Organic Psychosis in A Male Adolescent With Cerebral Palsy: A Case Report And Review of The Literature

Organic Psychosis in A Male Adolescent With Cerebral Palsy: A Case Report And Review of The Literature | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Organic Psychosis in A Male Adolescent With Cerebral Palsy: A Case Report And Review of The Literature Melek Hande Bulut Demir This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8310751/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Cerebral palsy (CP) is a neurodevelopmental condition associated with motor impairment and cognitive challenges. Although psychiatric comorbidities are common, psychotic symptoms are rarely documented. Early recognition of organic psychosis in CP is essential for effective intervention. Case Presentation: We report a 15-year-old male adolescent with spastic quadriplegic CP who presented with acute psychotic symptoms, including persecutory delusions, disorganized behavior, referential ideation, and presumed auditory hallucinations. Neuroimaging revealed chronic periventricular leukomalacia. Symptoms emerged following academic stress and social isolation. Treatment with risperidone and olanzapine led to significant clinical improvement. No major extrapyramidal side effects occurred aside from transient akathisia. Discussion: Psychosis in CP may arise from structural brain abnormalities, psychosocial stressors, and cognitive vulnerabilities. Differentiating organic psychosis from primary psychotic disorders is essential for treatment planning. Limited literature exists regarding psychopharmacology in CP, emphasizing the need for further research. Conclusion: This case highlights the complexity of managing psychosis in CP and underscores the importance of early identification, multidisciplinary care, and individualized treatment strategies. cerebral palsy psychosis child adolescent psychotropic treatment Figures Figure 1 1. INTRODUCTION Cerebral palsy (CP) is a neurodevelopmental condition and the leading cause of motor impairment in childhood( 1 ). It results from damage to the developing brain and leads to lifelong motor dysfunction( 2 ). According to the World Health Organization (WHO), approximately 10% of children worldwide—nearly 200 million—experience physical disabilities, cognitive impairments, or developmental delays( 3 ). Moreover, an estimated 80% of children and adolescents with disabilities reside in low-income countries( 4 ), suggesting a higher prevalence of CP in these regions( 5 ). Despite receiving medical, rehabilitative, and supportive interventions, individuals with CP continue to face functional limitations that restrict their ability to perform daily activities( 6 ). Among these limitations, the degree of gross motor impairment is a key determinant of future physical independence, mobility, and social participation for children at risk of CP( 7 ). Psychotic disorders are severe psychiatric conditions characterized by marked disturbances in thought, perception, and affect, accompanied by impaired reality testing; they typically emerge during adolescence or early adulthood( 8 ). Although often associated with adults, psychotic disorders can also arise in childhood and adolescence, significantly influencing cognitive, emotional, and social development( 9 ). The incidence, clinical presentation, and progression of psychosis in younger populations may differ from those seen in adults, and symptoms may initially resemble or be confused with neurodevelopmental or psychiatric conditions such as ADHD, autism spectrum disorder, or anxiety disorders( 10 ). Notably, psychosis beginning in adolescence carries a risk of progressing to schizophrenia or other chronic psychiatric disorders in later life( 11 ). Although the coexistence of cerebral palsy and psychotic disorders is uncommon, its impact on functioning and quality of life can be substantial( 12 ). This case report presents the school-related challenges, emerging psychotic symptoms, clinical characteristics, treatment course, and outcomes of a 15-year-old adolescent male diagnosed with both cerebral palsy and a psychotic disorder. 2. CASE REPORT The patient is a 15-year-old male adolescent, single, literate, and enrolled in the ninth grade of a high school Informatics Department. He lives with his biological mother, father, and older brother. He has cognitive developmental delay, cerebral palsy (CP), and spastic quadriplegia and is wheelchair-bound. He presented to the child and adolescent psychiatry outpatient clinic with acute-onset psychotic symptoms, including disorganized speech and behavior, paranoid delusions, delusions of reference, and auditory hallucinations. Recent academic difficulties and feelings of social isolation at school appeared to have negatively affected his mental state. He expressed fear of failing his second-term examinations and began to believe that his teacher was keeping a record about him. Consequently, he became increasingly irritable, accusatory toward his parents, and prone to temper outbursts. According to his parents, he had been more withdrawn, sluggish, reluctant to leave his room, unwilling to interact with his family, and preoccupied with the belief that others were listening to him or intended to cause harm—symptoms that reportedly started approximately one year before admission. Family-reported history indicated that persecutory and referential delusions first emerged one year earlier. He was taken to a child and adolescent psychiatry clinic in 2024 due to worsening symptoms and functional decline. His mother noted increased dysphoria, agitation, and episodes of covering his ears while speaking to himself. When questioned about distressing stimuli, he claimed he was mocked by teachers and friends and insisted that his teacher had written negative reports about him. School staff, however, denied any such incidents, although they confirmed increased irritability. In the following days, he became increasingly withdrawn, refused food and drink, and resisted assistance with personal hygiene. He spent most of the day irritably covering his ears and whispering to himself. He was evaluated in the child and adolescent psychiatry clinic and initiated on pharmacological treatment. His hostility toward his mother escalated, and he persisted in expressing persecutory thoughts. He was subsequently referred to both child neurology and child psychiatry. Premorbidly, he was described as quiet and calm. Although he had CP, he had no prior psychiatric hospitalizations or regular psychiatric follow-up. A school psychologist evaluated him in the past for frustration and self-esteem issues. No standardized cognitive assessment had previously been conducted. He had no history of suicide attempts, self-harm, or substance use. Family history was negative for neurological or psychiatric disorders. Perinatal history revealed that the mother experienced premature rupture of membranes at 32 weeks, and the patient required neonatal intensive care due to respiratory distress. CP was diagnosed after cranial computed tomography demonstrated features consistent with anoxic brain injury. Developmental milestones were globally delayed. According to his mother, he could write, perform basic calculations, and communicate in sentences, although motor contractures limited his functioning. Educationally, he is a ninth-grade student receiving instruction in computer science at a regular public school with integrated special education services. After experiencing bullying in primary school, he transferred to a school specializing in cerebral palsy four years prior. He receives occupational, physical, and speech therapy. He reportedly performed adequately both academically and socially during the previous academic year. Socially, his interactions were limited primarily to school and family. Medically, he experienced neonatal hypoxia but was not intubated and required CPAP for one day. He carries diagnoses of spastic quadriplegic CP and hypoxic-ischemic encephalopathy. He is followed in a neuromuscular clinic and has been receiving baclofen without recent dosage changes. Cranial diffusion MRI showed no diffusion-restricted lesions, indicating no acute or subacute infarction. Non-contrast cranial MRI demonstrated increased T2 signal intensity in the bilateral periventricular white matter, enlarged lateral ventricles, and irregular ventricular walls, consistent with periventricular leukomalacia. A 2016 MRI showed a thin, arched corpus callosum, irregular posterior horn ventricular contours, and chronic leukomalacia sequelae with sulcal widening consistent with cerebral atrophy. On mental status examination, he appeared his stated age, wore appropriate clothing, and demonstrated adequate self-care. He was wheelchair-bound with minimal upper-body movement. He avoided eye contact, intermittently covered his ears, and was only partially cooperative. His mood was depressive and irritable; affect was childish, variable, and inappropriate. His speech was reduced in rate, volume, and tone; he mumbled to himself and answered questions briefly and reluctantly. Attention and concentration were impaired, memory deficits were evident, and reality testing was disturbed. Thought processes were disorganized with persecutory and referential delusions. Insight and judgment were poor, and impulse control was moderate. School, peer, and family functioning were markedly impaired. Vital signs were normal, and neurological examination revealed no acute pathology. Routine blood tests showed elevated fasting glucose. MRI findings again confirmed periventricular leukomalacia. There was no history of psychotropic medication use. Given his congenital brain pathology, the diagnosis was considered consistent with organic psychosis (WHO ICD-11 6E61), secondary to cerebral palsy (8D2Z). He was started on risperidone 0.5 mg/day orally for organic psychotic disorder secondary to CP. Differential diagnoses included psychotic disorder and psychotic depression based on DSM-5 criteria. At baseline, sleep and appetite were normal, and mood was moderately impaired. Parents expressed surprise, noting that such behavioral changes had not occurred previously. He was anxious during the interview and expressed fear about leaving school. He endorsed delusions of reference involving the belief that his thoughts were being monitored. During the mental status evaluation, he attempted to suppress auditory hallucinations by covering his ears. He appeared irritable and mistrustful toward his parents, tried to prematurely terminate the interview, refused to complete clinical assessments, and stated that his academic life was over. Risperidone 1 mg/day and olanzapine 5 mg/day were prescribed. One week later, irritability and self-talking had decreased, though he continued to believe that his teacher kept a report about him and expressed shame regarding clinic visits. Sedation and increased appetite were noted as side effects. Two weeks later, disorganized speech, referential delusions regarding phone monitoring, suspiciousness, and irritability persisted. Medication was adjusted to risperidone 0.5 mg three times daily and olanzapine 5 mg three times daily. After one month, auditory hallucinations and paranoid ideation decreased but persisted. He continued to cover his ears and told his family not to “listen to his thoughts.” He refused to continue school, and the family pursued a school transfer. Medication was increased to risperidone 2 mg/day and olanzapine 10 mg/day. At the next visit, auditory and referential delusions and irritability had markedly improved; he no longer covered his ears during interviews, although he continued to do so when his father spoke on the phone. He answered questions appropriately but appeared mildly sedated. After six months, family members reported nearly 90% improvement. No extrapyramidal side effects were observed, although he developed new-onset enuresis nocturna. Medication was adjusted to risperidone 0.5 mg twice daily and olanzapine 5 mg twice daily. When school reopened in September, symptoms were exacerbated, including social withdrawal, ear-covering behaviors, irritability toward caregivers and teachers, and knife-threatening behavior related to delusional ideation. Akathisia was observed in the lower extremities, attributed to antipsychotic treatment. Medication was adjusted to risperidone 2.5 mg/day and olanzapine 12.5 mg/day. At follow-up, symptoms improved but residual auditory and referential delusions and akathisia persisted. Doses were increased to risperidone 4 mg/day and olanzapine 20 mg/day; biperiden 2 mg three times daily and desmopressin 120 µg/day were added. The family was counseled about extrapyramidal side effects. The patient is currently awaiting inpatient psychiatric admission. Throughout follow-up, significant clinical improvement was observed after antipsychotic initiation, with no psychotic exacerbations. Current treatment includes risperidone 1 mg three times daily, olanzapine 5 mg four times daily, biperiden 2 mg three times daily, and Lioresal. Further evaluation includes EEG to rule out epileptic pathology, neuropsychological testing for possible cognitive decline, complete blood count and metabolic screening for medical contributors to psychosis, and toxicology screening. Informed consent was obtained from the patient and his family. 2.1.Brief Report In summary, this 15-year-old male adolescent—diagnosed with spastic quadriplegia secondary to an anoxic brain injury at birth—presented with acute-onset psychotic symptoms, including disorganized speech and behavior, persecutory and referential delusions, and presumed auditory hallucinations. His clinical history was characterized by mood fluctuations, atypical behaviors, and prominent internal preoccupation. Several psychosocial stressors preceded the onset of illness, including significant threats to his academic and social self-esteem and family-related anxieties regarding long-term caregiving. At presentation, he demonstrated a rapid therapeutic response to risperidone and olanzapine, although initiation of treatment was initially delayed due to concerns related to his neuromuscular condition. 3. DISCUSSION This case highlights several diagnostic and therapeutic challenges encountered when an adolescent with cerebral palsy presents with psychotic symptoms. Cerebral palsy is an umbrella term describing nonprogressive brain lesions arising during early development that disrupt gross motor and postural functions and frequently impair cognitive processes( 13 ). One definition conceptualizes cerebral palsy as “a group of disorders affecting movement and posture, causing activity limitations, and attributable to nonprogressive disturbances occurring in the developing fetal or infant brain”( 14 ). Motor impairments in cerebral palsy are often accompanied by disturbances in sensation, cognition, communication, perception, and behavior, as well as seizure disorders( 15 ). According to the Centers for Disease Control and Prevention, its median prevalence in 2004 was 3.3 per 1,000 eight-year-old children. Although psychiatric comorbidities are known to be common in children with cerebral palsy, the literature has historically emphasized physical rather than psychological symptoms, despite cerebral palsy being an organic brain disorder( 16 ). Elevated rates of psychiatric disorders have been reported in this population( 17 ). The psychiatric consequences of childhood neurodevelopmental disorders may arise from multiple mechanisms, including characteristics of the underlying brain lesion, associated intellectual disability, comorbid conditions, impairments in sensorimotor or speech-language functions, parental psychopathology and family functioning, and broader environmental risk and protective factors( 18 ). Rutter’s seminal Isle of Wight study (1970) reported that approximately half of children with cerebral palsy had a psychiatric disorder( 19 ). Low IQ and reading difficulties further increase risk, with hyperkinetic disorder identified as the most frequent comorbidity( 17 ). In a more recent multicenter cross-sectional study of 818 children aged 8–12 years, one-quarter exhibited significant psychological symptoms on the Strengths and Difficulties Questionnaire, with higher scores associated with moderate-to-severe intellectual disability, absence of siblings or having a disabled sibling, and severe physical pain ( 20 ). A key question is whether psychiatric disorders, including mood and psychotic symptoms, represent characteristic features of cerebral palsy( 21 ). Some evidence suggests possible links between neuropathological changes implicated in cerebral palsy and white matter abnormalities reported in juvenile-onset bipolar disorder, as proposed by Craven et al. (2002)( 22 ). Several mechanisms may underlie the emergence and treatment response of severe psychiatric symptoms in this population. Foster et al. (2010) described a 15-year-old girl with cerebral palsy who exhibited acute psychotic symptoms and marked mood instability, responding favorably to a combination of antipsychotic and anticonvulsant medications( 23 ). An additional consideration concerns whether adolescents with cerebral palsy require distinct pharmacological approaches for the management of psychosis compared with neurotypical adolescents( 24 – 28 ). Antipsychotic medications, while necessary, may exacerbate extrapyramidal symptoms and potentially worsen preexisting motor and postural impairments. Given the limited available literature on pharmacological management in this context, further research is needed to establish the safety and efficacy of psychotropic medications in adolescents with cerebral palsy( 25 ). It is also important to acknowledge that this patient’s symptoms emerged amid substantial psychosocial stressors, including concerns about his family’s caregiving capacity, limited peer relationships, and diminished self-esteem( 29 – 32 ). Prior research indicates that individuals with cerebral palsy often experience difficulties in social and familial adjustment, alongside reduced self-esteem. His cognitive delays and physical limitations related to quadriplegia may have further increased his vulnerability to emotional dysregulation and mood disturbances( 33 – 35 ). This case represents a rare instance of an adolescent with cerebral palsy exhibiting psychotic symptoms. Academic difficulties, social isolation, and psychosocial stressors likely contributed to the onset of his psychiatric presentation. Early initiation of treatment and consistent follow-up were critical for stabilizing his mental state. 4. CONCLUSION In conclusion, further research is required to better characterize the prevalence, clinical course, and phenomenology of psychiatric disorders in youth with Cerebral Palsy, in order to clarify risk and protective factors and to guide the development of effective treatment strategies. In the follow-up of this adolescent patient with Cerebral Palsy, the combination of significant school-related difficulties and emerging psychotic symptoms necessitated a comprehensive multidisciplinary approach. Throughout treatment and follow-up, psychosocial support and educational interventions tailored to his unique developmental and medical needs played a critical role in achieving a favorable therapeutic response. This case report provides an important contribution to clinical practice by illustrating the complexities of managing co-occurring Cerebral Palsy and psychotic disorders and underscores the importance of individualized, integrative care in such presentations. Declarations Consent for Publication: On behalf of all the contributors I will act and guarantor and will correspond with the journal from this point onward. This work has not been published or submitted to any other journal. Each author listed on the manuscript has seen and approved the manuscript. We hereby transfer, assign, or otherwise convey all copyright ownership, including any and all rights incidental thereto, exclusively to the journal, in the event that such work is published by the journal. Conflict of Interest: None of the authors had conflict of interest. Funding : The authors declared that this study received no financial support. References Grody MB, Coffey BJ. Presentation and treatment of acute psychosis in an adolescent girl with cerebral palsy. J Child Adolesc Psychopharmacol. 2012;22(2):175–8. Tiger A, Dalman C, Wicks S. Length during early childhood and later development of non-affective psychotic disorder. Schizophr Res. 2018;195:560–1. 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Cerebral Palsy Link to Sensorimotor System, Cognition, Emotion and Nociplastic Pain. Children 12.6 (2025): 702. Additional Declarations No competing interests reported. Supplementary Files GRAPHICALABSTRACT.png Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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16:08:18","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1292747,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8310751/v1/c3843564-6127-456d-afe5-025d9395b009.pdf"},{"id":97873414,"identity":"372b59f8-282d-4665-aef9-0a1b2700e6d4","added_by":"auto","created_at":"2025-12-10 10:43:28","extension":"png","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":1852238,"visible":true,"origin":"","legend":"","description":"","filename":"GRAPHICALABSTRACT.png","url":"https://assets-eu.researchsquare.com/files/rs-8310751/v1/6c635f7100613cf4bd43607e.png"}],"financialInterests":"No competing interests reported.","formattedTitle":"Organic Psychosis in A Male Adolescent With Cerebral Palsy: A Case Report And Review of The Literature","fulltext":[{"header":"1. INTRODUCTION","content":"\u003cp\u003eCerebral palsy (CP) is a neurodevelopmental condition and the leading cause of motor impairment in childhood(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). It results from damage to the developing brain and leads to lifelong motor dysfunction(\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). According to the World Health Organization (WHO), approximately 10% of children worldwide\u0026mdash;nearly 200 million\u0026mdash;experience physical disabilities, cognitive impairments, or developmental delays(\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Moreover, an estimated 80% of children and adolescents with disabilities reside in low-income countries(\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e), suggesting a higher prevalence of CP in these regions(\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eDespite receiving medical, rehabilitative, and supportive interventions, individuals with CP continue to face functional limitations that restrict their ability to perform daily activities(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Among these limitations, the degree of gross motor impairment is a key determinant of future physical independence, mobility, and social participation for children at risk of CP(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e\u003cp\u003ePsychotic disorders are severe psychiatric conditions characterized by marked disturbances in thought, perception, and affect, accompanied by impaired reality testing; they typically emerge during adolescence or early adulthood(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Although often associated with adults, psychotic disorders can also arise in childhood and adolescence, significantly influencing cognitive, emotional, and social development(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). The incidence, clinical presentation, and progression of psychosis in younger populations may differ from those seen in adults, and symptoms may initially resemble or be confused with neurodevelopmental or psychiatric conditions such as ADHD, autism spectrum disorder, or anxiety disorders(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Notably, psychosis beginning in adolescence carries a risk of progressing to schizophrenia or other chronic psychiatric disorders in later life(\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eAlthough the coexistence of cerebral palsy and psychotic disorders is uncommon, its impact on functioning and quality of life can be substantial(\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). This case report presents the school-related challenges, emerging psychotic symptoms, clinical characteristics, treatment course, and outcomes of a 15-year-old adolescent male diagnosed with both cerebral palsy and a psychotic disorder.\u003c/p\u003e"},{"header":"2. CASE REPORT","content":"\u003cp\u003eThe patient is a 15-year-old male adolescent, single, literate, and enrolled in the ninth grade of a high school Informatics Department. He lives with his biological mother, father, and older brother. He has cognitive developmental delay, cerebral palsy (CP), and spastic quadriplegia and is wheelchair-bound. He presented to the child and adolescent psychiatry outpatient clinic with acute-onset psychotic symptoms, including disorganized speech and behavior, paranoid delusions, delusions of reference, and auditory hallucinations.\u003c/p\u003e\u003cp\u003eRecent academic difficulties and feelings of social isolation at school appeared to have negatively affected his mental state. He expressed fear of failing his second-term examinations and began to believe that his teacher was keeping a record about him. Consequently, he became increasingly irritable, accusatory toward his parents, and prone to temper outbursts. According to his parents, he had been more withdrawn, sluggish, reluctant to leave his room, unwilling to interact with his family, and preoccupied with the belief that others were listening to him or intended to cause harm\u0026mdash;symptoms that reportedly started approximately one year before admission.\u003c/p\u003e\u003cp\u003eFamily-reported history indicated that persecutory and referential delusions first emerged one year earlier. He was taken to a child and adolescent psychiatry clinic in 2024 due to worsening symptoms and functional decline. His mother noted increased dysphoria, agitation, and episodes of covering his ears while speaking to himself. When questioned about distressing stimuli, he claimed he was mocked by teachers and friends and insisted that his teacher had written negative reports about him. School staff, however, denied any such incidents, although they confirmed increased irritability. In the following days, he became increasingly withdrawn, refused food and drink, and resisted assistance with personal hygiene. He spent most of the day irritably covering his ears and whispering to himself.\u003c/p\u003e\u003cp\u003eHe was evaluated in the child and adolescent psychiatry clinic and initiated on pharmacological treatment. His hostility toward his mother escalated, and he persisted in expressing persecutory thoughts. He was subsequently referred to both child neurology and child psychiatry. Premorbidly, he was described as quiet and calm. Although he had CP, he had no prior psychiatric hospitalizations or regular psychiatric follow-up. A school psychologist evaluated him in the past for frustration and self-esteem issues. No standardized cognitive assessment had previously been conducted.\u003c/p\u003e\u003cp\u003eHe had no history of suicide attempts, self-harm, or substance use. Family history was negative for neurological or psychiatric disorders.\u003c/p\u003e\u003cp\u003ePerinatal history revealed that the mother experienced premature rupture of membranes at 32 weeks, and the patient required neonatal intensive care due to respiratory distress. CP was diagnosed after cranial computed tomography demonstrated features consistent with anoxic brain injury. Developmental milestones were globally delayed. According to his mother, he could write, perform basic calculations, and communicate in sentences, although motor contractures limited his functioning.\u003c/p\u003e\u003cp\u003eEducationally, he is a ninth-grade student receiving instruction in computer science at a regular public school with integrated special education services. After experiencing bullying in primary school, he transferred to a school specializing in cerebral palsy four years prior. He receives occupational, physical, and speech therapy. He reportedly performed adequately both academically and socially during the previous academic year.\u003c/p\u003e\u003cp\u003eSocially, his interactions were limited primarily to school and family. Medically, he experienced neonatal hypoxia but was not intubated and required CPAP for one day. He carries diagnoses of spastic quadriplegic CP and hypoxic-ischemic encephalopathy. He is followed in a neuromuscular clinic and has been receiving baclofen without recent dosage changes.\u003c/p\u003e\u003cp\u003eCranial diffusion MRI showed no diffusion-restricted lesions, indicating no acute or subacute infarction. Non-contrast cranial MRI demonstrated increased T2 signal intensity in the bilateral periventricular white matter, enlarged lateral ventricles, and irregular ventricular walls, consistent with periventricular leukomalacia. A 2016 MRI showed a thin, arched corpus callosum, irregular posterior horn ventricular contours, and chronic leukomalacia sequelae with sulcal widening consistent with cerebral atrophy.\u003c/p\u003e\u003cp\u003eOn mental status examination, he appeared his stated age, wore appropriate clothing, and demonstrated adequate self-care. He was wheelchair-bound with minimal upper-body movement. He avoided eye contact, intermittently covered his ears, and was only partially cooperative. His mood was depressive and irritable; affect was childish, variable, and inappropriate. His speech was reduced in rate, volume, and tone; he mumbled to himself and answered questions briefly and reluctantly. Attention and concentration were impaired, memory deficits were evident, and reality testing was disturbed. Thought processes were disorganized with persecutory and referential delusions. Insight and judgment were poor, and impulse control was moderate. School, peer, and family functioning were markedly impaired.\u003c/p\u003e\u003cp\u003eVital signs were normal, and neurological examination revealed no acute pathology. Routine blood tests showed elevated fasting glucose. MRI findings again confirmed periventricular leukomalacia. There was no history of psychotropic medication use. Given his congenital brain pathology, the diagnosis was considered consistent with organic psychosis (WHO ICD-11 6E61), secondary to cerebral palsy (8D2Z).\u003c/p\u003e\u003cp\u003eHe was started on risperidone 0.5 mg/day orally for organic psychotic disorder secondary to CP. Differential diagnoses included psychotic disorder and psychotic depression based on DSM-5 criteria. At baseline, sleep and appetite were normal, and mood was moderately impaired. Parents expressed surprise, noting that such behavioral changes had not occurred previously. He was anxious during the interview and expressed fear about leaving school. He endorsed delusions of reference involving the belief that his thoughts were being monitored.\u003c/p\u003e\u003cp\u003eDuring the mental status evaluation, he attempted to suppress auditory hallucinations by covering his ears. He appeared irritable and mistrustful toward his parents, tried to prematurely terminate the interview, refused to complete clinical assessments, and stated that his academic life was over. Risperidone 1 mg/day and olanzapine 5 mg/day were prescribed.\u003c/p\u003e\u003cp\u003eOne week later, irritability and self-talking had decreased, though he continued to believe that his teacher kept a report about him and expressed shame regarding clinic visits. Sedation and increased appetite were noted as side effects. Two weeks later, disorganized speech, referential delusions regarding phone monitoring, suspiciousness, and irritability persisted. Medication was adjusted to risperidone 0.5 mg three times daily and olanzapine 5 mg three times daily.\u003c/p\u003e\u003cp\u003eAfter one month, auditory hallucinations and paranoid ideation decreased but persisted. He continued to cover his ears and told his family not to \u0026ldquo;listen to his thoughts.\u0026rdquo; He refused to continue school, and the family pursued a school transfer. Medication was increased to risperidone 2 mg/day and olanzapine 10 mg/day.\u003c/p\u003e\u003cp\u003eAt the next visit, auditory and referential delusions and irritability had markedly improved; he no longer covered his ears during interviews, although he continued to do so when his father spoke on the phone. He answered questions appropriately but appeared mildly sedated. After six months, family members reported nearly 90% improvement. No extrapyramidal side effects were observed, although he developed new-onset enuresis nocturna. Medication was adjusted to risperidone 0.5 mg twice daily and olanzapine 5 mg twice daily.\u003c/p\u003e\u003cp\u003eWhen school reopened in September, symptoms were exacerbated, including social withdrawal, ear-covering behaviors, irritability toward caregivers and teachers, and knife-threatening behavior related to delusional ideation. Akathisia was observed in the lower extremities, attributed to antipsychotic treatment. Medication was adjusted to risperidone 2.5 mg/day and olanzapine 12.5 mg/day.\u003c/p\u003e\u003cp\u003eAt follow-up, symptoms improved but residual auditory and referential delusions and akathisia persisted. Doses were increased to risperidone 4 mg/day and olanzapine 20 mg/day; biperiden 2 mg three times daily and desmopressin 120 \u0026micro;g/day were added. The family was counseled about extrapyramidal side effects. The patient is currently awaiting inpatient psychiatric admission.\u003c/p\u003e\u003cp\u003eThroughout follow-up, significant clinical improvement was observed after antipsychotic initiation, with no psychotic exacerbations. Current treatment includes risperidone 1 mg three times daily, olanzapine 5 mg four times daily, biperiden 2 mg three times daily, and Lioresal. Further evaluation includes EEG to rule out epileptic pathology, neuropsychological testing for possible cognitive decline, complete blood count and metabolic screening for medical contributors to psychosis, and toxicology screening. Informed consent was obtained from the patient and his family.\u003c/p\u003e\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003e2.1.Brief Report\u003c/h2\u003e\u003cp\u003eIn summary, this 15-year-old male adolescent\u0026mdash;diagnosed with spastic quadriplegia secondary to an anoxic brain injury at birth\u0026mdash;presented with acute-onset psychotic symptoms, including disorganized speech and behavior, persecutory and referential delusions, and presumed auditory hallucinations. His clinical history was characterized by mood fluctuations, atypical behaviors, and prominent internal preoccupation. Several psychosocial stressors preceded the onset of illness, including significant threats to his academic and social self-esteem and family-related anxieties regarding long-term caregiving. At presentation, he demonstrated a rapid therapeutic response to risperidone and olanzapine, although initiation of treatment was initially delayed due to concerns related to his neuromuscular condition.\u003c/p\u003e\u003c/div\u003e"},{"header":"3. DISCUSSION","content":"\u003cp\u003eThis case highlights several diagnostic and therapeutic challenges encountered when an adolescent with cerebral palsy presents with psychotic symptoms. Cerebral palsy is an umbrella term describing nonprogressive brain lesions arising during early development that disrupt gross motor and postural functions and frequently impair cognitive processes(\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). One definition conceptualizes cerebral palsy as \u0026ldquo;a group of disorders affecting movement and posture, causing activity limitations, and attributable to nonprogressive disturbances occurring in the developing fetal or infant brain\u0026rdquo;(\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Motor impairments in cerebral palsy are often accompanied by disturbances in sensation, cognition, communication, perception, and behavior, as well as seizure disorders(\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). According to the Centers for Disease Control and Prevention, its median prevalence in 2004 was 3.3 per 1,000 eight-year-old children.\u003c/p\u003e\u003cp\u003eAlthough psychiatric comorbidities are known to be common in children with cerebral palsy, the literature has historically emphasized physical rather than psychological symptoms, despite cerebral palsy being an organic brain disorder(\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Elevated rates of psychiatric disorders have been reported in this population(\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). The psychiatric consequences of childhood neurodevelopmental disorders may arise from multiple mechanisms, including characteristics of the underlying brain lesion, associated intellectual disability, comorbid conditions, impairments in sensorimotor or speech-language functions, parental psychopathology and family functioning, and broader environmental risk and protective factors(\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). Rutter\u0026rsquo;s seminal Isle of Wight study (1970) reported that approximately half of children with cerebral palsy had a psychiatric disorder(\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). Low IQ and reading difficulties further increase risk, with hyperkinetic disorder identified as the most frequent comorbidity(\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). In a more recent multicenter cross-sectional study of 818 children aged 8\u0026ndash;12 years, one-quarter exhibited significant psychological symptoms on the Strengths and Difficulties Questionnaire, with higher scores associated with moderate-to-severe intellectual disability, absence of siblings or having a disabled sibling, and severe physical pain (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eA key question is whether psychiatric disorders, including mood and psychotic symptoms, represent characteristic features of cerebral palsy(\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e). Some evidence suggests possible links between neuropathological changes implicated in cerebral palsy and white matter abnormalities reported in juvenile-onset bipolar disorder, as proposed by Craven et al. (2002)(\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). Several mechanisms may underlie the emergence and treatment response of severe psychiatric symptoms in this population. Foster et al. (2010) described a 15-year-old girl with cerebral palsy who exhibited acute psychotic symptoms and marked mood instability, responding favorably to a combination of antipsychotic and anticonvulsant medications(\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eAn additional consideration concerns whether adolescents with cerebral palsy require distinct pharmacological approaches for the management of psychosis compared with neurotypical adolescents(\u003cspan additionalcitationids=\"CR25 CR26 CR27\" citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). Antipsychotic medications, while necessary, may exacerbate extrapyramidal symptoms and potentially worsen preexisting motor and postural impairments. Given the limited available literature on pharmacological management in this context, further research is needed to establish the safety and efficacy of psychotropic medications in adolescents with cerebral palsy(\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eIt is also important to acknowledge that this patient\u0026rsquo;s symptoms emerged amid substantial psychosocial stressors, including concerns about his family\u0026rsquo;s caregiving capacity, limited peer relationships, and diminished self-esteem(\u003cspan additionalcitationids=\"CR30 CR31\" citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e). Prior research indicates that individuals with cerebral palsy often experience difficulties in social and familial adjustment, alongside reduced self-esteem. His cognitive delays and physical limitations related to quadriplegia may have further increased his vulnerability to emotional dysregulation and mood disturbances(\u003cspan additionalcitationids=\"CR34\" citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eThis case represents a rare instance of an adolescent with cerebral palsy exhibiting psychotic symptoms. Academic difficulties, social isolation, and psychosocial stressors likely contributed to the onset of his psychiatric presentation. Early initiation of treatment and consistent follow-up were critical for stabilizing his mental state.\u003c/p\u003e"},{"header":"4. CONCLUSION","content":"\u003cp\u003eIn conclusion, further research is required to better characterize the prevalence, clinical course, and phenomenology of psychiatric disorders in youth with Cerebral Palsy, in order to clarify risk and protective factors and to guide the development of effective treatment strategies. In the follow-up of this adolescent patient with Cerebral Palsy, the combination of significant school-related difficulties and emerging psychotic symptoms necessitated a comprehensive multidisciplinary approach. Throughout treatment and follow-up, psychosocial support and educational interventions tailored to his unique developmental and medical needs played a critical role in achieving a favorable therapeutic response. This case report provides an important contribution to clinical practice by illustrating the complexities of managing co-occurring Cerebral Palsy and psychotic disorders and underscores the importance of individualized, integrative care in such presentations.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConsent for Publication:\u003c/strong\u003e On behalf of all the contributors I will act and guarantor and will correspond with the journal from this point onward. This work has not been published or submitted to any other journal. Each author listed on the manuscript has seen and approved the manuscript. We hereby transfer, assign, or otherwise convey all copyright ownership, including any and all rights incidental thereto, exclusively to the journal, in the event that such work is published by the journal.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of Interest:\u003c/strong\u003e None of the authors had conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e: The authors declared that this study received no financial support.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eGrody MB, Coffey BJ. Presentation and treatment of acute psychosis in an adolescent girl with cerebral palsy. J Child Adolesc Psychopharmacol. 2012;22(2):175\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eTiger A, Dalman C, Wicks S. Length during early childhood and later development of non-affective psychotic disorder. 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Intelligence, functioning, and related factors in children with cerebral palsy. Arch Neuropsychiatry. 2017;54(1):33.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBax M, Goldstein M, Rosenbaum P, Leviton A, Paneth N, Dan B, et al. Proposed definition and classification of cerebral palsy, April 2005. Dev Med Child Neurol. 2005;47(8):571\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eDe Clercq LE, Soenens B, Dieleman LM, Prinzie P, Van der Kaap-Deeder J, Beyers W, et al. Parenting and child personality as modifiers of the psychosocial development of youth with cerebral palsy. Child Psychiatry Hum Dev. 2022;53(1):137\u0026ndash;55.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eDemeco A, Molinaro A, Ambroggi M, Frizziero A, Fazzi E, Costantino C, et al. Cognitive approaches in the rehabilitation of upper limbs function in children with cerebral palsy: a systematic review and meta-analysis. Eur J Phys Rehabil Med. 2024;60(3):445.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFerrari A, Cioni G, Masi G, Brovedani P. Emotional, behavioral and social disorders in children and adolescents with cerebral palsy. Spastic Forms Cereb Palsy A Guid to Assess Adapt Funct. 2010;181\u0026ndash;92.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBeckung E, White-Koning M, Marcelli M, McManus V, Michelsen S, Parkes J, et al. Health status of children with cerebral palsy living in Europe: a multi‐centre study. Child Care Health Dev. 2008;34(6):806\u0026ndash;14.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBoldyreva U, Streiner DL, Rosenbaum PL, Ronen GM. Quality of life in adolescents with epilepsy, cerebral palsy, and population norms. Dev Med Child Neurol. 2020;62(5):609\u0026ndash;14.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eCraven C, James A, Murphy M. Cerebral palsy and juvenile-onset bipolar disorder: A preliminary report. Eur Child Adolesc Psychiatry. 2002;11:134\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFoster JLH. Perpetuating stigma? Differences between advertisements for psychiatric and non-psychiatric medication in two professional journals. J Ment Heal. 2010;19(1):26\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHauptman AJ, Barkoudah E. The role of neuropsychiatry in the care of children and adults with cerebral palsy. BJPsych Open. 2022;8(4):e99.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGorter JW, Fehlings D, Ferro MA, Gonzalez A, Green AD, Hopmans SN, et al. Correlates of mental health in adolescents and young adults with cerebral palsy: a cross-sectional analysis of the MyStory project. J Clin Med. 2022;11(11):3060.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eOstojic K, Karem I, Paget S, Mimmo L, Berg A, Scott T, et al. A qualitative study investigating the experiences of unmet social needs for children with cerebral palsy and their families: Perspectives of parents and clinicians. Disabil Rehabil. 2025;47(9):2278\u0026ndash;87.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBhatnagar S, Mitelpunkt A, Rizzo JJ, Zhang N, Guzman T, Schuetter R, et al. Mental health diagnoses risk among children and young adults with cerebral palsy, chronic conditions, or typical development. JAMA Netw Open. 2024;7(7):e2422202\u0026ndash;2422202.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHaruna IBRAHIM, Adekola Kamil LASISI, Olubunmi Foluke BELLO. Stress Implication of Rearing Children with Cerebral-Palsy and Down-Syndrome: Perceptions of Caregivers in Ilorin, Nigeria. KONTAGORA Int J EDUCATIONAL Res. 2025;2(1):99\u0026ndash;110.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKim S et al. Standardized clinical data capture to describe cerebral palsy. \u003cem\u003emedRxiv\u003c/em\u003e (2024): 2024-08.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePizzighello S, et al. Psychiatric symptoms in adult patients with cerebral palsy: A cohort study. Front Neurol. 2022;13:998922.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSingh A, Jasleen Kaur B. Catatonia in Young Male with Cerebral Palsy and Intellectual Disability: A Case Report. Indian J Private Psychiatry. 2023;17(2):95\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWhitney DG, et al. Prevalence of mental health disorders among adults with cerebral palsy: a cross-sectional analysis. Ann Intern Med. 2019;171(5):328\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMoreira CA, Soares AR, Maia G. Acute psychosis in an adolescent with cerebral palsy. Eur Psychiatry. 2016;33S1:S348\u0026ndash;348.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRausch R, et al. The Mental Health of Children with Cerebral Palsy: A Review of the Last Five Years of Research. J Clin Med. 2025;14:4364.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAlito A, et al. Suicidal Ideation in Individuals with Cerebral Palsy: A Narrative Review of Risk Factors, Clinical Implications, and Research Gaps. J Clin Med. 2025;14:5587.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLaube W. and Mathilde Sengoelge. Cerebral Palsy Link to Sensorimotor System, Cognition, Emotion and Nociplastic Pain. \u003cem\u003eChildren\u003c/em\u003e 12.6 (2025): 702.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"cerebral palsy, psychosis, child, adolescent, psychotropic, treatment","lastPublishedDoi":"10.21203/rs.3.rs-8310751/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8310751/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cb\u003eBackground:\u003c/b\u003e\u003c/p\u003e\u003cp\u003eCerebral palsy (CP) is a neurodevelopmental condition associated with motor impairment and cognitive challenges. Although psychiatric comorbidities are common, psychotic symptoms are rarely documented. Early recognition of organic psychosis in CP is essential for effective intervention.\u003c/p\u003e\u003cp\u003e\u003cb\u003eCase Presentation:\u003c/b\u003e\u003c/p\u003e\u003cp\u003eWe report a 15-year-old male adolescent with spastic quadriplegic CP who presented with acute psychotic symptoms, including persecutory delusions, disorganized behavior, referential ideation, and presumed auditory hallucinations. Neuroimaging revealed chronic periventricular leukomalacia. Symptoms emerged following academic stress and social isolation. Treatment with risperidone and olanzapine led to significant clinical improvement. No major extrapyramidal side effects occurred aside from transient akathisia.\u003c/p\u003e\u003cp\u003e\u003cb\u003eDiscussion:\u003c/b\u003e\u003c/p\u003e\u003cp\u003ePsychosis in CP may arise from structural brain abnormalities, psychosocial stressors, and cognitive vulnerabilities. Differentiating organic psychosis from primary psychotic disorders is essential for treatment planning. Limited literature exists regarding psychopharmacology in CP, emphasizing the need for further research.\u003c/p\u003e\u003cp\u003e\u003cb\u003eConclusion:\u003c/b\u003e\u003c/p\u003e\u003cp\u003eThis case highlights the complexity of managing psychosis in CP and underscores the importance of early identification, multidisciplinary care, and individualized treatment strategies.\u003c/p\u003e","manuscriptTitle":"Organic Psychosis in A Male Adolescent With Cerebral Palsy: A Case Report And Review of The Literature","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-10 10:43:23","doi":"10.21203/rs.3.rs-8310751/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"5054ad8b-d60f-42ed-b4be-419f55f0116b","owner":[],"postedDate":"December 10th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-12-23T07:40:15+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-10 10:43:23","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8310751","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8310751","identity":"rs-8310751","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}