Human Experimentation↗

Auditory processing in spinal cord injury: a preliminary investigation from a sensory deprivation perspective.

Research on sensory deprivation suggests that the loss of somatosensory input to the central nervous system may have an impact on cortical reactivity and subsequent cognitive task efficiency. Individuals with spinal cord injury have a permanent loss of such input to varying degrees. However, there have been few investigations of cognitive processing in spinal cord injury. In this study, six outpatients with quadriplegia and 12 able-bodied controls were administered a dichotic listening task while auditory evoked response data and auditory threshold data were recorded. There were no differences between groups in terms of auditory threshold or auditory evoked responses. However, the outpatient quadriplegic group was more successful than the able-bodied controls in performing the dichotic listening task at one but not all levels of complexity. Results suggest that differences in cognitive processing ability between spinal cord injured and able-bodied individuals may reflect higher level motivational attention-concentration differences rather than more basic auditory and neurophysiologic processing differences.

Analysis of Variance↗

Neurophysiological and psychopharmacological approaches to sensory deprivation phenomena.

1. Research concerned with neurophysiological aspects of sensory deprivation phenomena is surveyed. 2. A theory is developed regarding the neurophysiological processes involved in sensory deprivation phenomena. It is postulated that the high amplitude bursts of slow waves observed in the visual cortex and lateral geniculate nucleus in deafferentation studies represent a PGO-like substrate of dream initiation. Concurrent neurochemical alterations are hypothesized to consist of a decrease in central serotonergic activity and an increase in norepinephrine level. 3. Hallucinogenic drugs, which produce subjective effects similar to those reported in sensory deprivation, are noted to induce neurochemical changes similar to those hypothesized for sensory deprivation. 4. New directions for research in this field are suggested.

Animals↗

Effects of sensory deprivation on the development of asymmetrical synapses in mouse barrels.

Alterations in the numerical density and structure of asymmetrical synapses were examined in thin sections through barrel D4 in six CD/1 mice, including three controls and three sensory deprived animals. Sensory deprivation was effected by once daily trimming of all large mystacial vibrissae on the contralateral side of the snout from P0. The mice were perfuse-fixed at P20, several days following the termination of rapid synaptic growth during barrel development (White et al., Somatosens Mot Res 14: 34-55, 1997). Cerebral hemispheres contralateral to the deprived side were osmicated, sectioned at 40 microm and embedded in plastic for thin sectioning. Sterio's (J Microsc 134: 127-136, 1984) procedure combined with serial thin section analysis (Braendgaard and Gundersen, J Neurosci Meth 18: 39-78, 1986), was applied blindly to systematic random samples of neuropil in barrel hollows and septa. No significant difference in the numerical density, estimated total number, or in the proportion of perforated postsynaptic densities was observed. However, a significant decrease in the diameters of asymmetrical postsynaptic densities was observed in hollow (P < 0.05) and septal (P < 0.05) neuropil of deprived animals. These results demonstrate a significant morphological alteration in asymmetrical synapses of a type consistent with a reduction in synaptic activity consequent to sensory deprivation.

Animals↗

EEG alpha activity and hallucinatory experience during sensory deprivation.

The relationship between hallucinatory experiences under sensory deprivation and EEG alpha activities was studied. Each of seven male students lived alone in an air conditioned, soundproof dark room for 72 hours. When hallucinatory experiences occurred, the students pressed a button at once. If they could not press the button during the experience, they were required to press it two times when the hallucinatory experience was finished. Spectral analysis was performed on the consecutive EEG samples from just before button-presses to 10 min. before them, and the average alpha band amplitudes were obtained for the four epochs (0-.5, .5-2, 2-5, 5-10 min.). For the single button-presses, the amplitude of alpha band increased 2 min. before the button-presses. Right-hemisphere EEG activation was observed in the occipital area for the double button-presses. The results suggest an association between the hallucinatory experiences under sensory deprivation and the amount of EEG alpha activity.

Adult↗

Sensory deprivation in spinal cord injury--an essay.

Due to altered or absent sensation below the level of the lesion, and varying degrees of preserved motor function, the spinal cord patient is limited in his/her ability to increase sensory feedback via interaction with the environment. The sequelae of this in the acute spinal cord patient could be likened to a state of sensory deprivation. Drawing inferences from the sensory deprivation literature of the 1950s and 1960s, in which university students volunteered to be placed in sensory deprivation chambers, is far from accurate. However, the research stimulates thought into the combined effects of immobilization, social isolation, and sensory deprivation-all of which the acute spinal cord patient is likely to experience. This state of sensory deprivation appears to lessen with time, regardless of the persistence of the impairment. The essay hypothesizes that neuroadaptive processes occur and proposes to the use of sensory stimulation, particularly in the spinal intensive care unit, to facilitate this adaptation.

Humans↗