Search Results

Abstract Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are characterised by progressive neuronal loss, cognitive decline, and motor dysfunction. While diverse in clinical presentation, these disorders share a common pathological denominator: mitochondrial dysfunction. Mitochondria, as the principal generators of cellular energy and regulators of apoptosis, are uniquely positioned at the intersection of metabolic stress, oxidative damage, and programmed cell death. This article explores the role of mitochondrial impairment in neurodegeneration, examining the breakdown of mitochondrial quality control, dysregulation of biogenesis, calcium homeostasis, and the permeability transition pore, while highlighting emerging therapeutic strategies. Introduction Neurons are the most metabolically demanding cells in the body, relying heavily on oxidative phosphorylation (OXPHOS) to power the constant, intense energy requirements of synaptic transmission, axonal transport, and plasticity. As the cell's principal energy generators, mitochondria occupy a central, non-negotiable role in neuronal survival. Beyond ATP production, these dynamic organelles are crucial regulators of intracellular calcium homeostasis, redox (reduction-oxidation) signalling, and the fundamental apoptotic pathway. To sustain the vast energy needs across extended neuronal structures, mitochondria constantly undergo a regulated cycle of fission and fusion (dynamics) and are actively transported along the axon. Given this complexity and the neuron's reliance on aerobic metabolism, even subtle mitochondrial perturbations can quickly escalate, initiating a cascade of dysfunction, including bioenergetic failure, chronic oxidative stress, and impaired quality control, that culminates in irreversible neuronal death. Mitochondrial impairment is therefore emerging not as a consequence of neurodegeneration, but as the convergent axis that ultimately precipitates cellular collapse across diverse disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS). Mitochondrial Bioenergetic Failure and Oxidative Stress The electron transport chain (ETC) is the pillar of mitochondrial ATP production. In neurodegenerative diseases, ETC dysfunction is a recurrent theme, arising from both genetic and environmental factors. Deficiencies in specific complexes, such as Complex I in PD (Bindoff et al., 1989; Greenamyre & Shachar, 2018) or Complex IV in AD (Davis & Williams, 2017), compromise ATP synthesis, destabilising ion gradients and impairing synaptic transmission. Crucially, defects can also stem from accumulated damage to the mitochondrial genome: mtDNA mutations and deletions are increasingly recognised as primary drivers of bioenergetic failure, evidenced by high levels found in the substantia nigra of Parkinson's patients (Bender et al., 2006; Kraytsberg et al., 2006). Moreover, partial ETC blockade leads to electron leakage, generating reactive oxygen species (ROS) such as superoxide and hydrogen peroxide (Abou-Sleiman et al., 2006). These ROS damage mitochondrial DNA, lipids, and proteins, creating a vicious feedback loop of escalating dysfunction (Anandatheerthavarada et al., 2003). The vulnerability of energy-dependent neurons is starkly demonstrated by toxins like MPTP, which replicates dopaminergic neuronal loss in PD models by inhibiting Complex I (Greenamyre & Shachar, 2018). This cumulative oxidative burden, often exacerbated by primary mtDNA defects, accelerates the aging-related degeneration characteristic of neurodegenerative disorders. Disruption of Mitochondrial Dynamics and Axonal Transport Aspect of Pathology Mechanism of Disruption Key Proteins Involved Fission Overload (AD) Amyloid-beta (Aβ ) induces the S-nitrosylation of Drp1 , directly promoting excessive mitochondrial fission and fragmentation. Drp1, Amyloid-beta (Aβ ) Axonal Blockade (AD) Hyperphosphorylated tau  detaches from microtubules, destabilising axonal tracks and physically obstructing mitochondrial trafficking. Tau Impaired Biogenesis (HD) Mutant Huntingtin protein  interferes with mitochondrial fusion and suppresses PGC-1-alpha , impairing energy renewal. Huntingtin, PGC-1-alpha Mitochondria are not static; they are subjected to continuous fission and fusion to maintain integrity and adapt to cellular demands. This dynamic equilibrium is regulated by proteins such as Drp1 (fission), Mfn1/2, and OPA1 (fusion) (Chen & Chan, 2004). In neurodegenerative conditions, this balance is lost, resulting in excessive fragmentation. A key link in this pathology involves the Alzheimer's-defining protein: amyloid-beta (A-beta) exposure has been shown to induce the nitrosylation of Drp1 (dynamin-related protein 1). This post-translational modification is critical, as it directly promotes Drp1 activity, thereby driving excessive mitochondrial fission and fragmentation, a morphological signature of neuronal distress (Cho et al., 2009).This damage is compounded by the mislocalisation of other key proteins. In AD, hyperphosphorylated tau detaches from microtubules, destabilising axonal tracks and obstructing mitochondrial trafficking to synapses (Berth & Lloyd, 2023). Similarly, in HD, the mutant Huntingtin protein interferes with mitochondrial fusion and suppresses PGC-1-alpha (PGC-1α) impairing biogenesis and energy renewal (Benchoua et al., 2006; Cui et al., 2006). These disruptions compromise mitochondrial distribution, particularly in distal axons, leading to synaptic failure and neuronal death long before the cell body is compromised. Mitochondrial Biogenesis and Transcriptional Collapse Mitochondrial biogenesis is regulated by PGC-1α, a transcriptional coactivator that regulates nuclear respiratory factors and TFAM, essential for mtDNA replication and transcription (Cui et al., 2006). In neurodegenerative conditions, PGC-1α expression is suppressed, impairing the renewal of mitochondrial populations and exacerbating energy deficits (Du et al., 2020). This transcriptional collapse leads to neurons incapable of adapting to metabolic stress. In HD, PGC-1α repression correlates with behavioural abnormalities and cellular dysfunction (Bae et al., 2005). Therapeutic upregulation of PGC-1α has shown promise in restoring mitochondrial function and mitigating neurodegeneration in preclinical models (Swerdlow, 2018). Calcium Dysregulation and the Mitochondrial Permeability Transition Pore Mitochondria sequester cytosolic calcium, maintaining intracellular homeostasis. However, sustained calcium influx often triggered by excitotoxicity, overwhelms mitochondrial capacity, leading to the opening of the permeability transition pore (Calì et al., 2013). This pore disrupts membrane potential, causes matrix swelling, and facilitates the release of cytochrome c, initiating apoptosis (Baev et al., 2022). In AD, amyloid-β exacerbates calcium dysregulation and sensitises mitochondria to pore opening, linking extracellular plaques to intracellular collapse (Alves et al., 2018). The confluence of calcium dysregulation and oxidative stress initiates irreversible neuronal damage. Mitophagy Failure and Accumulation of Damaged Organelles Mitophagy is the selective autophagic clearance of damaged mitochondria, regulated by PINK1 and Parkin. Mutations in these genes are causative in familial PD, highlighting the importance of mitochondrial quality control (Bacman et al., 2006). When mitophagy fails, dysfunctional mitochondria accumulate, increasing ROS production and triggering apoptosis (Calkins et al., 2011). In AD, impaired mitophagy correlates with increased mtDNA damage and reduced mitochondrial biogenesis (Cui et al., 2006). The persistence of damaged organelles disrupts cellular homeostasis and accelerates neurodegeneration (Bender et al., 2006). Disease-Specific Mitochondrial Signatures Each neurodegenerative disease exhibits a distinct mitochondrial profile. PD features Complex I deficiency, α-synuclein aggregation, and mitophagy failure (Du et al., 2020). AD is marked by tau pathology, amyloid-β-induced calcium overload, and altered ER-mitochondria tethering (Area-Gomez et al., 2012). HD presents with PGC-1α repression and mitochondrial fragmentation (Benchoua et al., 2006). ALS is characterised by mitochondrial swelling, cristae disruption, and impaired axonal transport (Bacman et al., 2006). Despite these differences, all converge on mitochondrial dysfunction as a central axis of pathology. Neurodegeneration and Dementia Mitochondrial Nexus Dementia, particularly Alzheimer’s disease and vascular dementia, is marked by progressive cognitive decline, synaptic failure, and neuronal death. Mitochondrial dysfunction is increasingly recognised as a central driver of this deterioration. In Alzheimer’s disease, mitochondrial fragmentation, impaired biogenesis, and defective mitophagy precede plaque formation and tau pathology (Alves et al., 2018; Anandatheerthavarada et al., 2003). Damaged mitochondria accumulate in hippocampal neurons, reducing ATP availability and increasing ROS burden, which in turn exacerbates amyloid precursor protein misprocessing and tau hyperphosphorylation (Calkins et al., 2011; Cho et al., 2009). Key mitochondrial elements Outer membrane Inner membrane with cristae Intermembrane space Matrix Mitochondrial DNA Ribosomes ATP synthase Transport proteins Diseased mitochondrion: Defective mitochondrion showing cristae collapse, swollen matrix, disrupted inner membrane, oxidative debris, and impaired ATP synthesis. Vascular dementia introduces an additional layer of metabolic insult. Chronic cerebral hypoperfusion impairs oxygen delivery, directly compromising oxidative phosphorylation and accelerating mitochondrial permeability transition pore opening (Kraytsberg et al., 2006). This leads to abrupt loss of membrane potential, calcium accumulation, and release of pro-apoptotic factors. The alignment of vascular compromise with pre-existing mitochondrial fragility leaves neurons exquisitely vulnerable to even minor ischaemic events (Fang et al., 2019). Moreover, mitochondrial dysfunction in dementia is not confined to energy failure. It disrupts lipid metabolism, impairs ER-mitochondria tethering, and alters calcium signalling, mechanisms that are increasingly implicated in early cognitive symptoms and synaptic disintegration (Calì et al., 2013; Area-Gomez et al., 2012). These findings suggest that mitochondrial collapse is not a subsequent consequence but a primary axis of dementia pathogenesis. Pathological Feature Mechanism Consequences Impaired Biogenesis Reduced synthesis of new mitochondria Energy deficit, reduced neuronal resilience Disrupted Dynamics Imbalanced fission/fusion processes Fragmentation, loss of mitochondrial network integrity Calcium Dysregulation Excessive mitochondrial calcium uptake ROS generation, membrane permeabilisation Mitophagy Failure Inefficient clearance of damaged mitochondria Accumulation of dysfunctional organelles, chronic stress Cristae Collapse Structural degradation of inner membrane folds Impaired ATP synthesis, reduced metabolic efficiency Oxidative Stress Excess reactive oxygen species (ROS) Lipid peroxidation, protein damage, DNA instability ATP Synthase Impairment Dysfunctional energy conversion machinery Synaptic failure, cognitive decline Matrix Swelling Osmotic imbalance and membrane rupture Release of pro-apoptotic factors, cell death Table 1. Key mitochondrial defects and their cellular consequences in neurodegeneration. Chemical Disruption Mechanism Impact on Neuronal Integrity ATP Depletion Impaired oxidative phosphorylation Synaptic failure, reduced repair capacity ROS Accumulation Excess electron leakage from ETC Oxidative damage to lipids, proteins, and mtDNA Calcium Overload Dysregulated mitochondrial calcium buffering Membrane rupture, apoptotic signalling Lipid Peroxidation ROS-induced damage to phospholipid membranes Loss of membrane fluidity, increased permeability NAD⁺/NADH Imbalance Disrupted redox cycling Impaired metabolic flux, reduced sirtuin activity Cytochrome c Release Membrane permeabilisation Activation of caspases, programmed cell death Iron Dysregulation Fenton reaction amplification Hydroxyl radical formation, ferroptosis Glutathione Depletion Exhausted antioxidant reserves Heightened vulnerability to oxidative stress Table 2. Electrochemical Disruption as a Catalyst of Neurodegeneration Therapeutic Strategies Targeting Mitochondria Mitochondria are increasingly recognised as therapeutic targets. Antioxidants such as MitoQ and CoQ10 aim to neutralise ROS and restore redox balance (Beal, 1995). Mitophagy enhancers like urolithin A promote the clearance of damaged organelles, improving cellular resilience (Calkins et al., 2011). Gene therapy approaches seek to restore PGC-1α and TFAM expression, revitalising biogenesis and transcriptional capacity (Cui et al., 2006). Artificial mitochondrial transfer, injecting healthy mitochondria into damaged neurons, has shown promise in preclinical models (Du et al., 2020). These strategies represent a paradigm shift from symptomatic relief to mechanistic intervention. Conclusion Mitochondrial dysfunction is not a peripheral anomaly but the metabolic fault line upon which neurodegeneration converges. Across Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and ALS, the mitochondrion is both a sentinel and a casualty, its collapse precipitating synaptic failure, oxidative overload, and apoptotic priming. The integration of impaired biogenesis, disrupted dynamics, calcium dysregulation, and mitophagy failure leaves neurons exquisitely vulnerable to even minor metabolic insults. Crucially, these mechanisms are not isolated; they form a feedback loop of escalating dysfunction, where oxidative stress impairs transcriptional renewal, and failed clearance of damaged organelles amplifies apoptotic signalling. Therapeutically, this offers clarity: interventions must restore mitochondrial function, not simply masks symptoms. From gene therapy targeting PGC-1α to mitophagy enhancers and artificial mitochondrial transfer, the future of neurodegenerative medicine lies in reclaiming the cell’s energetic core. To treat the brain, we must first repair its mitochondria. References Abou-Sleiman, P. M., Muqit, M. M. K., & Wood, N. W. (2006). Expanding insights of mitochondrial dysfunction in Parkinson's disease. Nature Reviews Neuroscience, 7(3), 207–219. Alves, S., Figueira, I., Sampaio-Marques, V., & Pedros, I. (2018). The role of mitochondrial dysfunction in Alzheimer's disease: From molecular mechanisms to clinical evidence. Current Neuropharmacology, 16(5), 558–571. Anandatheerthavarada, H. K., Biswas, G., Robin, M. A., & Avadhani, N. G. (2003). Mitochondrial targeting and a novel transmembrane arrest of Alzheimer's amyloid precursor protein impairs mitochondrial function in neuronal cells. The Journal of Cell Biology, 161(1), 41–54. Bae, B. I., Xu, H., Igarashi, S., Fujimuro, M., Agrawal, N., Taya, Y., ... & Sawa, A. (2005). p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease. Neuron, 47(381), 29–41. Bacman, S. R., Bradley, W. G., & Moraes, C. T. (2006). Mitochondrial involvement in Amyotrophic Lateral Sclerosis: Trigger or target? Molecular Neurobiology, 33(2), 113–128. Beal, M. F. (1995). Aging, energy, and oxidative stress in neurodegenerative diseases. Annals of Neurology, 38(3), 357–366. Benchoua, A., Trioulier, Y., Zala, D., Gaillard, M. C., Lefort, N., Dufour, N., ... & Brouillet, E. (2006). Involvement of mitochondrial complex II defects in neuronal death produced by N-terminus fragment of mutated huntingtin. Molecular Biology of the Cell, 17(1), 1674–1684. Bender, A., Krishnan, K. J., Morris, C. M., Taylor, G. A., Reeve, A. K., Perry, R. H., ... & Turnbull, D. M. (2006). High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease. Nature Genetics, 38(5), 515–517. Berth, S. H., & Lloyd, T. E. (2023). Disruption of axonal transport in neurodegeneration. Journal of Clinical Investigation, 133(10), e168554. Bindoff, L. A., Birch-Machin, M. A., Cartlidge, N. E. F., Parker, W. D., & Turnbull, D. M. (1989). Mitochondrial function in Parkinson's disease. The Lancet, 334(8674), 1030. Calkins, M. J., Manczak, M., Mao, P., Shirendeb, U., & Reddy, P. H. (2011). Impaired mitochondrial biogenesis, mitophagy, and increased mitochondrial DNA damage in Alzheimer’s disease transgenic mice. Journal of Alzheimer's Disease, 25(3), 449–460. Calì, T., Ottolini, D., & Brini, M. (2013). Calcium and endoplasmic reticulum-mitochondria tethering in neurodegeneration. DNA and Cell Biology, 32(4), 140–146. Chen, H., & Chan, D. C. (2004). Mitochondrial dynamics in cell death and disease. Cell Death & Differentiation, 11(4), S39–S45. Cho, D. H., Nakamura, T., Fang, J., Liu, H., Pei, W., Guo, L., ... & Lipton, S. A. (2009). S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal cell death. Science, 324(5923), 102–105. Cui, L., Jeong, H., Borovecki, F., Troutt, L. L., Peters, N. L., & Kordower, J. H. (2006). PGC-1α is a transcriptional regulator of mitochondrial function and prevents mHtt-induced mitochondrial toxicity. Nature Medicine, 12(1), 115–119. Davis, R. L., & Williams, C. L. (2017). The role of mitochondria in Alzheimer's disease. Journal of Alzheimer's Disease, 58(4), 957–975. Du, H., Gu, L., Wang, S., Fan, N., & Ye, X. (2020). Mitochondrial dysfunction and Parkinson's disease. International Journal of Molecular Sciences, 21(3), 875. Fang, H., Wang, J., Zhao, L., Zhao, B., Zhai, M., Zheng, X., ... & Zhang, Y. (2019). Mitochondrial dysfunction and neurodegenerative disorders. Journal of Biochemical and Molecular Toxicology, 33(10), e22380. Greenamyre, J. T., & Shachar, D. B. (2018). Mitochondrial dysfunction in Parkinson's disease. Seminars in Neurology, 38(4), 438–444. Halliwell, B. (2006). Oxidative stress and neurodegeneration: Where are we now? Journal of Neurochemistry, 97(6), 1634–1658. Kraytsberg, Y., Kudryavtseva, E., McKee, A. C., Geula, C., Kowall, N. W., & Khrapko, K. (2006). Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons. Nature Genetics, 38(5), 518–520.

Abstract Diogenes Syndrome (DS), also known as Senile Squalor Syndrome, is a complex behavioural disorder predominantly affecting older adults. It is characterised by extreme self-neglect, domestic squalor, hoarding of refuse (syllogomania), social withdrawal, and a marked lack of insight or shame regarding one’s condition. Despite an estimated annual incidence of 5 new cases for every 10,000 people over the age of sixty, DS remains absent from major diagnostic manuals such as the DSM-5 and ICD-11. This omission contributes to frequent misdiagnosis, particularly in the early stages, where DS is often conflated with psychotic disorders. This article presents a retrospective case analysis of twelve individuals initially misdiagnosed with psychosis but subsequently identified as exhibiting DS. The findings highlight the need for clearer diagnostic criteria and a reclassification of DS as a distinct neuropsychiatric-behavioural syndrome, with profound implications for clinical management and policy. Introduction Diogenes Syndrome (DS) occupies a paradoxical space in clinical psychiatry: simultaneously recognisable and yet diagnostically elusive. Though first described in the mid-twentieth century (MacMillan & Shaw, 1966), the syndrome remains uncodified in contemporary diagnostic frameworks. Clinically, DS manifests through a cluster of behaviours including severe self-neglect, domestic squalor, compulsive hoarding of non-functional items, and a profound withdrawal from social engagement. These features are often accompanied by a striking absence of insight or shame, further complicating clinical interpretation. The syndrome’s exclusion from the DSM-5 and ICD-11 has led to significant nosological ambiguity. In the absence of formal criteria, clinicians frequently rely on heuristic or phenomenological impressions, which can result in misclassification, most notably within the psychotic spectrum. This misdiagnosis carries tangible risks, including inappropriate pharmacological interventions and the neglect of capacity-led, psychosocial approaches more suited to the syndrome’s underlying pathology. This article seeks to address these diagnostic challenges by presenting a retrospective case series of twelve individuals initially referred for suspected psychosis but ultimately diagnosed with DS. Through this analysis, the paper aims to clarify the distinguishing features of DS, advocate for its recognition as a distinct clinical entity, and propose a framework for more accurate diagnosis and management. The Diagnostic Challenge The phenotypic similarity between DS and primary psychotic disorders has long confounded diagnostic clarity. Individuals with DS often present with aloofness, suspiciousness, and profound social withdrawal, features that may be misinterpreted as indicative of paranoid schizophrenia or schizoaffective disorder. Garrick and Heins (2017) observed that such behavioural presentations, particularly in conjunction with a distorted perception of reality, frequently lead to provisional diagnoses within the psychotic spectrum. Moreover, the hoarding of refuse and disregard for environmental hygiene are often construed as manifestations of disorganised thought or delusional content. Fond et al.  (2011) highlighted that clinicians may mistake the chaotic living conditions and refusal of assistance as evidence of a primary delusional disorder. Hanon et al.  (2004) proposed a transnosographic approach, suggesting that DS does not fit neatly within existing psychiatric categories and requires a more judicious diagnostic lens. Differential diagnosis in older adults further complicates the picture. DS must be distinguished from late-onset schizophrenia, alcohol-related brain damage, and behavioural-variant frontotemporal dementia (bvFTD). Vermeulen et al.  (2019) provided compelling evidence linking DS to frontal lobe dysfunction, a finding echoed by Cipriani et al.  (2019), who emphasised the syndrome’s neuropsychiatric aetiological roots. Crucially, the absence of Schneiderian first-rank symptoms such as auditory hallucinations or thought insertion, and the poor response to antipsychotic medication serve as key differentiators between DS and primary psychosis (Takahashi & Arai, 2016; Finney et al. , 2017). Methodology This study employed a retrospective review of clinical case notes and community health records for a cohort of twelve patients. All individuals were initially referred under the Mental Health Act (1983) for suspected psychosis, based on presentations of severe self-neglect, domestic squalor, and social withdrawal. Inclusion criteria required the presence of at least three core features of DS, as delineated by Clark et al.  (1975): extreme self-neglect, hoarding of refuse, and active refusal of assistance. Data were extracted regarding initial presenting features, provisional diagnoses, diagnostic criteria applied, final diagnoses, and treatment responses. The diagnostic evolution was assessed using the criteria proposed by Clark et al.  and later refined by Snowdon et al.  (2012). The study design aligns with methodologies employed by Ames and Snowdon (2015), who conducted similar analyses of domestic squalor in older populations. Ethical considerations were addressed through anonymisation of patient data and adherence to local governance protocols. Steele and Gray (2018) and Hurley et al.  (2000) have previously emphasised the importance of detailed clinical documentation in identifying DS. This study builds upon such work by offering a comparative analysis of diagnostic trajectories and treatment outcomes. Key Findings The analysis revealed a consistent pattern of misdiagnosis across the cohort. In ten of the twelve cases, patients were initially diagnosed with paranoid psychosis or delusional disorder. These diagnoses were based on features such as social withdrawal, refusal of care, and environmental squalor, behaviours that were interpreted as evidence of persecutory delusions or disorganised thought. However, further assessment revealed a lack of core psychotic features, such as hallucinations or systematised delusions, and a notable absence of response to antipsychotic medication. Instead, the patients exhibited high rates of comorbid affective disorders and cognitive impairments, particularly frontal lobe dysfunction. Vermeulen et al.  (2019) and Cipriani et al.  (2012) have previously linked DS to neurodegenerative processes, suggesting that the syndrome may be secondary to underlying neuropathology. In this context, six patients demonstrated signs consistent with behavioural-variant frontotemporal dementia, while four exhibited chronic affective disorders, including dysthymia and treatment-resistant depression. The therapeutic implications of accurate diagnosis were profound. In cases where DS was correctly identified, interventions shifted from pharmacological management to capacity-led approaches, including environmental remediation, social care planning, and legal interventions under the National Assistance Act (1948) and the Mental Capacity Act (2005). These strategies proved more effective in stabilising patients and improving quality of life than antipsychotic regimens, which had yielded minimal benefit. Takahashi and Arai (2016) argue that DS should be conceptualised as a syndrome of behavioural collapse, rather than a variant of psychosis. This perspective is supported by Finney et al.  (2017), whose cluster analysis demonstrated that DS occupies a distinct position within the spectrum of self-neglect syndromes. The findings of this study reinforce the need for diagnostic specificity and challenge the prevailing tendency to pathologise DS within psychotic frameworks. Conclusion Diogenes Syndrome represents a distinct neuropsychiatric-behavioural entity, often secondary to cognitive or affective disorders. Its clinical presentation though superficially similar to psychosis, requires a fundamentally different diagnostic and therapeutic approach. The misclassification of DS as a primary psychotic disorder not only obscures its unique pathology but also leads to inappropriate treatment and suboptimal outcomes. This paper advocates for the development of standardised diagnostic criteria and screening tools to facilitate accurate identification and management of DS. Future research should prioritise prospective studies to elucidate the neurobiological correlates of the syndrome and establish evidence-based care protocols that honour its complexity. **Context Note Legislation Primary Function in DS Cases Mental Capacity Act 2005 (MCA 2005) Provides the legal framework for making "best interests"  decisions and intervening (e.g., providing care, environmental remediation) for patients found to lack capacity  for those specific decisions. This is the main framework for capacity-led approaches. Mental Health Act 1983 (MHA 1983) Used for compulsory detention and treatment  when a patient is deemed to have a treatable mental disorder and is a risk to self or others. The major amendments to this Act were made by the MHA 2007  (e.g., introducing Community Treatment Orders). National Assistance Act 1948 Provides local authorities with powers to enter and clean premises in cases of severe domestic squalor and neglect. Academic References MacMillan, D., & Shaw, P. (1966). Senile breakdown in standards of personal and environmental cleanliness. British Medical Journal , 2(5521), 1032-1037. Clark, A.N., Mankikar, G.D., & Gray, I. (1975). Diogenes syndrome: A clinical study of gross neglect in old age. The Lancet , 1(7903), 366-368. Cybulska, E., & Rucinski, J. (1986). Gross self-neglect in old age. British Journal of Hospital Medicine , 36(6), 332-337. O'Brien, J.G. (1989). Diogenes syndrome: an aspect of self-neglect. The British Journal of Psychiatry , 155(5), 701-704. Drummond, I.A., Turnbull, G.J., & Sheldon, M. (1997). Diogenes syndrome: a load of rubbish? International Journal of Geriatric Psychiatry , 12(10), 999-1004. Reyes-Ortiz, C.A. (2001). Diogenes syndrome: the self-neglect elderly. Comprehensive Therapy , 27(2), 117-121. Snowdon, J. (2006). Severe domestic squalor: prevalence and risk factors in the Sydney Older Persons Study. International Psychogeriatrics , 18(3), 545-554. Cipriani, G., Lucetti, C., Vedovello, M., & Nuti, A. (2012). Diogenes syndrome in patients suffering from dementia. Dialogues in Clinical Neuroscience , 14(4), 438-444. Snowdon, J., Halliday, G., & Banerjee, S. (2012). Severe Domestic Squalor . Cambridge University Press. Ames, D., & Snowdon, J. (2015). Diogenes syndrome: A perspective for the century. International Psychogeriatrics , 27(1), 163-171. Takahashi, N., & Arai, H. (2016). Diogenes syndrome: Pathogenesis and clinical aspects. Psychogeriatrics , 16(1), 44-50. Garrick, T.R., & Heins, C.H. (2017). Diogenes Syndrome: A Special Manifestation of Hoarding Disorder. The American Journal of Psychiatry Residents' Journal , 12(8), 4-6. Vermeulen, E., van Zandvoort, M.J.E., van Wingen, G.A., & Kanning, S.K. (2019). The link between Diogenes Syndrome and Frontotemporal Dementia: a systematic review. Ageing Research Reviews , 56, 100965. Fond, G., Jollant, F., & Abbar, M. (2011). The need to consider mood disorders, and especially chronic mania, in cases of Diogenes syndrome (squalor syndrome). International Psychogeriatrics , 23(3), 505-507. Hanon, C., Pinquier, C., Gaddour, N., Saïd, S., Mathis, D., & Pellerin, J. (2004). Diogenes syndrome: a transnosographic approach. Encephale , 30(4), 315-322. Hurley, A.D., Vostanis, P., & Dean, C. (2000). Self-neglect and Diogenes Syndrome: A review of prevalence and associated factors. Journal of Mental Health , 9(4), 387-394. Cipriani, G., Nuti, A., & Danti, S. (2019). Clinical and ethical aspects of Diogenes syndrome: A narrative review. Neuropsychiatric Disease and Treatment , 15, 2529-2540. Steele, C., & Gray, I. (2018). Self-neglect and Diogenes syndrome: Clinical management. British Journal of General Practice , 68(673), 390-391. Lee, V., & Ooi, S. (2020). Hoarding and the law: A review of legal issues and implications in the United Kingdom. The Psychiatrist , 44(4), 184-188. Finney, C.M., Aakre, J.M., & Whiteside, S.P. (2017). Diogenes Syndrome is a syndrome of symptom overlap: A cluster analysis of cases. Journal of Affective Disorders , 217, 194-198.

A peaceful landscape inviting exploration Note from Rakhee LB Limited We appreciate your patience during periods of high inquiry. While immediate responses may not always be possible, we strive to respond within a defined time frame. Please leave us a message, email, or complete the online form so we can assist you as efficiently as possible. In today's rapidly changing world, effective communication is crucial for businesses. Fluctuating customer inquiries can create challenges, especially during peak periods. When queries skyrocket, responding to every message promptly can be tough. This blog post explores practical strategies to enhance communication during busy times, ensuring customers feel valued, even when immediate replies may not be feasible. Understanding the Challenge A surge in customer queries can lead to a significant backlog, creating stress for customer service teams vying to provide timely and accurate responses. For example, during the holiday season, businesses can see a 60% increase in inquiries compared to non-peak periods. This spike can overwhelm smaller teams, making it essential to find an effective communication strategy that balances inquiry volume with available resources. Effective communication becomes critical during these times. Acknowledging delays in response times and offering alternative ways for customers to contact the business can help manage expectations. For instance, letting customers know about a 24-hour response window can reduce frustration and improve their experience. The Importance of Clear Communication Clear communication lays the foundation for any successful business relationship. When customers know what to expect, they are more likely to be patient and understanding. Key points to consider include: Set Expectations : Inform customers about potential delays in response times. A simple message like, "Due to an increase in inquiries, our response time may take longer than usual," is effective in managing expectations, especially when projected delays could be up to 48 hours. Provide Alternatives : Motivate customers to leave messages, send emails, or fill out online forms. This not only empowers them but also helps organize and manage the inquiry process more effectively. Express Gratitude : Acknowledging a customer's patience can create goodwill. A line such as, "We appreciate your understanding during this busy time," strengthens the customer relationship. Utilising Technology for Better Communication Harnessing technology can dramatically improve communication during periods of high inquiry. Consider these solutions: Automated Responses Implementing automated responses can effectively manage customer expectations. When a customer sends a message, an automated reply stating that their inquiry has been received and an estimated response time (for example, 24-48 hours) goes a long way in reassuring them that their concerns are being taken seriously. Chatbots Chatbots serve as an effective tool for quickly addressing common inquiries. For example, chatbots can answer frequently asked questions about store hours, return policies, or shipping times instantly. This capability reduces unnecessary messages that require human attention, allowing customer service representatives to focus on more complex inquiries. Online Forms Encouraging customers to fill out online forms can collect essential information upfront. For instance, forms can request details such as order numbers or specific issues, ensuring representatives have all necessary data to provide accurate responses. This simplifies the inquiry process and can significantly cut down on follow-up questions. Prioritising Inquiries It is important to recognise that not all inquiries are equal. Some require immediate attention, while others can be addressed later. Implementing a system to prioritise inquiries can help businesses respond efficiently. Here are recommended strategies: Categorise Inquiries : Develop a categorisation system to classify inquiries based on urgency and complexity. For instance, issues affecting customer safety or account access should be addressed first. Use Tags : Utilise tags or labels to identify the nature of each inquiry. This helps assign the right team member and streamlines the response process. Monitor Response Times : Track response times for different categories of inquiries. Data analysis can reveal trends, helping teams identify areas needing improvement. For example, if technical support inquiries usually take longer to respond to, extra resources can be allocated during peak times. Training and Empowering Staff Investing in staff training is crucial for maintaining effective communication. Empower your team with these strategies: Provide Comprehensive Training Ensure that your customer service representatives are well-versed in handling various inquiries, including product knowledge, communication skills, and conflict resolution. A trained team can deliver responses more efficiently and with greater confidence. Encourage Team Collaboration Creating a supportive, collaborative environment enhances internal communication. Encourage team members to share insights or successful strategies for handling inquiries. Regular team meetings or brainstorming sessions can foster cohesion and lead to quicker response times. Recognise and Reward Efforts Acknowledging the hard work of your customer service representatives can boost morale. Consider implementing a recognition program to highlight top performers during busy periods. For example, reward employees who consistently meet or exceed response time benchmarks with incentives or recognition. Maintaining Customer Relationships Maintaining strong customer relationships remains vital, even during busy times. Consider these approaches to keep customers engaged: Follow Up After resolving an inquiry, follow up to ensure customer satisfaction. You could send a brief message like, "We hope your issue is resolved! If you need further assistance, please let us know." This not only shows you value their feedback but reinforces your commitment to excellent service. Personalise Communication Personalise your interactions by using customer's names and referencing previous interactions. A message such as, "Hi, Sarah! Thank you for your question about our return policy," helps promote a deeper connection with customers, making them feel valued. Solicit Feedback Encourage customers to provide feedback on their experience. You might include a short survey after a service interaction to gather insights. This not only highlights areas for improvement but also signals to customers that you value their opinions. Final Thoughts Enhancing communication during high inquiry periods is essential for sustaining customer satisfaction and loyalty. By setting clear expectations, harnessing technology, prioritising inquiries, training staff, and focusing on customer relationships, businesses can effectively manage busy times. Remember, while immediate responses may not always be possible, thoughtful communication can significantly impact customer experience. Thank you for your understanding as we strive to provide exceptional service during busy periods. Implementing these strategies can keep your business responsive to customer needs, even when inquiries are at their peak.

Diwali, also known as Deepavali, is one of the most cherished and widely observed festivals across India and beyond. The word ‘Deepavali’ derives from Sanskrit, meaning ‘row of lights’, a reference to the countless oil lamps, or diyas, that illuminate homes, temples, and streets during this time. It is a celebration of light over darkness, good over evil, and wisdom over ignorance. Though this theme is universal, the festival’s significance varies across traditions and regions, each marking a distinct mythic return. In the Ramayana, Diwali commemorates Lord Rama’s return to Ayodhya after fourteen years of exile and his victory over the demon king Ravana. The citizens lit rows of diyas to welcome him home, transforming the night into a beacon of joy and justice. In Southern India, the legend of Lord Krishna defeating Narakasura is honoured on Naraka Chaturdashi, the eve of Diwali. His victory liberated thousands and restored dharma. Many also worship Goddess Lakshmi, the deity of wealth and prosperity. It is believed she visits clean, brightly lit homes, bringing blessings for the year ahead. The rituals span five days, Dhanteras, Naraka Chaturdashi, Lakshmi Puja, Govardhan Puja, and Bhai Dooj, each a timestamp of devotion, renewal, and familial bond. Homes are cleaned, adorned with rangoli, and lit with lamps. Families gather for Lakshmi Puja, share sweets and gifts, and mark new beginnings. For many, especially within the business community, Diwali signals the start of a new financial year. A Diwali Wish To all who mark this festival, whether with clay lamps, LED garlands, or quiet reflection, may your homes be lit with clarity, your hearts with courage, and your paths with purpose. May the light you kindle today illuminate every threshold you cross, and may the year ahead be marked by rhythm, renewal, and sovereign joy. Happy Diwali 🪔

Abstract Factitious Disorder Imposed on Self, FDIS, historically known as Munchausen Syndrome, is a rare, yet clinically profound, mental health condition characterised by the intentional fabrication or induction of physical or psychological symptoms in the absence of obvious external incentives. The core motivation is psychological, stemming from a compulsive need to assume the sick role. FDIS presents a formidable challenge to healthcare systems globally, consuming vast resources through unnecessary, high-risk investigations and treatments. Contemporary research has illuminated strong links between FDIS and early life trauma, severe personality pathology, notably Borderline Personality Disorder, BPD, and a propensity for medical peregrination. Effective management necessitates a coordinated, multidisciplinary strategy, prioritising a non-confrontational approach and long-term psychotherapeutic engagement to address the underlying emotional distress. Introduction Factitious Disorder Imposed on Self, FDIS, represents one of the most complex diagnoses encountered in modern medicine, fundamentally disrupting the fiduciary nature of the doctor-patient relationship. First described by British psychiatrist Richard Asher in 1951, the term Munchausen Syndrome was coined after Baron von Munchausen, an 18th-century German nobleman renowned for his extravagant and false tales of adventure (Asher, 1951). The disorder is currently classified in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, DSM-5-TR, under the somatic symptom and related disorders (American Psychiatric Association, 2022). The central defining feature of FDIS is the deliberate act of deception, falsification, exaggeration, or induction of illness, sustained by the internal psychological need to be perceived as sick or injured (Feldman, 2018). This internal gain clearly differentiates FDIS from malingering, where the motivation is strictly for external rewards, such as avoiding work or obtaining financial compensation (Folks, Feldman, & Ford, 2000). Whilst historically considered a condition predominantly affecting men, contemporary large-scale database studies indicate a significant prevalence amongst females, frequently those with a background in the healthcare profession (Martin et al., 2021; De La Rivière et al., 2023). Due to the deceptive nature of the behaviour and the phenomenon of medical peregrination, the migration between numerous healthcare facilities, its true prevalence remains uncertain, though estimates range from 0.02% to 3% in inpatient settings (Yates & Bass, 2016; Sharma & Verma, 2022). Aetiology and Psychosocial Underpinnings The aetiology of FDIS is considered multifactorial, lacking a single verified organic cause, but strongly rooted in developmental psychology and personality pathology. Developmental and Trauma-Related Factors A recurring theme in the psychosocial history of individuals with FDIS is a background of significant childhood adversity, including emotional neglect, physical abuse, or early loss (Caselli et al., 2019). Feigning illness is hypothesised to serve as a deeply maladaptive coping mechanism, replicating a scenario where the individual received intense, unconditional care or attention that was otherwise absent in their formative years (Feldman & Eisendrath, 2024; Grosdidier, Bense, & Faget-Agius, 2024). One review of dialogue from online support communities noted that the vast majority of members described various forms of childhood emotional or physical abuse, supporting the hypothesis that the sick role becomes an acquired identity providing a sense of comfort, security, or self-worth (Yates & Feldman, 2019). Furthermore, a history of major childhood illness, resulting in prolonged hospitalisation and medical attention, may condition the individual to associate the patient role with receiving comfort and security, thereby reinforcing the behaviour (Kanaan & Wessely, 2010). Personality Pathology and Comorbidity There is a significant and consistently reported comorbidity between FDIS and Personality Disorders, particularly Borderline Personality Disorder, BPD (Gnanadesigan & Stoudemire, 2012). BPD features, such as emotional dysregulation, an unstable self-image, and a profound fear of abandonment, align closely with FDIS behaviours (Feldman & Feldman, 1995). The dramatic presentation, the urgency of medical complaints, and the clingy demand for hospitalisation may function as a desperate, though destructive, attempt to stabilise a fragile identity or cope with overwhelming interpersonal stress (Nadeau & Malingering, 2024; Sharma & Verma, 2022). One retrospective study of FDIS cases found that a large proportion of patients exhibited a high rate of prescribed psychotropic medications, including antidepressants (58.3%) and anxiolytics (66%), reflecting the significant burden of co-occurring depression and anxiety alongside the factitious behaviour (Martin et al., 2021). Clinical Presentations and Diagnostic Challenge The presentation of FDIS is highly varied, limited only by the individual's imagination and medical knowledge. The sophistication of deception, termed pseudologia fantastica, often necessitates extensive investigation to confirm the factitious origin of symptoms. Self-Induction and Harm Patients may induce severe, unexplained anaemia, sometimes referred to as Lasthénie de Ferjol syndrome (Feldman, 2018). This is achieved via occult bloodletting, self-inflicted injuries, or the surreptitious ingestion of anticoagulants (Asher, 1951). A 2025 case report highlighted the complex ethical dilemma of involuntary admission for a patient with recurrent life-threatening iron-deficiency anaemia eventually attributed to FDIS (Eng, Neo, & Chang, 2025). Factitious hypoglycaemia is a high-risk presentation where patients secretly self-inject insulin or ingest sulphonylurea medications (Lebowitz & Blumenthal, 1993). The critical diagnostic clue, often confirmed through endocrinology literature, is the laboratory finding of a low C-peptide level alongside high insulin or sulphonylurea levels, definitively proving the source is exogenous, non-self-produced (Wallach, 1994; BMJ Best Practice, 2023). Individuals may also induce sepsis or localised infections by contaminating wounds or intravenous access lines with foreign or faecal matter, leading to infections by unusual or polymicrobial pathogens that fail to respond to standard care (Sutherland & Rodin, 1990). Falsification and Exaggeration FDIS comprises the falsification of psychological symptoms. A 2024 case study described the late detection of FDIS in a patient feigning schizophrenia, presenting with bizarre and fluctuating complaints, such as commanding hallucinations (Shamsudin et al., 2024). The symptoms were observed to resolve rapidly when the patient's requests, such as specific medications, were granted, and worsen when they were denied, providing an objective window into the feigned nature of the illness. Tampering with medical evidence, such as spoiling urine samples with blood or manipulating medical records, is a common deceptive tactic (Pachkin & Zito, 2023). Diagnosis and Management Strategy Diagnosis rests not on a single test, but on a pattern of behaviour and a systematic approach to excluding organic disease whilst objectively confirming the presence of deception (Mayo Clinic Staff, 2024). Key elements include exclusion of genuine illness, identification of deception through objective evidence, and confirmation that the behaviour is driven by internal psychological need rather than external gain (Thompson & Wilson, 2022; Mayou & Farmer, 2024). Treatment is challenging and the prognosis is guarded. The primary organisational strategy involves a “Gatekeeper” Model, where a single physician coordinates all care (Feldman & Eisendrath, 2024). Psychotherapeutic intervention, particularly CBT, remains the primary modality (Yates & Feldman, 2019). The goal is to validate suffering without reinforcing deception, and to redirect focus toward trauma, identity disturbance, and coping skills. In life-threatening cases, involuntary psychiatric admission may be ethically justified under the Mental Health Act (Eng, Neo, & Chang, 2025). Conclusion Factitious Disorder Imposed on Self is a severe and often tragic psychological imperative rooted in a complex dynamic of developmental trauma, personality dysfunction, and a compulsive need to inhabit the sick role. Its deceptive nature places enormous diagnostic pressure on clinicians, consumes disproportionate healthcare resources, and subjects patients to significant iatrogenic risk. Effective management demands a high index of clinical suspicion, a rigorously coordinated medical strategy centred on a 'gatekeeper' system, and a persistent, non-judgmental psychotherapeutic commitment focused squarely on addressing the underlying emotional pathology. References Asher, R. (1951). Munchausen's syndrome. The Lancet, 1(6650), 339–341. Kaur, J., Gokarakonda, S. B., & Aslam, S. P. (2025). Factitious Disorder Overview. In StatPearls [Internet]. StatPearls Publishing. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.). American Psychiatric Publishing. De La Rivière, S., Auriacombe, M., Baccara-Dinet, M., & Jollant, F. (2023). Factitious disorder imposed on self: A retrospective study of 2232 cases from health insurance databases. ResearchGate. Martin, V., Pompili, M., Olie, J. P., et al. (2021). A descriptive, retrospective case series of patients with factitious disorder imposed on self. BMC Psychiatry, 21(1), 572. Eng, S. L., Neo, H. L. M., & Chang, C. W. L. (2025). Case Report: Area of focus - involuntary admission for severe Factitious Disorder imposed on self. Frontiers in Psychiatry, 16, 1649205. Sutherland, A. J., & Rodin, G. M. (1990). Factitious disorders in a general hospital setting: Clinical features and a review of the literature. Psychosomatics, 31(4), 392-399. Feldman, M. D. (2018). Factitious disorders (2nd ed.). American Psychiatric Publishing. Nadeau, M. M., & Malingering, H. E. (2024). Munchausen Syndrome: Understanding Factitious Disorder Imposed on Self. Clinical Neuropsychology: Open Access, 11(1). Pachkin, V., & Zito, T. (2023). Factitious Disorder. In StatPearls [Internet]. StatPearls Publishing. Yates, G., & Bass, C. (2016). Factitious Disorder: a systematic review of 455 cases in the professional literature. ResearchGate. Grosdidier, C., Bense, B., & Faget-Agius, C. (2024). Prevalence and risk factors for depression in factitious disorder: a systematic review. Frontiers in Psychiatry, 15, 1355243. Sharma, B. R., & Verma, S. (2022). Factitious Disorder Imposed on Self (Munchausen Syndrome): A Brief Review. Journal of Indian Academy of Forensic Medicine, 44(4), 438-442. Folks, G. D., Feldman, M. D., & Ford, C. V. (2000). Somatoform disorders, factitious disorders, and malingering. In Psychiatric care of the medical patient (2nd ed., pp. 459-475). Oxford University Press. Lebowitz, M. R., & Blumenthal, S. A. (1993). The molar ratio of insulin to C-peptide: An aid to the diagnosis of hypoglycemia due to surreptitious (or inadvertent) insulin administration. Archives of Internal Medicine, 153(5), 650-655. Kaur, J., Gokarakonda, S. B., & Aslam, S. P. (2023). Factitious Disorder Overview. In StatPearls [Internet]. StatPearls Publishing. Shamsudin, A. N., Harun, H., Razali, R., & Alwi, W. (2024). Case Study: Late detection of Factitious Disorder- Munchaussen's Syndrome with feigned schizophrenia. ASEAN Journal of Psychiatry, 25(1), 1–6. Wallach, J. (1994). Laboratory diagnosis of factitious disorders. Archives of Internal Medicine, 154(15), 1690-1696. BMJ Best Practice. (2023). Factitious disorders - Symptoms, diagnosis and treatment. Retrieved from https://bestpractice.bmj.com/ Mayou, R., & Farmer, A. (2024). Factitious disorders and malingering: Challenges for clinical assessment and management. The Lancet, 383(9926), 1425-1434. Mayo Clinic Staff. (2024). Factitious disorder - Diagnosis and treatment. Retrieved from https://www.mayoclinic.org/ Thompson, T., & Wilson, K. (2022). A systematic review of psychological treatments for women presenting with factitious disorder and factitious disorder imposed on another. Forensic Update, 1(141), 15-36. Gnanadesigan, M., & Stoudemire, A. (2012). Factitious Disorder: A Clinical Review. Psychiatric Clinics of North America, 35(2), 403–415. Feldman, M. D., & Feldman, J. M. (1995). Tangled in the web: Countertransference in the therapy of factitious disorders. International Journal of Psychiatry in Medicine, 25(4), 389–399. Eng, S. L., Neo, H. L. M., & Chang, C. W. L. (2025). Case Report: Area of focus - involuntary admission for severe Factitious Disorder imposed on self. PubMed Central, 12455358. Lee, J. Y., Sung, J., Cho, B., et al. (2022). Chronic recurrent diarrhea: A case of factitious disorder. Clinical Journal of Gastroenterology, 15(3), 459–468.

Abstract Frégoli Delusion Syndrome (FDS) is a rare and complex neuropsychiatric condition classified under the Delusional Misidentification Syndromes (DMS). It is defined by the fixed, paranoid belief that a known individual, typically a persecutor, repeatedly assumes the physical appearance of various strangers encountered by the patient. Fundamentally, FDS is a syndrome of hyper-identification, rooted in the pathological dissociation between accurate visual perception and the pathologically over-stimulated affective recognition system. Neurobiological research consistently implicates functional and structural disruption within the right cerebral hemisphere, specifically involving the anterior fusiform gyrus and a resulting temporolimbic-frontal disconnection. Cognitive neuropsychiatric models, such as the Dual-Route Model and the Two-Factor Theory, explain the delusion's emergence as the brain's attempt to rationalise an aberrant internal signal of familiarity (Factor 1), coupled with frontal lobe dysfunction that impairs the ability to reject this improbable belief (Factor 2). Management requires a meticulous, multidisciplinary approach, combining antipsychotic medication to modulate psychotic salience, alongside tailored psychological interventions, particularly Cognitive Behavioural Therapy (CBT), to address the fixed belief structure and mitigate the associated high risk of aggressive behaviour. Future work should focus on clarifying the underlying neurodevelopmental and genetic vulnerabilities shared with primary psychoses to inform targeted therapeutic strategies. 1. Introduction: Delusional Misidentification Syndromes and the Phenomenon of Frégoli Frégoli Delusion Syndrome (FDS), also known as Frégoli syndrome, is classified as a rare and complex neuropsychiatric condition belonging to the family of Delusional Misidentification Syndromes (DMS). DMS are psychotic conditions characterised by the pathological misidentification of people, objects, or locations, often unified by the concept of the sosie (double). FDS stands alongside Capgras delusion, Intermetamorphosis, and the syndrome of Subjective Doubles as one of the core subtypes of DMS. The syndrome was first described in 1927 by Courbon and Fail, who named it after the famous Italian actor Leopoldo Frégoli, renowned for his rapid changes in costume and character. FDS is defined by the patient’s fixed, often persecutory, delusional belief that a known individual, typically perceived as a threat, is consistently and repeatedly changing their physical appearance, masquerading as various strangers whom the patient encounters in their environment. The patient maintains the conviction of the psychological identity of the persecutor, even though they consciously perceive the physical appearance of the encountered stranger as being different from the known person's typical guise. This cognitive contradiction, the dissociation between visual perception and identity recognition, forms the central paradox of the syndrome. FDS is fundamentally categorised as a 'hyper-identification' syndrome. This designation refers to an aberrant excess of perceived familiarity directed towards unfamiliar individuals. This mechanism is in direct opposition to the characteristic 'hypo-identification' observed in Capgras syndrome, where a familiar person is perceived as psychologically unfamiliar and replaced by an imposter, suggesting a loss of the normal affective link. The presence of hyper-identification suggests a crucial functional breakdown: an overactive or pathologically disinhibited affective identification system, referred to in cognitive models as the Person Identity Node (PIN). When this affective system is pathologically hyper-stimulated by a novel face, the higher-order frontal systems responsible for reality testing must attempt to rationalise the resultant contradictory sensory data. The only internally consistent explanation that preserves the fixed identity is intentional deception and disguise, which explains the pervasive paranoid and persecutory nature of the delusion. 2. Clinical Spectrum, Aetiology, and Forensic Relevance 2.1 Aetiological Pathways and Differential Presentation The pathogenesis of FDS is complex and heterogenous, rarely existing in isolation (Ellis et al., 1994; Hudson & Grace, 2000). Clinically, FDS presents across a bimodal spectrum: either as a feature of primary psychiatric conditions or as a consequence of organic cerebral dysfunction (Corlett et al., 2010). A review of 119 FDS cases revealed that approximately 52% occur within the context of primary psychoses, such such as schizophrenia or bipolar I disorder (Hudson & Grace, 2000; Ellis et al., 1994; Corlett et al., 2010; Christodoulou et al., 2009; Forstl et al., 1994). Conversely, 42% of cases are secondary, stemming from defined organic brain disorders. The underlying aetiology correlates directly with the typical age of onset. FDS secondary to organic causes tends to present significantly later in life, showing a median onset age of 60, whereas cases associated with a primary psychiatric diagnosis typically have a median onset age of 33 (Forstl et al., 1994). This disparity suggests two distinct initiation pathways. For younger patients, FDS emerges from an underlying neurodevelopmental vulnerability interacting with the acute stress of a primary psychotic break. For older patients, the syndrome is often a catastrophic symptom of structural brain damage, such as neurodegeneration (e.g., Alzheimer's or Lewy body dementia) or acute vascular compromise. This crucial distinction mandates a bifurcated clinical investigation: early-onset FDS requires a thorough psychiatric evaluation for primary psychotic disorders, while late-onset FDS demands immediate and exhaustive neuroimaging (MRI/PET) to screen for structural lesions, such as the temporal lobe masses that have been reported to induce FDS (Hudson & Grace, 2000; Hentati et al., 2022). 2.2 Secondary (Organic) Risk Factors The occurrence of FDS secondary to neurological damage is well-documented. Specific insult sites include the right frontoparietal and adjacent regions (Hentati et al., 2022; Feinberg et al., 1999). FDS has been linked to Traumatic Brain Injury (TBI) (Feinberg et al., 1999) , cerebral lesions (such as a right temporal lobe mass with associated oedema suggestive of metastasis) (Hentati et al., 2022) , and cerebrovascular accidents. Beyond physical trauma, FDS has been reported secondary to infectious diseases like typhoid fever (Stanley & Andrew, 2002; Hentati et al., 2022) and systemic failure, demonstrated by a case associated with chronic kidney disease requiring haemodialysis (Papageorgiou et al., 2005). Furthermore, the condition may also be iatrogenic; certain medications, notably Levodopa, have been explicitly linked to the onset of FDS symptoms (Turkiewicz et al., 2009; Courbon & Fail, 1927). 2.3 Forensic and Clinical Behavioural Risks Due to the fundamental paranoid content of the delusion, the persistent belief that the patient is being actively tracked, monitored, and deceived by an individual disguised as multiple people (Courbon & Fail, 1927; Turkiewicz et al., 2009), patients exhibiting FDS are often considered to be at a particularly high risk for dangerousness, including verbal threats and aggressive behaviour. This is particularly pertinent in forensic populations and clinical settings. Patients in hospital environments frequently misidentify members of the treatment team (e.g., nurses or doctors) as the persecutor, leading to assaultive behaviour towards staff (Silva et al., 2012; Lykouras et al., 2002). Documented risk factors for aggression in DMS patients include male sex, a long-standing history of the delusion, a primary diagnosis of schizophrenia, and co-morbid substance use (Forstl et al., 1994). Recognition and early treatment of this relatively uncommon delusional syndrome are thus essential for mitigating assault risk and ensuring patient safety (Silva et al., 2012). 3. Neurobiological Substrates and Functional Disconnection (Neuroscience) The scientific investigation into FDS and other DMS has shifted dramatically over the decades, moving from purely psychodynamic explanations to identifying clear neurophysiological and neuroimaging correlates (Hentati et al., 2022). The current understanding firmly roots FDS in a functional and structural breakdown of specific pathways within the right cerebral hemisphere. 3.1 Anatomical Localisation and Structural Damage Neuroimaging studies consistently report identifiable neurological lesions or functional abnormalities in DMS patients, predominantly lateralised to the right hemisphere (Hentati et al., 2022; Stanley & Andrew, 2002). Specific regions implicated include the right temporal lobe, right fusiform gyrus, and right frontoparietal cortex (Stanley & Andrew, 2002; Hentati et al., 2022; Hudson & Grace, 2000; Christodoulou et al., 2009). In cases of co-occurring FDS and Capgras syndrome, structural MRI findings have revealed periventricular and subcortical white matter hyperintensities concentrated in the right frontotemporal region, alongside bilateral frontotemporal volume loss (Stanley & Andrew, 2002; Silva et al., 2012; Lykouras et al., 2002). Functional studies (SPECT) in patients with misidentification delusions also suggest bilateral hypoperfusion in the superior and inferior temporal lobes, corresponding precisely to the location of the fusiform face area (FFA) (Papageorgiou et al., 2005; Turkiewicz et al., 2009). 3.2 Disruption of Face Recognition Pathways FDS is understood fundamentally as a failure within the brain's visual processing network. Visual perception is organised into two main pathways: the dorsal (spatial) pathway and the temporal-occipital ventral pathway, which is critical for object and face recognition. The pathology in FDS localises to the ventral stream, particularly involving the anterior part of the right fusiform gyrus (Christodoulou et al., 2009; Forstl et al., 1994). This region is home to the FFA, a highly specialised area dedicated to face identification. Lesions here are thought to result in an inability to attribute perceptual uniqueness to a specific face (Papageorgiou et al., 2005; Langdon et al., 2014). The visual misidentification phenomena in FDS are explained by the disruption of connections between these highly specialised visual areas (like the FFA) and the anterior, inferior, and medial parts of the right temporal lobe (Christodoulou et al., 2009). This latter region is crucial for storing long-term visual recognition memory and retrieving the information necessary for the recognition of faces. The consequence is a loss of function in the associative nodes, the biological links that connect the perception of a specific familiar face to all stored identity information about that person. 3.3 The Temporolimbic-Frontal Disconnection Hypothesis The most compelling mechanistic explanation is the right temporolimbic-frontal disconnection hypothesis (Stanley & Andrew, 2002; Silva et al., 2012; Lykouras et al., 2002). This functional disconnection creates an impairment in the high-order nervous system function responsible for identification. In FDS, the sensory/perceptual recognition system registers a novel physical appearance, but the limbic-frontal affective and memory systems pathologically register this input as deeply familiar (Stanley & Andrew, 2002). This disjunction prevents the patient from correctly associating established long-term memories of the familiar person with the contradictory new perceptual information (the stranger’s face). Electrophysiological evidence supports this view, with studies noting abnormal event-related potentials (P300) in DMS patients, indicating underlying working memory dysfunction in the frontal and parietal regions (Turkiewicz et al., 2009; Hentati et al., 2022). The misidentification symptoms are therefore the brain's effort to reconcile conflicting internal signals arising from structural or functional disconnection in this critical circuit. 4. Cognitive Neuropsychiatric Models Cognitive neuropsychiatry seeks to explain delusions by mapping them onto specific disruptions of normal cognitive processes. FDS is a paradigm case for such models, offering a cognitive error that must then be rationalised as a delusion. 4.1 The Dual-Route Model and Hyper-Identification Building upon earlier models of face processing, Langdon and colleagues (2014) proposed a dual-route model specifically tailored to explain disorders of person identification. This framework delineates separate routes for overt (conscious) and covert (affective/subconscious) face recognition. FDS is explained within this model as a syndrome of hyper-identification, arising from an impaired cognitive system that possesses a pathological propensity to over-excite certain internal representations known as Person Identity Nodes (PINs) (Feinberg et al., 1999; Turkiewicz et al., 2009). The model asserts that FDS stems from a breakdown in the identification process leading to an inability to attribute visual uniqueness to a face (Papageorgiou et al., 2005). When any face bearing some level of perceived similarity to the persecutor is encountered, the hyper-vigilant PIN associated with the persecutor is pathologically activated. The brain consequently misidentifies the unfamiliar individual as the known person, leading to the fixed, irrational belief that the familiar person is employing multiple physical disguises (Feinberg et al., 1999; Langdon et al., 2014; Hentati et al., 2022). 4.2 The Two-Factor Theory and Belief Maintenance The formation and maintenance of monothematic delusions like FDS are often discussed within the framework of the Two-Factor Theory (TFT) (Langdon et al., 2014; Turkiewicz et al., 2009; Christodoulou et al., 2009). TFT posits that two independent neuropsychological impairments are necessary: Factor 1, which generates the aberrant perceptual content, and Factor 2, which ensures the formation and tenacious maintenance of the belief. In FDS, Factor 1 is clearly the perceptual anomaly resulting from the disconnection between the visual processing area (FFA) and the limbic system, leading to the hyper-familiarity signal (Turkiewicz et al., 2009; Christodoulou et al., 2009). This signal provides the initial bizarre content, the stranger feels like the familiar person. Factor 2, the failure to evaluate and reject this highly improbable belief, is associated with dysfunction in the right dorsolateral prefrontal cortex (rDLPFC) and potentially the ventromedial prefrontal cortex (vmPFC) (Hentati et al., 2022; Langdon et al., 2014; Turkiewicz et al., 2009; Christodoulou et al., 2009). This frontal pathology prevents the patient from appropriately weighing the objective visual evidence against the internal feeling of recognition, thereby locking the persecutory, bizarre delusion of disguise into place (Hentati et al., 2022; Turkiewicz et al., 2009). While TFT remains a strong explanatory tool, recent neurocognitive findings challenge the strict modularity of the two factors. Studies show that neurological lesions frequently span multiple regions, affecting both perceptual and evaluative circuits simultaneously. This suggests that the impairments contributing to the delusion may not be strictly independent processes, but rather integrated components of a single, structurally or functionally disconnected circuit (Langdon et al., 2014; Turkiewicz et al., 2009; Christodoulou et al., 2009). 4.3 Computational Models: Aberrant Prediction Error Beyond structural models, computational psychiatry offers a sophisticated mechanism for delusion formation based on prediction error (Corlett et al., 2010). Delusions are seen as resulting from aberrations in how brain circuits specify hierarchical predictions and how they compute the prediction error, the mismatch between expectation and sensory experience. In the context of FDS, the pathological hyper-activation of the PIN generates a powerful internal expectation ("Person X is here and is persecuting me"). However, external sensory data (the stranger's physical appearance) generates a significant prediction error (Corlett et al., 2010). Normal cognitive function would use this high error signal to update and reject the initial expectation. Dysfunction in the frontostriatal circuits, however, compromises the patient's ability to process or correctly respond to this prediction error, leading to a failure to update the belief (Corlett et al., 2010). Consequently, the brain defaults to the least likely, yet internally satisfying, conclusion: that the visual discrepancy is the result of an external, elaborate plot of disguise and deception, thus maintaining the fixed delusion (Corlett et al., 2010; Hentati et al., 2022). 5. Evidence-Based Management and Therapeutic Outcomes (Treatment Research) The complexity and heterogeneity of FDS, coupled with its relatively low prevalence, mean that no standardised, single-pronged treatment regimen exists (Courbon & Fail, 1927). Effective management requires an individualised, multidisciplinary approach that targets both the psychotic and behavioural symptoms. 5.1 Pharmacological Strategies Antipsychotic medication forms the cornerstone of pharmacological treatment, supplemented sometimes by antidepressants or antiseizure medications, especially when there is evidence of structural brain injury or organic aetiology. However, robust, syndrome-specific clinical trials comparing drug efficacy in FDS are scarce (Papageorgiou et al., 2005). Treatment protocols are often extrapolated from research on general delusional disorders (DD) and co-morbid primary psychoses. Systematic reviews covering DD indicate that antipsychotics, as a class, are effective, but show no clear superiority for any one specific agent. Tentative evidence suggests that First-Generation Antipsychotics (FGAs) may show a slight advantage over Second-Generation Antipsychotics (SGAs), with good response rates reported at 39% versus 28%, respectively, in general delusional disorder cohorts. Dosage typically requires careful titration, often over several weeks, to manage persistent symptoms. In one case involving a patient treated with Risperidone, the dose had to be escalated from 2 mg to 6 mg daily to achieve a partial decrease in delusional activity and reactivity (Silva et al., 2012). Critically, while the patient achieved remission in hallucinatory activity, the core delusional belief remained partially present but no longer influenced their behaviour. Given the high associated risk for aggressive behaviour, clinicians must employ intensive monitoring, particularly regarding medication adherence and potential drug abuse history (Silva et al., 2012; Lykouras et al., 2002). Furthermore, adjusting medication, such as changing levodopa if it is identified as a trigger, may be necessary in secondary cases (Courbon & Fail, 1927). Clinical insight: Levodopa, while essential for managing motor symptoms, can trigger dopamine dysregulation syndrome, delusions, and psychiatric effects in some patients. A 2025 case report documented a patient developing Frégoli syndrome alongside drug dependence and hallucinations after prolonged levodopa/carbidopa use and self-adjusted dosing (Springer, 2025). When the levodopa dosage was reduced or discontinued, delusional symptoms including misidentification diminished. 📌 Implication for clinicians: If Frégoli symptoms appear, especially in Parkinson’s patients, reviewing and adjusting levodopa dosing is not just advisable, it may be essential. This is not just about psychiatric overlay, it is about dopaminergic overload and its distortion of identity perception. 5.2 Psychological and Non-Pharmacological Interventions Pharmacological intervention, even when successful, often manages the severity and reactivity of the delusion, rather than eradicating the fixed belief entirely. Therefore, psychological therapy is essential to address the distorted thoughts and associated behaviour patterns. Cognitive Behavioural Therapy (CBT) is considered crucial for FDS, particularly when comorbid with schizophrenia, where the combination of CBT and antipsychotics proves significantly more effective than medication alone (Lykouras et al., 2002). CBT aims to help the patient evaluate the non-bizarre elements of their thoughts, challenge the persecutory inferences derived from the misidentification error, and restructure their response to the belief (Courbon & Fail, 1927). For patients with complex clinical histories, including trauma or chronic non-adherence, personalised interventions, such as trauma-focused care, are necessary (Lykouras et al., 2002; Schmitt et al., 2023). Additionally, some case reports suggest that adjunctive treatments such as hypnosis may be helpful alongside traditional pharmaceutical and cognitive therapies (Courbon & Fail, 1927). The ultimate measure of therapeutic success is often redefined from complete delusion eradication to substantial reduction in patient reactivity, functional impairment, and associated violence risk. 6. Conclusion and Future Directions Frégoli Delusion Syndrome is a striking example of a monothematic delusion, classified as a hyper-identification DMS, rooted in a fundamental disruption of the cerebral circuits responsible for face recognition and identity processing. The current evidence overwhelmingly points to a critical functional and structural failure within the right hemisphere, specifically involving the fusiform gyrus and its connections to the right temporolimbic and frontal structures. This disconnection prevents the integration of visual discrepancy with identity confirmation, resulting in the brain's rationalisation of the fixed identity through a bizarre, persecutory narrative of disguise. The clinical heterogeneity of FDS, arising either from primary neurodevelopmental vulnerabilities (schizophrenia/bipolar disorder) or secondary organic insults (TBI/neurodegeneration), necessitates a stringent differential diagnostic protocol tailored by age of onset. Management must be multidisciplinary, relying on antipsychotics to modulate the salience of the delusion (likely by reducing prediction error signalling) and robust psychological intervention, chiefly CBT, to manage the fixed belief structure and mitigate high risks of aggressive behaviour. Summary of Aetiological and Therapeutic Concepts Domain Aetiology/Model Primary Correlates Therapeutic Implication Neuroanatomy Right Hemisphere Dysfunction Lesions in Fusiform Gyrus; Temporolimbic-frontal disconnection Mandatory neuroimaging (MRI) to rule out structural causes (e.g., mass lesions). Cognitive Model Dual-Route / Hyper-PIN Activation Over-excitation of Person Identity Nodes; Failure to attribute visual uniqueness Cognitive Behavioural Therapy (CBT) to challenge and restructure the fixed belief. Pharmacological Psychotic Vulnerability / Prediction Error Dopaminergic dysregulation; Schizophrenia comorbidity Antipsychotic medication (FGAs or SGAs) to modulate delusional salience and reactivity.   Directions for Prospective Research To advance the understanding and treatment of FDS, future efforts should be concentrated on three key areas. Firstly, further investigation into the familial genetic risk shared between DMS and core psychotic disorders (such as Schizophrenia and Bipolar Disorder) is required to clarify the underlying neurodevelopmental vulnerability. Secondly, specific, controlled clinical trials are necessary to compare the efficacy of modern antipsychotics (SGAs) against FGAs and adjunctive agents in homogenous DMS cohorts, moving beyond reliance on general delusional disorder data. Finally, the continued application of computational psychiatry, utilising advanced neuroimaging techniques, holds promise for refining the understanding of aberrant prediction error mechanisms, thereby offering clearer neurobiological targets for future pharmacological and neuromodulatory interventions. References Courbon, P., & Fail, G. (1927). Syndrome d'illusion de Frégoli et schizophrénie. Bulletin de la Société Clinique de Médicine Mentale, 15(1), 121–125. Langdon, R., Connaughton, E., & Coltheart, M. (2014). The Fregoli Delusion: A Disorder of Person Identification and Tracking. Topics in Cognitive Science, 6(4), 615–631. Hudson, A. J., & Grace, G. M. (2000). Misidentification syndromes related to face specific area in the fusiform gyrus. Journal of Neurology, Neurosurgery, and Psychiatry, 69(5), 645–648. Reactions Weekly. (2025). Levodopa/carbidopa/rotigotine: Various toxicities including Frégoli syndrome – case report. Reactions Weekly, 2070, p.299. Springer Nature. https://doi.org/10.1007/s40278-025-87367-2 Stanley, P. C., & Andrew, A. E. (2002). Fregoli syndrome: A rare persecutory delusion in a 17-year-old sufferer of psychosis associated with typhoid fever at Jos University Teaching Hospital, Jos, Nigeria. Nigerian Journal of Medicine, 11(1), 33–34. Forstl, H., Almeida, O. P., Owen, A. M., Burns, A., & Howard, R. (1994). Psychiatric, neurological, and medical aspects of misidentification syndromes: A review of 260 cases. Psychological Medicine, 24(05), 903–910. Christodoulou, G. N., Margariti, M., Kontaxakis, V. P., & Christodoulou, N. G. (2009). The delusional misidentification syndromes: a review of available neurological data. European Archives of Psychiatry and Clinical Neuroscience, 259(1), 12-19. Silva, J. A., Leong, G. B., Weinstock, R., Sharma, K. K., & Klein, R. L. (2012). Delusional misidentification syndromes and dangerousness. Journal of Forensic Sciences, 57(3), 779–783. Chen Avni & Paz Toren. (2025). Who’s Who in Doctor Who: Rethinking the Fregoli Delusion Through the Lens of Regeneration. Academic Psychiatry, 49, 178–182. https://doi.org/10.1007/s40596-025-02120-y Feinberg, T. E., Eaton, L. A., Roane, D. M., & Giacino, J. T. (1999). Multiple Fregoli delusions after traumatic brain injury. Cortex, 35(3), 373–387. Lykouras, L., Typaldou, M., Gournellis, R., et al. (2002). Coexistence of Capgras and Fregoli syndromes in a single patient: Clinical, neuroimaging, and neuropsychological findings. European Psychiatry, 17(4), 234–235. Papageorgiou, C., Lykouras, L., Ventouras, E., et al. (2005). Psychophysiological differences in schizophrenics with and without delusional misidentification syndromes: A P300 study. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 29(4), 593–601. Mojtabai, R. (1994). Fregoli syndrome. Australasian Psychiatry, 28(3), 458–462. Teixeira-Dias, M., Dadwal, A.K., Bell, V., & Blackman, G. (2022). Neuropsychiatric Features of Fregoli Syndrome: An Individual Patient Meta-Analysis. The Journal of Neuropsychiatry and Clinical Neurosciences, 35(2), 171–177. Turkiewicz, G., et al. (2009). Coexistent Capgras and Frégoli syndromes in a female patient with paranoid schizophrenia and brain MRI findings. Revista de Psiquiatria Clínica, 36(6), 240–243. Ellis, H. D., Luauté, J., & Retterstøl, N. (1994). Delusional misidentification syndromes. Journal of Neurology, Neurosurgery, and Psychiatry, 57(1), 74–77. Corlett, P. R., Taylor, J. R., & Fletcher, P. C. (2010). Delusions and the maintenance of belief: a computational perspective. Progress in Neurobiology, 92(3), 323–338. Hentati, S., Masmoudi, R., Guermazi, F., Cherif, F., Feki, I., Baati, I., Sallemi, R., & Masmoudi, J. (2022). Fregoli syndrome in schizophrenia: about a case report. Archives of Psychiatry and Mental Health, 6(1), 1-5.

Navaratri Stuti Nava rātri, shubh kāl, jagadambe namah. (Nine nights, an auspicious time, salutations to the Mother of the world.) Durgā mā, tejasvini, shakti rūpā. (Mother Durga, radiant and powerful, in the form of pure energy.) Shailaputrī, pratham rūpa, parvat putrī. (Shailaputri, the first form, daughter of the mountains.) Brahmachāriṇī, tapasvinī, gyāna dāyinī. (Brahmacharini, the ascetic, bestower of wisdom.) Chandraghaṇṭā, vīra rūpā, bhaya nāshinī. (Chandraghanta, the courageous form, destroyer of fear.) Kuṣmāṇḍā, brahmāṇḍa sraṣṭā, tejomayī. (Kushmanda, creator of the universe, full of light.) Skandamātā, mātṛ rūpā, snehapūrṇā. (Skandamata, in the form of a mother, full of love.) Kātyāyanī, satya vādā, dushṭa nāshinī. (Katyayani, speaker of truth, destroyer of evil.) Kālarātrī, ghora rūpā, agyāna hantrī. (Kalaratri, the fierce form, killer of ignorance.) Mahāgaurī, shānta rūpā, kshamā dāyinī. (Mahagauri, the peaceful form, bestower of forgiveness.) Siddhidātrī, sarva siddhī, moksha dāyinī. (Siddhidatri, the giver of all perfections, bestower of liberation.) Nava rūpa, eka śakti, devi tvam. (Nine forms, one power, you are the Goddess.) Sarva mangala, sarva shubh, jaya Durge. (All auspiciousness, all goodness, victory to Durga.) He mā, tvām namāmi, śaraṇam gacchāmi. (Oh Mother, I bow to you, I take refuge in you.) Abstract This article analyses Navratri as a multifaceted socio-spiritual phenomenon, deconstructing it from a religious festival into a profound ritual of sacred reorientation. Drawing from foundational texts like the Devi Mahatmya, it examines the mythic arc of Goddess Durga's emergence as a response to cosmic imbalance. The paper asserts that the nine-night observance, dedicated to the Navadurga, functions as a structured praxis for individual and collective transformation. It further explores the festival's diverse regional and diasporic manifestations, from the symbolic Durga Puja in Bengal to global community celebrations, demonstrating how the core themes of divine feminine power, moral clarity, and the defeat of fragmentation are perpetuated across cultural and geographic boundaries. Introduction Navratri, Sanskrit for "nine nights," is one of the most significant Hindu festivals, observed twice annually. While its widespread celebration often focuses on music, dance, and communal feasts, its deeper significance lies in its complex theological and philosophical foundations. This paper argues that Navratri transcends a simple liturgical calendar event, instead operating as a rich cultural text that encodes narratives of cosmic order, the primacy of Shakti (divine feminine energy), and the journey of the devotee from chaos to clarity. The subsequent sections will provide a detailed exposition of its historical origins, ritual structure, and evolving socio-cultural resonance for contemporary practitioners. The Mythos of Durga and the Devi Mahatmya The central narrative of Navratri is inextricably linked to the Devi Mahatmya (Glory of the Goddess), a pivotal text from the Markandeya Purana dated to the 5th-6th century CE. It recounts the story of Mahishasura, a buffalo demon who, through intense asceticism, secured a boon of invincibility from Lord Brahma against any man or god. His subsequent usurpation of the celestial realms and disruption of cosmic harmony necessitated a divine intervention of unparalleled power. The gods, rendered powerless, pooled their radiant energies to manifest Durga, a warrior goddess with ten arms, each wielding a weapon gifted by a different deity. This myth is not only a chronicle of a battle; it is a profound symbolic narrative. Mahishasura represents unchecked ego and ignorance, a chaotic force (tamas) that can only be vanquished by the integrated clarity and righteous action of Shakti. Durga's victory symbolises the triumph of dharma (cosmic order) and the essential role of feminine power in universal preservation. Navratri as a Ritual and Socio-Spiritual Praxis The nine nights of Navratri constitute a structured ritual arc dedicated to the Navadurga, nine distinct forms of Durga. This ritual progression is a blueprint for the devotee's internal journey. Each day is a threshold, beginning with Shailaputri, who embodies grounded strength, and culminating in Siddhidatri, the granter of wisdom and liberation. The daily focus on a specific form, from the asceticism of Brahmacharini to the fierce protection of Kalaratri, provides a framework for spiritual discipline and introspection. The Nine Nights: Navadurga and the Spiritual Arc Each night of Navratri is dedicated to a form of Durga, collectively known as the Navadurga . These forms are not simply theological abstractions but portals of emotional and spiritual transformation: Shailaputri  – Daughter of the Himalayas; symbol of grounded strength Brahmacharini  – Ascetic devotee; embodiment of discipline and penance Chandraghanta  – Warrior grace; dispeller of fear and protector of peace Kushmanda  – Cosmic creator; source of vitality and joy Skandamata  – Mother of Kartikeya; nurturer and guardian Katyayani  – Fierce justice; remover of obstacles and injustice Kalaratri  – Dark destroyer; annihilator of ignorance and evil Mahagauri  – Pure and serene; symbol of forgiveness and restoration Siddhidatri  – Granter of wisdom and supernatural powers These nine forms represent a spiritual progression, from rootedness to transcendence, from discipline to liberation. Devotees engage with each form through fasting, prayer, and reflection, seeking strength, clarity, and transformation. The Austerity of the Fast: Purifying the Body and Mind A central component of this ritual praxis is the fast (vrat), a practice of self-discipline that complements the worship of the nine goddesses. The fast is not simply a dietary restriction, but a conscious act of spiritual purification. By abstaining from specific foods, particularly grains, pulses, and table salt, devotees engage in a form of physical detoxification. This process is believed to cleanse the body of tamasic (inertial) and rajasic (overly active) qualities, promoting sattvic (pure and balanced) energy. This dietary regimen is a symbolic withdrawal from worldly attachments, allowing for a heightened state of mental clarity and spiritual focus. The fast thereby serves as a corporeal manifestation of the internal battle that Durga waged against the demon, with the devotee's body becoming a site for the triumph of self-control over base desires. Regional and Diasporic Manifestations Navratri’s core themes manifest across a wide spectrum of regional and global practices. In Eastern India, particularly Bengal, the festival culminates in Durga Puja, a five-day event that reframes the goddess not only as a warrior but as a beloved daughter returning home. The elaborate rituals, from the Nabapatrika (the ritual of nine plants) to the Sandhi Puja (a critical moment symbolising Durga's victory), culminate in the idol immersion (visarjan), a symbolic farewell that signifies both a departure and an enduring blessing. In contrast, Gujarat's Navratri is celebrated with Garba and Dandiya Raas, dynamic circle dances that symbolise the cyclical nature of life and the cosmic rhythm. In Tamil Nadu, the festival is observed through Golu, an elaborate tiered display of dolls that represents the divine hierarchy and cosmic order. In Gujarat and many countries, Navratri is celebrated through Garba, a circular dance performed in honour of the goddess. Deeply rooted in agricultural rhythms and devotional choreography, Garba is more than celebration; it is ritual in motion. Dancers move around a central lamp or image of Durga, symbolising the cyclical nature of time and the constancy of Shakti. Whether in village courtyards or diasporic auditoriums, Garba becomes a communal invocation, threading rhythm, memory, and spiritual clarity into every step. Circular choreography, communal clarity, Navratri threaded https://www.youtube.com/watch?v=VRRnuJph8kQ&list=RDVRRnuJph8kQ&start_radio=1 https://www.youtube.com/watch?v=rz1hAo3Hiy4&list=RDQMsFg1Fg2Okyk&index=3 Globally, diasporic communities have adapted the festival, recreating pandals and organising community-wide events that serve as vital cultural anchors. In cities like London, Toronto, and New York, the celebration blends traditional liturgy with contemporary formats, making the festival accessible to younger generations. The goddess is invoked not only in Sanskrit but also in English, Gujarati, and other languages, her story retold through podcasts, blogs, and cultural performances, thereby expanding her resonance as a transnational symbol of resistance and care. Conclusion Navratri is a deeply layered phenomenon that serves as a powerful testament to the enduring appeal of the divine feminine. Its historical roots in the Devi Mahatmya provide a mythic foundation for a rich, nine-night ritual praxis that facilitates personal and collective transformation. By studying its diverse regional expressions and its continued evolution in the diaspora, we see how the core principles of overcoming chaos, embracing clarity, and celebrating the power of Shakti remain universally relevant. The festival is, therefore, not only a celebration of a historical victory, but a perennial call to recalibration and renewal for the devotee. Note: While traditional depictions show Maa Durga atop a lion, the surfing board serves as a modern, metaphorical representation of her power. She is not just a static deity; she is an active, dynamic force gracefully riding the waves of chaos and change.

The wave bows gently to the morning light,    Mind adrift where sea and silence meet,    Each breath a rhythm, each fall a flight. Abstract Outdoor activities have long been celebrated for their capacity to elevate mood, reduce stress, and promote a sense of connection with the natural world. This article examines the psychological benefits of surfing and similar nature-based pursuits, drawing from a multidisciplinary array of research spanning psychology, neuroscience, and environmental studies. By weaving together empirical evidence and philosophical reflection, we argue that outdoor recreation is not merely a pastime, it is a profound therapeutic modality. Surfing, in particular, emerges as a compelling case study in how physical engagement with nature can recalibrate the mind, restore emotional equilibrium, and cultivate resilience. With a tone that balances academic rigor and lighthearted eloquence, this article invites readers to reconsider the beach not as a luxury, but as a laboratory of mental restoration. Introduction In a world increasingly dominated by screens, schedules, and synthetic environments, the human psyche finds itself yearning for something elemental. The rise of anxiety, depression, and burnout in modern societies is not only a consequence of individual pathology but a symptom of collective disconnection from nature, movement, and the present moment. Outdoor activities offer a contrast to this malaise, providing not only physical exertion but also psychological respite. Among these, surfing stands out as a particularly rich source of mental nourishment. It is a sport, yes, but also a ritual, a dance with the ocean that demands presence, humility, and adaptability. The surfer does not conquer the wave; they collaborate with it. This dynamic interaction between human and nature support a unique psychological state, one that is both exhilarating and meditative. In exploring the mental health benefits of surfing, we uncover broader truths about the healing power of outdoor engagement. Theoretical Framework To understand why outdoor activities like surfing have such a profound impact on mental health, we must first consider the theoretical framework that supports this phenomenon. The Biophilia Hypothesis, proposed by Edward O. Wilson, proposes that humans possess an inherent tendency to seek connections with nature and other forms of life. This affinity is not merely aesthetic, it is deeply psychological, rooted in our evolutionary history. When we immerse ourselves in natural environments, we activate neural pathways associated with calm, curiosity, and joy. Similarly, the Attention Restoration Theory developed by Rachel and Stephen Kaplan suggests that natural settings replenish our cognitive resources, particularly those depleted by the demands of urban living. Unlike the overstimulation of cityscapes, nature offers "soft fascination," stimuli that gently engage the mind without overwhelming it. Finally, Mihaly Csikszentmihalyi’s Flow Theory provides a lens through which to view surfing as a peak experience. Flow is the state of complete absorption in an activity, where time dilates, self-consciousness fades, and performance reaches its zenith. Surfing, with its unpredictable waves and demand for skillful navigation, is a quintessential flow activity, offering surfers a potent cocktail of focus, fulfillment, and freedom. Surfing as Psychotherapy Surfing is more than a sport; it is an expression of mindfulness in motion. Each wave presents a new challenge, requiring the surfer to attune to their breath, balance, and surroundings. This acute awareness mirrors the principles of mindfulness-based stress reduction, a therapeutic approach pioneered by Jon Kabat-Zinn. In the ocean, there is no room for rumination or distraction; the surfer must be fully present, lest they be swept away. This enforced presence cultivates a mental clarity that is often elusive on land. Moreover, the physical exertion involved in paddling, balancing, and manoeuvring triggers the release of neurochemicals such as serotonin and endorphins, which are known to elevate mood and reduce anxiety. Sunlight exposure further boosts vitamin D levels, contributing to overall wellbeing. But beyond the biochemical, surfing teaches psychological resilience. The ocean is indifferent to human plans, it crashes, recedes, and surprises. Learning to ride its waves requires not only skill but also surrender. The dialogue with uncertainty mirrors life itself, and in mastering it, surfers often find themselves better equipped to handle emotional turbulence on shore. Sociocultural Dimensions The mental health benefits of surfing are not confined to the individual; they ripple outward into the social sphere. Surfing communities, often characterised by inclusivity, camaraderie, and shared passion, provide a sense of belonging that is crucial for psychological wellbeing. In an era marked by social fragmentation and loneliness, these communities offer a rare space for authentic connection. Initiatives such as The Wave Project in the UK have harnessed this potential, using surf therapy to support young people facing mental health challenges. By combining physical activity with mentorship and group support, these programs demonstrate that surfing can be both a personal and collective healing practice. Moreover, the culture of surfing, its ethos of respect for nature, its celebration of spontaneity, stands in sharp contrast to the hyper-competitive, achievement-oriented norms of modern life. In embracing the unpredictability of the sea, surfers cultivate a worldview that values adaptability over control, experience over outcome. This shift in perspective can be profoundly liberating, offering a new lens through which to view not only mental health but also the human condition. Limitations and Future Research While the anecdotal and qualitative evidence supporting the mental health benefits of surfing is compelling, the field would benefit from more rigorous empirical investigation. Randomised controlled trials, longitudinal studies, and neuroimaging research could help quantify the psychological and neurological changes associated with regular surfing. Additionally, future research should explore the differential impacts of surfing across age groups, genders, and cultural contexts. Is the therapeutic effect universal, or does it vary based on individual background and environmental factors? Furthermore, while surfing is accessible in coastal regions, it remains geographically limited. Expanding research to include other nature-based activities, such as hiking, wild swimming, and rock climbing, could help identify common mechanisms of mental restoration and inform public health strategies. Finally, there is a need to examine the sustainability of surf therapy programs and their integration into mainstream mental health services. Can the joy of riding waves be prescribed, scaled, and sustained? Conclusion Outdoor activities are not indulgences to be enjoyed in spare moments; they are essential practices for mental hygiene. Surfing, in particular, offers a poetic convergence of body, mind, and nature. It is a reminder that healing does not always require a therapist’s couch or a pharmaceutical pill; sometimes, it requires a board, a wave, and the courage to let go. In the words of surfer and philosopher Gerry Lopez, “Surfing is attitude dancing.” And perhaps, it is also soul healing. As we navigate the complexities of modern life, we would do well to remember that the ocean is not just a body of water, it is a mirror, a teacher, and a sanctuary. To surf is to surrender, to celebrate, and ultimately, to restore. References Wilson, E. O. (1984). Biophilia. Harvard University Press. Kaplan, R., & Kaplan, S. (1989). The Experience of Nature: A Psychological Perspective. Cambridge University Press. Csikszentmihalyi, M. (1990). Flow: The Psychology of Optimal Experience. Harper & Row. Kabat-Zinn, J. (2003). Mindfulness-Based Interventions in Context: Past, Present, and Future. Clinical Psychology: Science and Practice, 10(2), 144–156. Wiley. Young, S. N. (2007). How to Increase Serotonin in the Human Brain Without Drugs. Journal of Psychiatry & Neuroscience, 32(6), 394–399. Canadian Medical Association. Levine, P. A. (2015). Trauma and Surfing: Somatic Healing in Motion. Somatic Experiencing Trauma Institute. Putnam, R. D. (2000). Bowling Alone: The Collapse and Revival of American Community. Simon & Schuster. The Wave Project. (n.d.). Surf Therapy for Young People. Retrieved from https://www.waveproject.co.uk

In an era defined by rapid technological advancements, many find themselves struggling with a troubling paradox. As we stand on the cusp of incredible breakthroughs in artificial intelligence (AI) and quantum computing, human life feels more fragile than ever. A world seemingly full of promise and innovation also exposes deep vulnerabilities, raising critical questions about our dependence on technology and what it truly means to be human. The Illusion of Control in a Tech-Dominated World We live in a society that glorifies control, yet technological progress often reveals our increased fragility. Take, for instance, the rise of AI. Algorithms are designed to optimise our daily lives, from smart assistants managing our schedules to advertising targeting our preferences. However, this convenience comes at a price. We often surrender our decision-making power to machines that operate on data we do not fully understand. Digital platforms create an illusion of control. We now “choose” what to consume, but behind that choice are algorithms that predict and manipulate our behaviour. Studies have shown that individuals exposed to consistent algorithm-driven content exhibit decreased emotional resilience and an increased sense of anxiety. As technology wields influence over our decisions, it raises the question: Are we truly in control, or have we become inconsequential passengers on a ride we cannot steer? High angle view of a digital landscape representing the complexity of artificial intelligence The Emotional Toll of Digital Dependency The convenience of technology has created an emotional toll that many are beginning to recognise. Our constant connectivity promotes a culture of immediate gratification but ends up highlighting our loneliness and disconnect. Studies indicate that social media, while designed to connect us, often leads to feelings of isolation and inadequacy. Far from the utopia promised by technology, we find ourselves navigating the mental health implications of digital dependency. Moreover, the pandemic offered a clear lens through which to view this fragility. While technology enabled remote work and communication, it also exacerbated feelings of anxiety and uncertainty. People suddenly found themselves reliant on digital tools for social interaction and work, further deepening their emotional vulnerability. This dependency on technology reveals the paradox of progress: in our pursuit of convenience, we often trade away integral human experiences that promote or highlight resilience and support. Close-up view of a person working remotely, highlighting the digital dependency during the pandemic The Fragility Exposed by Global Crises Recent global crises, including pandemics, cyber threats, and climate change, have laid bare the vulnerabilities that often lurk beneath the surface of modern society. Consider the increase in ransomware attacks that paralyse critical infrastructure. These incidents highlight how our reliance on technology can become a double-edged sword. While technology promises efficiency and convenience, it also introduces new risks that can leave entire systems vulnerable in moments of crisis. The pandemic illustrated another facet of this fragility. Sudden shifts in social structures and economic systems exposed weaknesses in our reliance on interconnected networks. Many industries struggled to adapt, and communities faced unprecedented challenges as they navigated both the health crisis and its economic fallout. These moments of disruption reveal a harsh reality: the more we lean on technology, the more fragile our societal fabric becomes. Ethical Maturity vs. Technological Power As we advance towards a future dominated by AI and quantum computing, we must confront an uncomfortable truth: our technological power often outpaces our ethical maturity. In our pursuit of innovation, ethical considerations frequently take a back seat. This is particularly concerning in the realm of AI, where biases embedded in algorithms can perpetuate discrimination or lead to unintended consequences. Imagine a world where decision-making about healthcare or law enforcement rests in the hands of algorithms that lack contextual understanding or ethical grounding. The consequences can be far-reaching, affecting lives in ways we may not fully grasp. As we develop increasingly complex systems, we must acknowledge the responsibility that comes with such power. The disconnect between technological advancement and ethical frameworks not only endangers individuals but can also undermine societal cohesion. Eye-level view of a city showcasing advanced technology infrastructure, symbolising ethical challenges in progress Navigating the Paradox: Recommendations for a Resilient Future To navigate the paradox of progress, we must strive for a balanced approach that embraces technology while nurturing our humanity. Here are some actionable recommendations: Digital Literacy Education : Encourage curricula that focus on teaching digital literacy from a young age. Understanding how technology works and recognising the implications of algorithmic decisions can empower individuals to make informed choices. Promote Ethical AI Development : Advocate for frameworks that require ethical considerations in AI development. Transparency and accountability should be integral to technological advancement to prevent harm and protect vulnerable populations. Promote Community Connections : As technology offers convenience, we must also prioritise real-world connections. Engage in local community activities and support initiatives that reinforce social ties, strengthening resilience against technological isolation. Encourage Mindfulness Practices : In a world filled with digital distractions, mindfulness practices can enhance emotional wellbeing. Techniques such as meditation, journaling, and regular digital detoxes empower individuals to reconnect with themselves and their surroundings. Participate in Policy Discussions : Stay informed and engaged in discussions about technology policy. Advocate for regulations that protect individuals from the vulnerabilities created by technology, ensuring that innovation serves humanity rather than dictates it. As we continue to innovate, we must ask ourselves what it means to be human in a world increasingly dependent on systems we barely understand. Can technology truly protect us from the vulnerabilities it creates? The answer is not simple. We may find ourselves crafting a smarter world at the cost of a more humane one, but it is our conscious efforts that will shape the balance we seek. Wide angle view of a city skyline, symbolising the integration and challenges of technology in urban life Actionable Recommendations for Societal Responsibility As we advance into an era shaped by artificial intelligence and quantum computing, the responsibility to harness these technologies for the greater good lies with us all. Here are actionable ways to support societal responsibility: Support Inclusive Access : Advocate for initiatives that provide equitable access to technology and digital education, ensuring communities are not left behind.    Champion Ethical Standards : Encourage organisations and governments to adopt ethical frameworks prioritising human rights, privacy, and wellbeing. Promote Public Dialogue : Participate in forums and discussions about the societal impacts of emerging technologies. Informed voices influence responsible innovation. Hold Institutions Accountable : Demand transparency from corporations about technology deployment, supporting independent audits to ensure ethical compliance. Cultivate a Culture of Empathy : Support understanding in both online and offline communities by promoting respect and kindness within digital citizenship. By embracing these recommendations, society can steer technological progress toward outcomes that uplift humanity and ensure innovation aligns with our values. Even in social settings, digital devices can create a barrier between individuals. In a world increasingly shaped by technological systems and algorithmic governance, the fragility of human life is no longer confined to biological vulnerability, it is existential. Our bodies remain susceptible to harm, yet it is our social, emotional, and ethical foundation that now appears most exposed. The speed and scale of modern systems from digital surveillance to automated warfare have outpaced our capacity for reflection and restraint. We inhabit environments where decisions are made faster than comprehension allows, and where the consequences of those decisions ripple through lives with irreversible force. This dissonance between technological capability and human vulnerability accentuates a deeper truth: progress, when divorced from empathy and ethical foresight, can render the human experience precarious. In such a landscape, the imperative is not only to innovate, but to safeguard the dignity and resilience of those who live within the systems we create. This is not a call to reject progress, but to redefine it. In a time characterised by rapid digital transformation, it is vital to remember that innovation must be tempered by compassion. Let us anchor our technological ambitions in ethical frameworks and a commitment to understanding the emotional toll of our digital lives. Only through this balance can we navigate the future with resilience and purpose, ensuring that our advancements contribute to a world that values not just intelligence, but the human spirit itself.

Rakhee LB Limited Our new site for Rakhee LB Limited has a fresh look, in terms of simplicity, compassionate, and designed with you in mind. With clearer navigation and tailored services for dementia and mental health support, we have created a space that is both easy to explore and emotionally attuned. We invite you to take a look, breathe it in, and feel the difference.

🎂 🌻A sunflower, bold and upright, turning always toward the light. It mirrors you, Rekha: rooted in truth, radiant in presence, and quietly defiant in the face of heat. A symbol not just of joy, but of endurance. At this hour, the Earth turns once more to honour a woman whose presence has reshaped systems, restored broken spaces, and dignified the invisible. Not just a birth, but the beginning of a legacy, clarity, reform, and quiet brilliance stitched into every structure she’s touched. This is not a milestone. It’s a moment of becoming. Rekha has honoured emotional labour, challenged the scaffolding of services, and turned grief into ritual. Her life is a living archive of resilience, where adversity becomes architecture and frontline strain becomes a blueprint for dignity. In every domain she enters, be it policy, care, or community, she brings a rare brilliance: one that dignifies the overlooked, restores the broken, and insists that respect is not a courtesy, but a cornerstone. Her leadership is not loud, but luminous. Not performative, but profound. We mark this hour not in minutes, but in meaning: A turning of the Earth in quiet celebration A life layered with insight, grit, and grace A legacy felt in every life touched, every truth spoken As the moment arrives, we bear witness, not just to her birth, but to her becoming. A ceremonial pause. A whispered invocation. A gesture rooted in soil and memory. A quiet sitting, where lived truth settles like dew on mulberry leaves. ENJOY YOUR SPECIAL DAY, SWEET! Lots and Lots of Love, Team Rakhee LB 🌻 xxxx

Emergency Contacts Dear Valued Customers and Colleagues, Rakhee LB Limited will be temporarily closed for the summer holiday from Monday 11 August 2025 to Thursday 11 September 2025 . During this time, we will not be responding to messages or inquiries. We would like to sincerely thank all our customers and colleagues for your dedication, trust, and support throughout the year. Your continued engagement means the world to us, and we look forward to reconnecting in September with renewed energy and our ongoing commitment to dignity, clarity, and compassionate care. If your message is urgent or relates to health, wellbeing or social care, please contact one of the following services: Your GP NHS 111 Your Local Crisis Team Your Local Mental Health Services Your Local Authority (Social Services) Your Local Samaritans (call 116 123 – free, confidential, 24/7) Important Message If you are currently participating in a research study, please contact your university or research coordinator directly for support or updates. We appreciate your understanding and look forward to reconnecting in September with renewed energy and continued commitment to dignity, clarity, and care. Warm regards, Team Rakhee LB