Disturbance Of Skin Sensation
Introduction
Section titled “Introduction”Disturbances of skin sensation refer to alterations in the normal perception of touch, pressure, temperature, or pain through the skin. These conditions can manifest in various forms, including reduced sensation, known as hypoesthesia, or abnormal, often unpleasant sensations, termed dysesthesia.[1] Such disturbances are not uncommon and can arise from a variety of causes, impacting an individual’s quality of life and daily functioning.
Biological Basis
Section titled “Biological Basis”The skin’s ability to sense environmental stimuli relies on a complex network of specialized nerve endings and sensory receptors that transmit signals through peripheral nerves to the central nervous system. When these intricate pathways are damaged or dysfunctional, normal sensation can be profoundly disturbed. Growing evidence suggests that genetic factors play a significant role in an individual’s susceptibility to these sensory alterations.[1]Genome-wide association studies (GWAS) have been instrumental in identifying common genetic variations, known as single nucleotide polymorphisms (SNPs), that are associated with differences in sensory perception. For example, specific SNPs such asrs502281 and rs2063640 have been linked to hypoesthesia, with these variants located within or near genes like ARID1B and ZPLD1.[1] Dysesthesia has been associated with SNPs such as rs2677879 , which is found within the METTL4 gene.[1] While the precise functions of some of these genes in sensory processing are still under investigation, these findings underscore the genetic underpinnings of how individuals experience sensation. Other research further supports the idea that complex skin-related physiological traits, like electrodermal activity, are influenced by multiple genes.[2]
Clinical Relevance
Section titled “Clinical Relevance”Disturbances of skin sensation hold significant clinical relevance across various medical and surgical specialties. A prominent example is their frequent occurrence following bilateral sagittal split ramus osteotomy (BSSRO), a common surgical procedure performed to correct jaw deformities.[1] After BSSRO, patients often experience sensory disturbances, particularly hypoesthesia and dysesthesia, in the lower lip and mental area, even in cases without overt nerve injury.[1] The frequency of these symptoms can be substantial, with hypoesthesia reported in 16.8% and dysesthesia in 49.2% of patients in some studies.[1] The evaluation of these disturbances often involves specialized objective tests, such as the Semmes-Weinstein pressure aesthesiometer test, used for assessing tactile sensation.[1] A deeper understanding of the genetic predispositions to these complications can inform personalized patient counseling, enhance risk assessment, and guide the development of preventative strategies and treatments.
Social Importance
Section titled “Social Importance”The impact of disturbed skin sensation extends far beyond the physical symptoms, significantly affecting daily activities and overall quality of life. Individuals experiencing hypoesthesia may face challenges with tasks requiring fine motor control or be at an increased risk of injury due to a diminished awareness of pressure, temperature, or pain. Dysesthesia, characterized by unpleasant or painful sensations, can severely impair an individual’s well-being, influencing basic functions like eating and speaking, and impacting social interactions. Given that many individuals undergoing procedures like BSSRO are young and otherwise healthy, these sensory disturbances can represent a substantial and chronic burden.[1] Continued research into the genetic and biological basis of these conditions is vital for developing more effective interventions, improving patient care, and ultimately enhancing the lives of those affected by sensory disturbances.
Limitations
Section titled “Limitations”The current understanding of genetic factors influencing disturbance of skin sensation, particularly in the context of post-surgical recovery, is subject to several important limitations that warrant careful consideration when interpreting research findings. These limitations span methodological constraints, specificity of phenotypic assessment, and challenges related to generalizability and the complex interplay of genetic and environmental factors.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Research into sensory disturbances often faces significant methodological and statistical limitations that can impact the reliability and breadth of findings . A single nucleotide polymorphism (SNP) likers377715874 can influence the CCDC138 gene’s function by altering its expression levels or the structure of the resulting protein, potentially impacting its ability to interact with other cellular components.[3] Such disruptions could affect the delicate balance required for normal nerve function or the structural integrity of skin tissues, thereby contributing to disturbances in skin sensation, such as dysesthesia or hypoesthesia, which are often investigated through genome-wide association studies.[1] The rs7780160 variant is located in the ZNF277-AS1 gene, which produces a long non-coding RNA (lncRNA). LncRNAs are regulatory molecules that do not code for proteins but instead influence gene expression by interacting with DNA, RNA, or proteins, often affecting the transcription or stability of nearby protein-coding genes, such as ZNF277.[3] These regulatory roles are crucial for a wide array of biological processes, including those involved in neurological function and the maintenance of healthy skin. A variant like rs7780160 within ZNF277-AS1 could alter the lncRNA’s stability, its binding affinity to target molecules, or its processing, leading to modified expression of genes vital for sensory neuron development, repair, or overall skin homeostasis.[3] Variations in such regulatory elements can underlie individual differences in susceptibility to conditions affecting skin sensation, including sensitive skin and other dermatological disorders.[3]
Defining Sensory Disturbances
Section titled “Defining Sensory Disturbances”Disturbances of skin sensation encompass a range of abnormal perceptions experienced on the skin, often indicating an underlying neurological or dermatological condition. Key terms include hypoesthesia, defined as a diminished sensitivity to stimuli, and dysesthesia, characterized by any abnormal, unpleasant sensation, whether spontaneous or evoked.[4] These conditions represent a departure from normal tactile sensation and can significantly impact an individual’s quality of life. Such disturbances are not merely subjective experiences but are recognized clinical phenomena, with their presence suggesting potential issues in sensory pathways.[4] The conceptual framework for understanding these disturbances acknowledges both their subjective nature and objective manifestations. For instance, following surgical procedures like bilateral sagittal split ramus osteotomy (BSSRO), sensory disturbances, particularly hypoesthesia and dysesthesia in the lower lip and mental area, are frequently observed.[4]These post-surgical sensations are often categorized as a form of neuropathic pain or sensory deficit, varying significantly among individuals and suggesting a role for genetic predispositions alongside environmental factors.[4] Beyond surgical contexts, broader skin sensitivity, such as “self-reported sensitive skin” or “skin sensitivity to sun,” also falls under this umbrella, representing a heightened or altered response to various external stimuli.[3]
Classification and Severity Grading
Section titled “Classification and Severity Grading”Classification systems for disturbances of skin sensation typically involve distinguishing between different types of abnormal perceptions and grading their severity. For specific neurological deficits, such as those affecting the inferior alveolar nerve, conditions are primarily classified into categories like hypoesthesia and dysesthesia.[4] These are often treated as distinct subtypes, though they can co-occur or represent different facets of a broader sensory impairment. The severity of sensory function can be dimensionally assessed using standardized scales, moving beyond a simple presence or absence of symptoms.[4] A notable example of severity gradation is the Bell scale, which classifies sensory function into five distinct grades.[4] In clinical and research settings, specific thresholds derived from such scales are used to define the presence of a disturbance. For instance, hypoesthesia is operationally defined as a classification into grades worse than the second grade (e.g., 2.83 Fmg) on the Bell scale.[4] This allows for a categorical diagnosis (e.g., “hypoesthesic” vs. “not hypoesthesic”) based on a dimensional measurement, facilitating consistent diagnostic criteria for both clinical practice and genome-wide association studies.[4]
Measurement Approaches and Diagnostic Criteria
Section titled “Measurement Approaches and Diagnostic Criteria”Diagnostic and measurement criteria for skin sensation disturbances employ various techniques to objectively and subjectively assess sensory function. A primary method for evaluating tactile sensitivity is the Semmes-Weinstein monofilaments pressure aesthesiometer test, where different filament thicknesses apply varying forces to the skin.[4] A patient is considered to have tactile sensitivity if they perceive any stimulation, regardless of whether it feels like a normal sensation.[4] Hypoesthesia, for example, is identified when an individual’s perception falls below a specific threshold, such as being worse than the second grade (2.83 Fmg) on the Bell scale.[4] Dysesthesia, conversely, is typically identified through a patient’s self-report of spontaneously recognizing abnormal sensations.[4] Beyond direct tactile assessment, other physiological and subjective measures contribute to the understanding and diagnosis of skin sensation. Electrodermal activity (EDA), which includes skin conductance level (SCL) and skin conductance response (SCR), measures skin’s electrical conductivity and is linked to various dermatological and neurological conditions.[5] Operational definitions for EDA involve recording skin conductance with Ag-AgCl electrodes and quantifying responses based on amplitude and frequency, often with specific micro-Siemens (µS) thresholds for detection.[5] Furthermore, subjective reports captured through surveys and questionnaires are crucial for conditions like “self-reported sensitive skin”.[3] while “skin sensitivity to sun” can be assessed using a phototype score.[6] highlighting the multifaceted nature of diagnosing and characterizing these disturbances.
Neural Pathways and Mechanisms of Sensory Perception
Section titled “Neural Pathways and Mechanisms of Sensory Perception”Skin sensation is a complex biological process mediated by an intricate network of specialized nerve fibers and receptors that transmit information from the periphery to the central nervous system. Disruptions to these pathways can lead to various sensory disturbances, such as hypoesthesia, characterized by reduced sensation, and dysesthesia, involving abnormal or unpleasant sensations.[4] These conditions are frequently observed following procedures that impact peripheral nerves, like the inferior alveolar nerve after bilateral sagittal split ramus osteotomy (BSSRO), even in the absence of overt nerve injury.[4] Early scientific investigations, such as Waller’s experiments on nerve sectioning, provided fundamental insights into the structural alterations that occur in nerve fibers following injury, laying the groundwork for understanding nerve regeneration and pathology.[7] The evaluation of skin sensibility employs methods like the Semmes-Weinstein monofilaments, which precisely measure pressure perception and can identify subtle differences in sensory thresholds, even between the dominant and non-dominant digits.[8]This detailed assessment helps characterize the extent and nature of sensory deficits. The overall integrity and function of these neural pathways are crucial for maintaining normal tactile, thermal, and pain perception, and their disruption can significantly impact an individual’s quality of life. Understanding the specific nerve fibers involved, their distribution, and their response to injury or disease is paramount to elucidating the mechanisms behind disturbed skin sensation.
Cellular and Molecular Processes in Sensory Regulation
Section titled “Cellular and Molecular Processes in Sensory Regulation”The regulation of skin sensation at the cellular and molecular level involves a sophisticated interplay of specialized cells, signaling pathways, and key biomolecules. Electrodermal activity (EDA), for example, provides a physiological measure of sympathetic nervous system arousal primarily through its influence on eccrine sweat glands within the skin.[5] This activity reflects the dynamic functioning of these cellular units and their neural control. Specific neurochemical systems, such as the serotonergic pathway, are integral to modulating sensory responses, with genetic polymorphisms like the 5-HT1A CG variant influencing electrodermal reactivity.[9] The accurate recording of skin conductance, a direct measure of the skin’s electrical properties, is achieved using specialized Ag-AgCl electrodes and conductive mediums like NaCl electrolyte paste.[5]This method allows for the assessment of underlying cellular functions related to sweat gland activity and neural transmission. Critical biomolecules, including various neurotransmitters, their receptors, and enzymes, orchestrate the transmission and interpretation of sensory information, thereby playing a fundamental role in both normal sensation and its dysregulation. Disturbances in these molecular signaling cascades can lead to altered sensory perception, contributing to conditions like sensitive skin or neuropathic pain.
Genetic and Epigenetic Modulators of Sensory Sensitivity
Section titled “Genetic and Epigenetic Modulators of Sensory Sensitivity”Individual predisposition and vulnerability to disturbances in skin sensation are significantly influenced by genetic and epigenetic factors. Genome-wide association studies (GWAS) have been instrumental in identifying specific single-nucleotide polymorphisms (SNPs) associated with traits such as self-reported sensitive skin and post-surgical sensory disturbances.[3] For instance, variants located at chromosome 2p21 have been linked to sensitive skin in certain populations.[3] while specific SNPs near the ARID1B and ZPLD1 genes on chromosomes 6 and 3, respectively, have been identified as candidate loci for hypoesthesia.[4] Furthermore, dysesthesia has been associated with an SNP, rs2677879 , located within the METTL4 gene on chromosome 18.[4]This particular SNP is a nonsynonymous polymorphism, meaning it leads to an amino acid substitution (Gln to Lys) in the encoded protein, which could alter its function.[4] METTL4, a methyltransferase-like protein, may be involved in methyltransferase activity, potentially influencing genomic DNA methylation and thereby modulating neural transmission relevant to sensory disturbances.[4]Beyond direct genetic variations, epigenomic profiling has revealed that DNA methylation changes are associated with conditions like major psychosis, suggesting that epigenetic mechanisms can also play a crucial role in the broader context of sensory processing and neurological function.[10]
Pathophysiological Links and Systemic Implications
Section titled “Pathophysiological Links and Systemic Implications”Disturbances of skin sensation are not isolated phenomena but are frequently intertwined with a spectrum of pathophysiological processes and broader systemic conditions, reflecting widespread disruptions in bodily homeostasis. Anomalies in electrodermal activity, for instance, are observed in various dermatological conditions, including psoriasis and epidermal damage, indicating a compromised skin barrier and altered neural responses.[11]Beyond dermatological issues, sensory disturbances are also linked to severe neurological conditions such as coma, cerebral vascular diseases, Huntington’s disease, and multiple sclerosis, highlighting the profound impact of central and peripheral nervous system pathologies on sensory perception.[5] The heritability of electrodermal response lability suggests a genetic predisposition to altered physiological reactivity, which can manifest across diverse clinical presentations.[12]Such genetic architectures also play a role in the vulnerability to neuropathic pain and other psychiatric disorders, illustrating the complex interplay between genetic factors and physiological outcomes.[4]Understanding these multifaceted connections between specific genetic polymorphisms, cellular dysfunctions, and systemic disease states is crucial for comprehending the complete biological landscape of disturbed skin sensation and its impact on overall health and well-being.
Neuro-Immune Signaling and Inflammatory Responses
Section titled “Neuro-Immune Signaling and Inflammatory Responses”The disturbance of skin sensation often originates from or is exacerbated by intricate neuro-immune signaling pathways that mediate inflammatory responses in the skin. A critical pathway involves the caspase recruitment domain family member 14 (CARD14), where a gain-of-function mutation can lead to spontaneous psoriasis-like skin inflammation through an enhanced keratinocyte response to IL-17A.[13] This mechanism highlights how receptor activation by cytokines like IL-17A initiates intracellular signaling cascades within keratinocytes, driving inflammatory pathology that can profoundly alter sensory perception and skin integrity.
Another significant inflammatory signaling cascade involves tumor necrosis factor-alpha (TNF-a), a potent pro-inflammatory cytokine.TNF-a has been shown to downregulate the expression of key skin barrier proteins, filaggrin and loricrin, through the activation of the c-Jun N-terminal kinase (JNK) pathway.[14] This pathway dysregulation directly contributes to compromised skin barrier function, a common feature in inflammatory dermatological conditions, and consequently influences skin sensitivity and the experience of sensations.
Epidermal Barrier Homeostasis and Gene Regulation
Section titled “Epidermal Barrier Homeostasis and Gene Regulation”Maintaining the epidermal barrier is fundamental for normal skin sensation, and its integrity is largely dependent on the precise regulation of structural proteins like filaggrin and loricrin. The expression of the profilaggrin gene, which is the precursor to filaggrin, is tightly controlled by complex interactions between epidermal POU domain and activator protein 1 (AP1) transcription factors.[15] This intricate transcriptional regulation ensures the proper differentiation of keratinocytes and the formation of a robust skin barrier, with any disruption potentially leading to altered sensory function.
Environmental factors and metabolic processes also play a crucial role in modulating skin barrier proteins. For instance, exposure to urban particulate matter can downregulate filaggrin expression via the induction of COX2 and subsequent PGE2 production, resulting in impaired skin barrier function.[16] Additionally, the MAPK pathway is deeply involved in the epidermal terminal differentiation of normal human epidermal keratinocytes.[17] These pathways underscore the sophisticated network of gene regulation and metabolic flux control that underpins epidermal homeostasis, and whose dysregulation can manifest as disturbances in skin sensation.
Epigenetic and Post-Translational Regulatory Mechanisms
Section titled “Epigenetic and Post-Translational Regulatory Mechanisms”Beyond direct genetic variations, epigenetic and post-translational mechanisms provide critical layers of regulatory control over gene expression and protein function relevant to skin sensation. Epigenomic profiling has revealed DNA-methylation changes associated with neurological and psychiatric conditions.[10] Given that sensory disturbances, such as those affecting the inferior alveolar nerve, can have a genetic basis.[4]it is plausible that similar DNA methylation changes could modulate genes encoding receptors, ion channels, or signaling molecules crucial for peripheral nerve function and skin sensory processing.
Furthermore, post-translational modifications, particularly protein methylation, represent another significant regulatory mechanism. Chemogenetic analysis has identified human protein methyltransferases, enzymes that modify proteins by adding methyl groups.[18] These modifications can alter protein activity, stability, subcellular localization, or interactions with other molecules, thereby finely tuning the function of proteins involved in sensory transduction and nerve signaling. Dysregulation of these protein modification pathways could contribute to the altered responsiveness or transmission of sensory information in the skin.
Systems-Level Dysregulation and Disease Pathogenesis
Section titled “Systems-Level Dysregulation and Disease Pathogenesis”Disturbances in skin sensation often arise from the systems-level integration and crosstalk between various molecular pathways, leading to emergent properties characteristic of complex dermatological and neurological conditions. For example, the interplay of inflammation-related pathways, such as the CARD14-IL-17A axis or TNF-a-JNK pathway, with epidermal barrier integrity, as governed by filaggrin and loricrin regulation, illustrates a hierarchical regulation where inflammatory signals can directly impair the physical and functional properties of the skin.[13]This network interaction contributes to conditions like psoriasis and atopic dermatitis, which are associated with altered electrodermal activity and other sensory disturbances.[5]The dysregulation of these integrated networks is central to disease pathogenesis. Loss-of-function variants infilaggrin, for instance, are well-established mechanisms contributing to atopic dermatitis.[19] a condition characterized by significant skin barrier dysfunction and altered tactile and pruritic sensations. Understanding these pathway dysregulations can also reveal therapeutic targets. The observation that TNF-a antagonists can improve skin barrier function by mitigating the downregulation of filaggrin and loricrin suggests that modulating specific inflammatory pathways can have systemic benefits on skin health and potentially normalize sensory perception.[14]
Clinical Assessment and Prognosis
Section titled “Clinical Assessment and Prognosis”The evaluation of skin sensation disturbances holds significant clinical relevance for diagnosis, monitoring disease progression, and predicting patient outcomes. Electrodermal activity (EDA), measured through skin conductance level (SCL) and skin conductance response (SCR), serves as an objective marker for various medical and neurological conditions. For instance, abnormal EDA responses are associated with dermatological issues like psoriasis and epidermal damage, as well as severe neurological states such as coma, cerebral vascular diseases, Huntington’s disease, and multiple sclerosis.[11]Standardized sensory evaluations, such as the Semmes-Weinstein monofilaments pressure aesthesiometer, are crucial for assessing tactile sensitivity, while the McGill Pain Questionnaire can quantify subjective abnormal sensations like dysesthesia, particularly in post-surgical contexts such as after bilateral sagittal split ramus osteotomy.[1] Monitoring strategies for sensory disturbances are essential, as demonstrated in patients undergoing procedures affecting nerve integrity. For example, the assessment of hypoesthesia and dysesthesia after inferior alveolar nerve surgery at specific post-operative time points, such as four weeks, helps to understand nerve regeneration and avoid confounding factors like Wallerian degeneration.[1]Furthermore, skin intrinsic fluorescence (SIF), a non-invasive marker, is strongly associated with the accumulation of advanced glycation end products in individuals with diabetes, correlating with the severity of microvascular complications, autonomic neuropathy, and distal symmetrical polyneuropathy.[20] This makes SIF a valuable tool for identifying diabetic patients at risk for developing complications that can manifest as sensory disturbances, providing prognostic value beyond traditional risk scores.[21]
Genetic Insights and Risk Stratification
Section titled “Genetic Insights and Risk Stratification”Genetic factors play a substantial role in predisposing individuals to disturbances of skin sensation and influencing their clinical course, offering avenues for personalized medicine and risk stratification. Electrodermal activity (EDA), a physiological correlate of skin sensation, exhibits significant heritability, suggesting a complex genetic architecture influenced by multiple genes rather than single polymorphisms with large effects.[2] Genome-wide association studies (GWAS) have begun to identify specific genetic variants linked to sensory disturbances, such as rs2677879 which has shown associations with dysesthesia following inferior alveolar nerve surgery, with candidate loci identified near or within the ARID1B and ZPLD1 gene regions.[1]However, the power of such studies can be limited by sample size, necessitating larger cohorts for robust associations.
Beyond specific single nucleotide polymorphisms (SNPs), broader genetic profiles and demographic factors contribute to risk stratification. In conditions like Charcot-Marie-Tooth Disease type 1A, specific subphenotypes, including “burning or tingling in feet or hands,” are influenced by modifier genes.[22]Moreover, patient age and sex are significant covariates, with disease severity often increasing with age, and females more likely to experience certain sensory and motor symptoms, while males may present with higher likelihood of foot deformity.[22]Understanding these genetic and demographic influences allows for the identification of high-risk individuals and the potential development of targeted prevention or intervention strategies, although the genetic basis of EDA, for instance, has not yet revealed strong associations with genes in specific neurotransmitter systems or with conditions like substance dependence or schizophrenia.[2] However, a polymorphism in the HTR1A gene has been linked to electrodermal reactivity.[9]
Systemic and Neurological Disease Associations
Section titled “Systemic and Neurological Disease Associations”Disturbances of skin sensation are frequently comorbid with a wide array of systemic, dermatological, and neurological conditions, serving as indicators or complications of underlying pathologies. Electrodermal activity (EDA) anomalies are recognized in dermatological conditions such as psoriasis and epidermal damage, highlighting the skin’s role as an interface for physiological and pathological processes.[11]Neurological conditions like coma, cerebral vascular diseases, Huntington’s disease, and multiple sclerosis also present with altered EDA, underscoring its utility in assessing central nervous system function and dysfunction.[23]Furthermore, sensory disturbances are integral to the clinical presentation of psychiatric disorders, with EDA anomalies consistently linked to schizophrenia and severe mood disorders.[11]In metabolic diseases, such as type 1 and type 2 diabetes mellitus, skin intrinsic fluorescence (SIF) acts as a non-invasive marker for the accumulation of advanced glycation end products and is strongly associated with the development of micro- and macrovascular complications, including autonomic and distal symmetrical polyneuropathy.[20] These associations demonstrate that changes in skin sensation and related physiological parameters are not isolated phenomena but rather reflect complex interactions with various systemic and neurological pathologies, often representing crucial overlapping phenotypes or complications.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs377715874 | CCDC138 | disturbance of skin sensation |
| rs7780160 | ZNF277-AS1 | disturbance of skin sensation |
Frequently Asked Questions About Disturbance Of Skin Sensation
Section titled “Frequently Asked Questions About Disturbance Of Skin Sensation”These questions address the most important and specific aspects of disturbance of skin sensation based on current genetic research.
1. Why do I feel weird sensations after surgery, but my friend doesn’t?
Section titled “1. Why do I feel weird sensations after surgery, but my friend doesn’t?”Genetic factors play a significant role in how individuals experience sensation. Specific variations in genes, such as ARID1B, ZPLD1, or METTL4, can make some people more susceptible to reduced or abnormal sensations even without obvious nerve damage. Your unique genetic makeup can influence how your body reacts and recovers from such procedures.
2. Can these strange skin feelings make it hard for me to eat or talk?
Section titled “2. Can these strange skin feelings make it hard for me to eat or talk?”Yes, if you experience dysesthesia, which involves abnormal and often unpleasant sensations, it can severely impact your well-being. These feelings, especially in areas like the lower lip or mental area, can make basic functions like eating and speaking quite challenging and uncomfortable.
3. Am I more likely to get hurt if I can’t feel my skin properly?
Section titled “3. Am I more likely to get hurt if I can’t feel my skin properly?”Yes, if you have hypoesthesia, meaning reduced sensation, you might be at an increased risk of injury. This is because your awareness of pressure, temperature, or pain is diminished, making it harder to detect potential harm from everyday activities.
4. If my family has this, am I more likely to get it too?
Section titled “4. If my family has this, am I more likely to get it too?”Research suggests that genetic factors significantly influence your susceptibility to these sensory disturbances. While it’s complex, if close family members have experienced them, it indicates a potential genetic predisposition that could increase your own risk.
5. Is it normal to have weird feelings in my jaw after surgery?
Section titled “5. Is it normal to have weird feelings in my jaw after surgery?”Yes, it’s quite common to experience sensory disturbances like hypoesthesia or dysesthesia in the lower lip and mental area after certain jaw surgeries, such as bilateral sagittal split ramus osteotomy (BSSRO). Studies show that a significant percentage of patients, up to nearly 50% for dysesthesia, report these symptoms.
6. How can doctors actually tell if my skin sensation is off?
Section titled “6. How can doctors actually tell if my skin sensation is off?”Doctors use specialized objective tests to evaluate skin sensation. For instance, the Semmes-Weinstein pressure aesthesiometer test is commonly used to assess tactile sensation, helping to quantify any reduced feeling you might be experiencing.
7. Can these skin issues affect my job or hobbies requiring precision?
Section titled “7. Can these skin issues affect my job or hobbies requiring precision?”Absolutely. If you have reduced sensation (hypoesthesia), you might face challenges with tasks requiring fine motor control or a precise sense of touch. Unpleasant sensations (dysesthesia) can also impair your overall well-being, indirectly affecting concentration and performance in detailed activities.
8. Can knowing my genes help prevent or treat these sensations?
Section titled “8. Can knowing my genes help prevent or treat these sensations?”Yes, understanding your genetic predispositions can be very helpful. This knowledge allows doctors to offer personalized counseling, assess your risk more accurately, and guide the development of preventative strategies or more targeted treatments for your specific sensory disturbances.
9. Will these strange sensations ever go away, or are they permanent?
Section titled “9. Will these strange sensations ever go away, or are they permanent?”The duration of these sensations can vary greatly. While some may resolve over time, for many individuals, especially those undergoing procedures like jaw surgery, these disturbances can become a substantial and chronic burden, impacting long-term quality of life.
10. Why do my unpleasant sensations feel so different from what others describe?
Section titled “10. Why do my unpleasant sensations feel so different from what others describe?”Your experience of unpleasant sensations, or dysesthesia, is highly subjective and inherently patient-reported. While there are common patterns, the specific quality and intensity of these feelings can vary significantly between individuals, making your personal description crucial for understanding.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Kobayashi, D. “Genome-wide association study of sensory disturbances in the inferior alveolar nerve after bilateral sagittal split ramus osteotomy.” Mol Pain, 2013.
[2] Vaidyanathan, U. “Heritability and molecular genetic basis of electrodermal activity: a genome-wide association study.” Psychophysiology, 2014.
[3] Li, B. et al. “A Genome-Wide Association Study Finds Variants at 2p21 Associated with Self-Reported Sensitive Skin in the Han Chinese population.” Journal of Investigative Dermatology, 2021.
[4] Kobayashi D, Nishizawa D, Fukuda K, Kasai S, Hasegawa J, Aoki Y, Nishi A, Saita N. “Genome-wide association study of sensory disturbances in the inferior alveolar nerve after bilateral sagittal split ramus osteotomy.” Mol Pain, vol. 10, no. 1, 2014, p. 43.
[5] Vaidyanathan U, Malone SM, Iacono WG. “Heritability and molecular genetic basis of electrodermal activity: a genome-wide association study.” Psychophysiology, vol. 52, no. 1, 2015, pp. 10–23.
[6] Galvan-Femenia, I. et al. “Multitrait genome association analysis identifies new susceptibility genes for human anthropometric variation in the GCAT cohort.” Journal of Medical Genetics, 2018.
[7] Waller, A. “Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog, and observations of the alterations produced thereby in the structure of their primitive fibres.” Phil Trans R Soc Lond, vol. 140, 1850, pp. 423–429.
[8] Hage, JJ., et al. “Difference in sensibility between the dominant and nondominant index finger as tested using the Semmes-Weinstein monofilaments pressure aesthesiometer.” Hand Surg Am, vol. 20, 1995, pp. 227–229.
[9] Schmitz, A., et al. “The 5-HT1A C(1019)G polymorphism, personality and electrodermal reactivity in a reward/punishment paradigm.” International Journal of Neuropsychopharmacology, vol. 12, 2009, pp. 383–392.
[10] Assadzadeh A, Flanagan J, Schumacher A, Wang SC, Petronis A. “Epigenomic profiling reveals DNA-methylation changes associated with major psychosis.”Am J Hum Genet, vol. 82, no. 3, 2008, pp. 696–711.
[11] Cambrai, M., et al. “Skin impedance and phoreographic index in psoriasis.” Archives of Dermatological Research, 1979.
[12] Crider, A., et al. “Stability, consistency, and heritability of electrodermal response lability in middle-aged male twins.” Psychophysiology, vol. 41, 2004, pp. 501–509.
[13] Wang M, Zhang S, Zheng G, Huang J, Songyang Z, Zhao X. “Gain-of-Function Mutation of Card14 Leads to Spontaneous Psoriasis-like Skin Inflammation through Enhanced Keratinocyte Response to IL-17A.” Immunity, vol. 49, no. 1, 2018, pp. 66–79.e5.
[14] Howell MD, Guttman-Yassky E, Gilleaudeau PM, Cardinale IR, Boguniewicz M, Krueger JG, Leung DY. “TNF-a downregulates filaggrin and loricrin through c-Jun N-terminal kinase: role for TNF-a antagonists to improve skin barrier.” J Invest Dermatol, vol. 131, no. 6, 2011, pp. 1272–79.
[15] Jang SI, Karaman-Jurukovska N, Morasso MI, Steinert PM, Markova NG. “Complex interactions between epidermal POU domain and activator protein 1 transcription factors regulate the expression of the profilaggrin gene in normal human epidermal keratinocytes.” J Biol Chem, vol. 275, no. 20, 2000, pp. 15295–304.
[16] Lee C-W, Lin Z-C, Hu SC-S, Chiang Y-C, Hsu L-F, Lin Y-C. “Urban particulate matter down-regulates filaggrin via COX2 expression/PGE2 production leading to skin barrier dysfunction.” Sci Rep, vol. 6, 2016, p. 2840.
[17] Meng X, Qiu L, Song H, Dang N. “MAPK Pathway Involved in Epidermal Terminal Differentiation of Normal Human Epidermal Keratinocytes.” Open Med (Wars), vol. 13, 2018, pp. 189–95.
[18] Richon VM, Johnston D, Sneeringer CJ, Jin L, Majer CR, Elliston K, Jerva LF, Scott MP, Copeland RA. “Chemogenetic analysis of human protein methyltransferases.” Chem Biol Drug Des, vol. 78, no. 2, 2011, pp. 199–210.
[19] Drislane C, Irvine AD. “The role of filaggrinin atopic dermatitis and allergic disease.”Ann Allergy Asthma Immunol, vol. 124, no. 1, 2020, pp. 36–43.
[20] Roshandel, D. “New Locus for Skin Intrinsic Fluorescence in Type 1 Diabetes Also Associated With Blood and Skin Glycated Proteins.” Diabetes, 2016.
[21] Gerrits, E. G., et al. “Skin autofluorescence: a tool to identify type 2 diabetic patients at risk for developing microvascular complications.” Diabetes Care, 2008.
[22] Tao, F. “Modifier Gene Candidates in Charcot-Marie-Tooth Disease Type 1A: A Case-Only Genome-Wide Association Study.”J Neuromuscul Dis, 2019.
[23] Schuri, U., and D. von Cramon. “Electrodermal responses to auditory stimuli with different significance in neurological patients.” Psychophysiology, 1981.