# Sensory Deprivation and the Brain: Neurobiological Mechanisms, Psychological Effects, and Clinical Implications

**Authors:** Donatella Marazziti, Gerardo Russomanno, Matteo Gambini, Francesca Rita Digiuseppe, Enrico Fazio, Riccardo Gurrieri

PMC · DOI: 10.3390/brainsci16020122 · Brain Sciences · 2026-01-23

## TL;DR

Sensory deprivation affects brain function and mental health, with outcomes depending on context, duration, and individual factors.

## Contribution

This review highlights sensory deprivation's dual role as a risk factor and potential therapeutic tool under controlled conditions.

## Key findings

- Sensory deprivation alters neurotransmitter systems and the HPA axis, increasing vulnerability to depression and anxiety.
- Short-term voluntary sensory restriction may promote relaxation and emotional regulation.
- Individual differences like baseline resilience and trait anxiety modulate the effects of sensory deprivation.

## Abstract

Background/Objectives: Sensory deprivation, defined as a reduction or absence of external sensory input across one or more modalities, has long been investigated in extreme and experimental settings. More recently, its relevance has expanded to clinical contexts and environmental conditions. The present narrative review aims to synthesize current evidence on the neurobiological mechanisms, psychological effects, and clinical implications of sensory deprivation, with particular attention to its dual role as both a risk factor and, under controlled conditions, a potential therapeutic tool. Methods: A narrative literature search was conducted using PubMed, Scopus, and PsycINFO, covering studies published up to August 2025. Search terms included sensory deprivation, neuroplasticity, neurotransmitters, HPA axis, neuro-inflammation, circadian rhythms, psychopathology, extreme environments, and spaceflight. Preclinical and clinical studies examining biological, cognitive, and psychological consequences of reduced sensory stimulation were included. Data were synthesized thematically without quantitative meta-analysis. Results: Evidence indicates that sensory deprivation induces widespread neurobiological adaptations involving neurotransmitter systems (particularly dopaminergic pathways), dysregulation of the hypothalamic–pituitary–adrenal axis, neuroimmune activation, circadian rhythm disruption, and structural and functional brain changes, notably affecting the hippocampus. These alterations are associated with increased vulnerability to depression, anxiety, hallucinations, dissociative symptoms, and cognitive impairment. Duration, voluntariness, and individual differences (e.g., baseline vulnerability/resilience, trait anxiety, and prior psychiatric history) critically modulate outcomes. However, short-term and voluntary sensory restriction, such as Floatation-REST, may promote relaxation and emotional regulation under specific conditions. Conclusions: Sensory deprivation exerts complex, context-dependent effects on brain function and mental health. Duration, individual vulnerability, and voluntariness critically modulate outcomes. Understanding these mechanisms is increasingly relevant for clinical practice and for developing preventive strategies in extreme environments, including future long-duration space missions.

## Linked entities

- **Diseases:** depression (MONDO:0002050), anxiety (MONDO:0005618)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, Il1a (interleukin 1 alpha) [NCBI Gene 16175] {aka Il-1a}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Il17a (interleukin 17A) [NCBI Gene 16171] {aka Ctla-8, Ctla8, IL-17, IL-17A, Il17}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Il3ra (interleukin 3 receptor, alpha chain) [NCBI Gene 16188] {aka CD123, CDw123, SUT-1}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Tlr9 (toll-like receptor 9) [NCBI Gene 81897], Il13 (interleukin 13) [NCBI Gene 16163] {aka Il-13}, Th (tyrosine hydroxylase) [NCBI Gene 21823], IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, H2 (histocompatibility-2, MHC) [NCBI Gene 111364] {aka H-2, MHC-II}, CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, Tlr5 (toll-like receptor 5) [NCBI Gene 53791], Tlr4 (toll-like receptor 4) [NCBI Gene 21898] {aka Lps, Ly87, Ran/M1, Rasl2-8}, Fcgr3 (Fc receptor, IgG, low affinity III) [NCBI Gene 14131] {aka CD16}, Tlr3 (toll-like receptor 3) [NCBI Gene 142980], Cd14 (CD14 antigen) [NCBI Gene 12475], Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, Lilrb4a (leukocyte immunoglobulin-like receptor, subfamily B, member 4A) [NCBI Gene 14728] {aka CD85K, Gp49b, HM18, ILT3, LIR-5, Lilrb4}, Tlr6 (toll-like receptor 6) [NCBI Gene 21899], GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Tlr8 (toll-like receptor 8) [NCBI Gene 170744], GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, Ddc (dopa decarboxylase) [NCBI Gene 13195] {aka Aadc}
- **Diseases:** Parkinson's disease (MESH:D010300), congenitally blind (MESH:D057130), disturbances in abstract thinking (MESH:D014832), mitochondrial dysfunction (MESH:D028361), like (MESH:C537419), sleep disturbances (MESH:D012893), anhedonia (MESH:D059445), pain (MESH:D010146), auditory, visual, vestibular, or other sensory dysfunctions (MESH:D014786), immunodeficiency (MESH:D007153), delusions (MESH:D063726), volume loss (MESH:D016388), anosmia) and/or taste (MESH:D013651), Hallucinations (MESH:D006212), injury to (MESH:D014947), neuro-inflammatory (MESH:C536203), HPA axis (MESH:C566610), DSL (MESH:D009105), inflammation (MESH:D007249), loss of smell (MESH:D000086582), Neuroinflammation (MESH:D000090862), schizophrenia (MESH:D012559), Anxiety (MESH:D001007), atrophy (MESH:D001284), autism (MESH:D001321), sensory deficits (MESH:D012678), COVID-19 (MESH:D000086382), ADHD (MESH:D001289), deafness or blindness (MESH:D054062), psychotic (MESH:D011618), sense (MESH:D020886), Polar T3 syndrome (MESH:D005067), musical ears syndrome (MESH:D004427), ischemic stroke (MESH:D002544), paranoia (MESH:D010259), agitation (MESH:D011595), impaired leucopoiesis (MESH:D060825), deafness (MESH:D003638), irritability (MESH:D001523), dementia (MESH:D003704), System (MESH:D015619), accidents (MESH:D000081084), CBS (MESH:D000075562), sensory loss (MESH:C580162), executive dysfunction (MESH:D006331), reduction in cortical (MESH:D054220), winter-over syndrome (MESH:D006963), seasonal affective disorder (MESH:D016574), Depression (MESH:D003866), Sensory (MESH:D009477), Sensory Deprivation (MESH:D012892), leukopenia (MESH:D007970), social phobia (MESH:D000072861), mood disorders (MESH:D019964), speech difficulties (MESH:D013064), concentrating impairments (MESH:C567712), hypoxia (MESH:D000860), mood lability (MESH:D005166), impairments in attention and memory (MESH:D008569), of olfaction (MESH:D000857)
- **Chemicals:** [(11)C]-raclopride (-), corticosterone (MESH:D003345), cortisol (MESH:D006854), catecholamine (MESH:D002395), endocannabinoids (MESH:D063388), CO2 (MESH:D002245), norepinephrine (MESH:D009638), dopamine (MESH:D004298)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090], human gammaherpesvirus 4 (Epstein Barr virus, no rank) [taxon 10376]
- **Cell lines:** /6J — Homo sapiens (Human), Cutaneous melanoma, Cancer cell line (CVCL_W797)

## Full text

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## References

257 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938772/full.md

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Source: https://tomesphere.com/paper/PMC12938772