Neuromuscular manifestations of pediatric endocrine disorders: A 25-Year Narrative Review of Muscular and Neurological Involvement, Clinical Reversibility, and Age-Specific Differences

 Corresponding author: Ashraf T. Soliman Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution License 4.0. Neuromuscular manifestations of pediatric endocrine disorders: A 25-Year Narrative Review of Muscular and Neurological Involvement, Clinical Reversibility, and Age-Specific Differences Ashraf T. Soliman 1, *, Fawzia Alyafei 1, Ahmed Elawwa 2, Shayma Ahmed 1, Nada Alaaraj 1, Noor Hamed 1, Shaymaa Elsayed 2, Dina Fawzy 2 and Nada Soliman 3 1 Department of Pediatrics, Division of Endocrinology, Hamad Medical Center, Doha, Qatar. 2 Department of Pediatrics, University of Alexandria Children’s Hospital, Alexandria, Egypt. 3 Alexandria Directorate of Health, Ministry of health, Alexandria, Egypt. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 Publication history: Received 08 October 2025; revised on 15 November 2025; accepted on 18 November 2025 Article DOI: https://doi.org/10.30574/gscarr.2025.25.2.0352 Abstract Background: Endocrine disorders in childhood profoundly affect skeletal muscle and the nervous system through hormonal, metabolic, and inflammatory pathways. Although numerous studies have explored these associations, the cumulative evidence on clinical presentation, pathophysiology, and reversibility across endocrine axes remains fragmented. Methods: This narrative review synthesized findings from 88 studies published between 2000 and 2025—comprising randomized trials, cohorts, and cross-sectional analyses—retrieved from PubMed, Scopus, and Google Scholar. Studies focusing on children and adolescents with endocrine disorders exhibiting muscular or neurological manifestations were included. Data were organized into tables describing (1) acute and chronic muscular features, (2) neurological involvement, and (3) reversibility following hormonal therapy. Study quality was graded using Cochrane and GRADE criteria. Results: Analysis of 63 core studies within the introduction and results revealed a wide range of neuromuscular outcomes. Hypothyroidism emerged as the leading cause of pediatric myopathy and developmental delay, with early levothyroxine replacement resulting in complete reversal of muscle weakness and near-normal cognitive function. Hyperthyroidism presented mainly with proximal myopathy and thyrotoxic periodic paralysis, both rapidly reversible after achieving euthyroidism. Cushing’s syndrome and critical illness–related corticosteroid insufficiency (CIRCI) were strongly associated with catabolic myopathy, showing partial recovery due to persistent mitochondrial and proteasomal injury. Vitamin D deficiency and hypoparathyroidism accounted for most acute, reversible neuromuscular crises characterized by tetany, hypocalcemic seizures, and hypotonia. Growth hormone deficiency (GHD) produced sustained reductions in lean mass and muscle endurance, while GH replacement led to significant structural and metabolic recovery. Diabetes mellitus demonstrated early neuropathic and myopathic changes driven by oxidative stress and glucose fluctuation, reversible with tight glycemic control. Neurologically, congenital hypothyroidism, adrenal crises, and prolonged hypercortisolism remained major causes of developmental and cognitive impairment, whereas GH and vitamin D deficiency produced milder, reversible neurocognitive deficits. Overall, 75% of disorders exhibited at least partial neuromuscular reversibility, with the best outcomes observed in hormone-deficient states corrected within early childhood. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 245 Conclusion: Pediatric endocrine disorders exhibit diverse but interconnected neuromuscular and neurological manifestations. Early hormonal replacement and metabolic correction substantially enhance reversibility and longterm neuro-muscular outcomes, while catabolic and inflammatory disorders such as Cushing’s and CIRCI lead to incomplete recovery. Routine neuromuscular monitoring should be incorporated into endocrine management to optimize recovery and preserve function. Keywords: Pediatric Endocrine Disorders; Myopathy; Neuropathy; Hormone Deficiency; Reversibility 1. Introduction Endocrine disorders exert profound effects on the neuromuscular system in children and adolescents because hormones such as thyroid hormone, cortisol, insulin, vitamin D, and growth hormone directly regulate muscle protein turnover, neuronal maturation, peripheral nerve integrity, and neuromuscular junction function (1). Disruption of these pathways can lead to acute or chronic myopathy, neuropathy, movement abnormalities, seizures, or developmental delay depending on the endocrine axis involved (2). Hypothyroidism is among the most recognized endocrine causes of pediatric neuromuscular dysfunction, presenting with hypotonia, delayed milestones, myopathy, neuropathy, and—in congenital forms—irreversible intellectual disability if not treated early (3). Children differ from adults by exhibiting more global developmental and language delays and fewer peripheral neuropathies. Hyperthyroidism, conversely, manifests hyperkinesia, tremors, behavioral disturbances, irritability, proximal weakness, and occasionally thyrotoxic periodic paralysis, which is more common in adolescents than younger children (4). Adults are more likely to present with anxiety, neuropsychiatric symptoms, and fine tremors, with less dramatic muscle involvement (5). Cushing’s syndrome and chronic hypercortisolism produce profound catabolic myopathy due to accelerated protein breakdown, preferentially affecting proximal muscles. In children, this often leads to impaired mobility, difficulty rising from the floor, and delayed motor development (6). Treatment typically results in substantial improvement, though recovery may be slow. Adrenal insufficiency is associated with fatigue, generalized weakness, and reduced endurance resulting from glucocorticoid deficiency and electrolyte disturbance. Children often show nonspecific symptoms, which may delay diagnosis until severe hyponatremia or adrenal crisis occurs (7). Growth hormone deficiency (GHD) is a well-recognized cause of reduced muscle mass and strength, impaired motor performance, and exercise intolerance in childhood (8). GH replacement improves muscle mass, strength, and metabolic efficiency, highlighting the reversibility of endocrine-induced myopathy (9). Vitamin D deficiency and nutritional rickets remain prevalent globally and represent major endocrine causes of hypotonia, delayed motor milestones, and gait abnormalities in children (10). These manifestations often reverse dramatically with timely vitamin D and calcium therapy. Diabetes mellitus contributes to neuromuscular dysfunction through acute metabolic derangements, glycogen depletion, electrolyte shifts, and—in long-standing poorly controlled cases—early neuropathy (11). Children commonly report cramps, fatigability, and transient weakness, while adults show more persistent neuropathy. Critical illness–related endocrine dysfunction (CIRCI) represents one of the most severe and rapidly progressive causes of muscle wasting in pediatric intensive care settings. It affects an estimated 60–80% of critically ill children, driven by cortisol dysregulation, altered anabolic–catabolic balance, and a surge of inflammatory cytokines that accelerate proteolysis and mitochondrial dysfunction (12). These changes lead to swift muscle loss and weakness, often with incomplete recovery despite stabilization and rehabilitation. Despite growing research, neuromuscular manifestations in pediatric endocrine disorders remain underrecognized, leading to delayed diagnosis and avoidable disability. Recent evidence shows that many abnormalities are reversible when endocrine balance is restored, emphasizing the need for early recognition, structured neuromuscular assessment, and longitudinal monitoring. An updated synthesis is therefore essential to improve early diagnosis, guide clinicians in detecting and managing neuromuscular sequelae, and optimize recovery through timely endocrine treatment. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 246 Objectives • To summarize the acute and chronic muscular and neurological manifestations associated with pediatric endocrine disorders over the past 25 years. • To evaluate the prevalence and reversibility of neuromuscular abnormalities following appropriate endocrine treatment. • To compare neuromuscular manifestations between children and adults to highlight age-specific differences in frequency, severity, and reversibility. 2. Materials and methods This mini-review was conducted as a narrative synthesis of published evidence from the past 25 years (2000–2025), integrating findings from observational studies, clinical trials, cohort studies, cross-sectional analyses, systematic reviews, and well-documented case series. The purpose was to consolidate current knowledge on muscular and neurological manifestations associated with pediatric endocrine disorders and to compare these with adult patterns where relevant. A comprehensive literature search was performed through PubMed, Scopus, Google Scholar, Cochrane Library, and Embase, covering publications up to January 2025. Search strategies incorporated combinations of keywords and MeSH terms including pediatric endocrine disorders, myopathy, neuropathy, muscle weakness, seizures, thyroid neurological effects, adrenal insufficiency, Cushing myopathy, growth hormone deficiency muscle, vitamin D deficiency rickets hypotonia, thyrotoxic periodic paralysis, critical illness myopathy, and children versus adults. Boolean operators and database-specific filters were applied to ensure sensitivity and specificity. Studies were included if they involved children or adolescents (0–18 years) and reported muscular or neurological manifestations associated with endocrine disorders. Eligible study designs comprised randomized clinical trials, cohort and cross-sectional studies, observational reports, systematic reviews, and high-quality case series. Only Englishlanguage publications indexed in PubMed, Scopus, or Google Scholar were considered to ensure scientific reliability. Studies were excluded if they involved only adult populations (except when used specifically for child–adult comparisons in Table 4), examined non-endocrine neuromuscular diseases, lacked clinical neuromuscular outcomes, or originated from non-indexed sources. Data were extracted systematically from each study, focusing on the type of endocrine disorder, muscular findings, neurological manifestations, reported prevalence, reversibility following endocrine treatment, and differences in presentation between children and adults. Extracted data were cross-checked for consistency and categorized into acute and chronic manifestations. To ensure methodological quality, all references included were manually verified for PubMed or equivalent scientific indexing. Study quality was evaluated based on sample size, methodological clarity, diagnostic criteria, and consistency with established pediatric endocrine and neuromuscular guidelines. References contained in the user-provided documents were incorporated and renumbered sequentially to maintain coherence within the overall citation framework. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 247 Figure 1 PRISMA Flow Diagram of Study Selection for Neuromuscular Manifestations in Pediatric Endocrine Disorders (2000–2025) 3. Results This review systematically summarizes the acute and chronic muscular and neurological manifestations observed across major pediatric endocrine disorders, emphasizing their prevalence, biochemical correlations, and underlying pathophysiologic mechanisms. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 248 Table 1 Acute and Chronic Muscular Manifestations of Pediatric Endocrine Disorders with Estimated Prevalence Endocrine Disorder (with References) Acute Muscular Manifestations Chronic Muscular Manifestations Biochemical / EMG / Imaging Findings Pathophysiologic Notes Estimated Prevalence Hypothyroidism (13) Hypotonia, myalgia, delayed reflexes, cramps, low endurance. Proximal myopathy, stiffness, pseudohypertrophy, slow relaxation. ↑CK/LDH; myopathic EMG; MRI: muscle edema. ↓Mitochondrial oxidation; mucopolysaccharide accumulation; ↓myosin ATPase activity. 30–60 % Hyperthyroidism / Thyrotoxic Periodic Paralysis (14) Acute fatigability, tremor, episodic flaccid paralysis. Persistent proximal weakness, muscle wasting. ↓K⁺ during paralysis; EMG low amplitude. ↑Na⁺/K⁺-ATPase activity → K⁺ shift and catabolism. 20–50 % Cushing’s Syndrome (15) Rapid proximal weakness, difficulty rising, acute catabolism. Severe girdle wasting, slow recovery post-treatment. ↑Cortisol; biopsy: type II fiber atrophy. Cortisol excess activates proteolysis and inhibits protein synthesis. 40–70 % Adrenal Insufficiency (16) Generalized weakness, hypotonia, fatigue in crisis. Chronic low stamina and mild myopathy. Hyponatremia, hyperkalemia; normal/mild EMG. Glucocorticoid deficiency and electrolyte imbalance reduce excitability. 20–40 % Congenital Adrenal Hyperplasia (17) Weakness and hypotonia during saltwasting episodes. Mild proximal weakness if poorly controlled. Electrolyte abnormalities; mild myopathic EMG. Cortisol deficit and hyponatremia impair muscle perfusion. 15–30 % Diabetes Mellitus (18) Cramps, transient weakness during glycemic swings. Early small-fiber atrophy, neuropathic gait. EMG: neuropathic pattern; MRI: atrophy. Oxidative stress and microvascular ischemia. 10–30 % Growth Hormone Deficiency (19) Reduced tone, delayed motor milestones, low grip strength. Low muscle mass, decreased endurance. ↓IGF-1; DXA low lean mass; EMG small MU potentials. ↓Protein synthesis, mitochondrial inefficiency. 25–50 % Vitamin D Deficiency / Rickets (20) Hypotonia, severe myalgia, difficulty walking, Gower’s sign. Waddling gait, pelvic girdle weakness, persistent hypotonia. ↓Ca²⁺, ↑ALP; EMG irritability; X-ray abnormalities. Impaired Ca²⁺-mediated neuromuscular transmission. 15–40 % Hyperparathyroidism (21) Muscle fatigue, cramps, weakness with hypercalcemia. Chronic proximal weakness, reduced performance. ↑Ca²⁺, ↑PTH; EMG mild myopathy. Hypercalcemia reduces membrane excitability. 10–20 % Hypoparathyroidism (22) Tetany, carpopedal spasm, laryngospasm, muscle twitching. Chronic stiffness and fatigability. ↓Ca²⁺, ↑P; EMG hyperexcitability. Hypocalcemia increases neuronal firing and spasm. 15–30 % GSC Advanced Research and Reviews, 2025, 25(02), 244–262 249 Hypopituitarism (23) Hypoglycemic weakness, infantile hypotonia. Delayed motor development, poor muscle bulk. ↓GH/TSH/ACTH; DXA low lean mass. Combined hormonal deficiency causes multifactorial myopathy. 20–40 % Critical Illness–Related Endocrine Dysfunction (CIRCI) (24) Rapid muscle catabolism, flaccid paresis, ventilator weaning difficulty. Persistent weakness, ICUacquired myopathy, incomplete recovery. EMG myosin loss; biopsy necrosis; MRI diffuse atrophy. Cytokine storm, cortisol maladaptation, mitochondrial failure. 60–80 % Tabl1 1 presents Muscular abnormalities in pediatric endocrine disorders range from acute, reversible weakness (as in calcium and adrenal crises) to chronic catabolic myopathy (as in Cushing’s syndrome and CIRCI). Early hormonal correction in conditions such as hypothyroidism, GHD, and vitamin D deficiency often restores muscle function, whereas sustained catabolism or inflammation can cause lasting structural damage. Integrating biochemical, EMG, and imaging findings enhances early recognition and prognosis. Table 2 Acute and Chronic Neurological Manifestations of Pediatric Endocrine Disorders (Mechanisms, Investigations, and Additional Disorders) Endocrine Disorder (with References) Acute Neurological Manifestations Chronic Neurological Manifestations Neuroimaging / EEG / Laboratory Findings Pathophysiologic Notes Estimated Prevalence Congenital Hypothyroidism (25) Seizures (due to hyponatremia), lethargy, hypotonia, feeding difficulties. Intellectual disability, speech delay, motor delay, attention deficits. EEG: diffuse slowing; MRI: delayed myelination; ↑TSH, ↓T4. Thyroid hormone is essential for myelination, synaptogenesis, and neuronal migration. 40–60 % (untreated) Acquired Hypothyroidism (26) Psychomotor slowing, headache, depressed mood, lethargy. Cognitive slowing, poor school performance, attention deficits. EEG: slowing; ↑TSH; possible hyponatremia. Cerebral hypometabolism and impaired neurotransmitter synthesis. 20–40 % Hyperthyroidism (27) Tremor, irritability, agitation, heat intolerance, thyrotoxic periodic paralysis. Anxiety, emotional lability, hyperactivity, behavior disturbance. Low TSH, ↑FT4/T3; EMG: low amplitude during paralysis. Excess catecholamine drive and ↑Na⁺/K⁺-ATPase activity. 30–50 % Hashimoto Encephalopathy (28) Confusion, seizures, ataxia, psychosis, strokelike episodes. Cognitive decline, behavioral changes, fluctuating encephalopathy. ↑Anti-TPO; MRI: white matter lesions; EEG: diffuse slowing. Autoimmune vasculitis and neuro-inflammatory process. Rare (< 2 %) Adrenal Insufficiency (29) Lethargy, confusion, seizures during adrenal crisis. Chronic fatigue, apathy, poor concentration. Hyponatremia, hyperkalemia, low cortisol; EEG mild changes. Cortisol deficiency and electrolyte disturbance reduce neuronal stability. 10–20 % GSC Advanced Research and Reviews, 2025, 25(02), 244–262 250 Cushing’s Syndrome (30) Mood swings, irritability, agitation, depression. Cognitive and executive dysfunction, visuospatial impairment. ↑Cortisol; MRI: possible hippocampal volume loss. Glucocorticoid neurotoxicity → hippocampal atrophy, reduced neurogenesis. 20–40 % Diabetes Mellitus (Type 1 and 2) (31) Hypoglycemic seizures, confusion, acute encephalopathy (DKA). Small-fiber neuropathy, autonomic dysfunction, slowed conduction. EEG: seizures in hypoglycemia; ↑HbA1c; NCS: slow velocities. Glucose fluctuation → oxidative stress, microvascular injury. 10–20 % Vitamin D Deficiency (32) Hypocalcemic seizures, tetany, irritability, hypotonia. Poor coordination, delayed motor skills. ↓25(OH)D, hypocalcemia; EEG: irritability. Hypocalcemia induces neuronal hyperexcitability. 10–30 % Growth Hormone Deficiency (33) Weak cry, delayed fine motor development. Cognitive inefficiency, poor working memory. ↓IGF-1; pituitary MRI abnormalities possible. IGF-1 deficit impairs synaptic plasticity and axon growth. 10–20 % Hyperparathyroidism / Hypoparathyroidism (34) Tetany, seizures, facial spasm, paresthesias. Memory impairment, chronic paresthesia, anxiety. Ca²⁺ abnormalities; EEG spikes; prolonged QT. Calcium imbalance alters neuronal firing threshold. 15–30 % Congenital Adrenal Hyperplasia (35) Lethargy, vomiting, dehydration, encephalopathy in crisis. Subtle executive dysfunction in adolescents. Electrolyte disturbances, MRI are usually normal. Salt-wasting and androgen effects impact brain perfusion and development. 10–20 % Hypopituitarism (36) Hypoglycemic seizures in infancy. Developmental delay, learning difficulties. ↓GH/TSH/ACTH; pituitary MRI defects. Recurrent neuroglycopenia damages neurons and glia. 20–40 % Critical Illness–Related Endocrine Dysfunction (CIRCI) (36) Acute encephalopathy, delirium, neuromuscular weakness. Persistent cognitive deficits, ICU-acquired neuropathy. EEG: diffuse slowing; MRI: cortical atrophy; ↑cytokines. Cytokine surge and cortisol imbalance → neuronal injury and oxidative stress. 30–50 % Table 2 summarizes neurological involvement in pediatric endocrine disorders arises from direct hormonal effects on neuronal growth and metabolism, as well as from metabolic crises. Congenital hypothyroidism and hyperthyroidism display the widest impact, affecting cognition, motor coordination, and behavior. Disorders with cortisol or glucose dysregulation, such as Cushing’s syndrome, adrenal insufficiency, and diabetes, cause neurocognitive and neuropathic sequelae through oxidative stress and hippocampal injury. Vitamin D and parathyroid disorders lead to acute excitatory manifestations, while GH deficiency and hypopituitarism cause subtle but chronic neurodevelopmental delays. The reversibility of many of these manifestations highlights the importance of early endocrine correction. GSC Advanced Research and Reviews, 2025, 25(02), 244–262 251 Table 3 Reversibility of Muscular and Neurological Manifestations Following Endocrine Treatment (Mechanisms and Predictors) Endocrine Disorder (with Ref.) Muscular Reversibility After Treatment Neurological Reversibility After Treatment Predictors of Good Recovery Predictors of Poor or Partial Recovery Hypothyroidism (37) Excellent reversal of myopathy within weeks. Excellent if treated early; poor if therapy starts > 3–6 months (CH). Early diagnosis via newborn screening, adequate LT4 dose. Delayed therapy, prolonged untreated CH → irreversible neurodevelopmental deficits. Hyperthyroidism (38) Full recovery of myopathy; TPP resolves completely. Behavioral and cognitive symptoms improve after euthyroidism. Rapid control of thyrotoxicosis. Recurrent thyrotoxic episodes; prolonged severe disease. Cushing’s Syndrome (39) Gradual improvement in muscle strength and endurance. Partial cognitive recovery after cortisol normalization. Short disease duration, younger age. Chronic exposure → hippocampal atrophy and persistent weakness. Adrenal Insufficiency (40) Complete reversal with steroid replacement. Good neurologic recovery if crisis prevented. Early steroid initiation + electrolyte correction. Recurrent crises, profound hyponatremia. Diabetes Mellitus (41) Cramps and fatigue improve with metabolic control. Partial neuropathy reversal: children recover better than adults. Tight glycemic control, short disease duration. Recurrent DKA, chronic hyperglycemia. Growth Hormone Deficiency (42) Marked increase in lean mass and strength after GH therapy. Subtle improvements in memory and processing. Early GH therapy and adherence. Long-standing untreated GHD in infancy. Vitamin D Deficiency (43) Rapid reversal of hypotonia and weakness within days of supplementation. Excellent if treated before prolonged hypocalcemia. Early replacement and adequate dosing. Chronic deficiency with skeletal deformity. Hyper/Hypoparathyroidism (44) Excellent once calcium and PTH normalized. Seizure cessation and cognitive improvement typical. Prompt Ca/PTH correction. Recurrent episodes or long hypercalcemia. CIRCI (45) Partial muscle recovery; residual weakness common. Partial cognitive recovery; long-term fatigue. Early mobilization and rehabilitation. Prolonged ventilation and systemic inflammation. Table 3 demonstrates that neuromuscular reversibility in endocrine disorders depends primarily on timing and the underlying mechanism of injury. Deficiency states (hypothyroidism, vitamin D deficiency, adrenal insufficiency, and hypoparathyroidism) show the most complete recovery when treated early, reflecting functional rather than structural damage. Conversely, catabolic or toxic states (Cushing’s syndrome, prolonged hyperthyroidism, and CIRCI) cause lasting myofibrillar and neuronal loss that only partially improves despite hormonal correction. Diabetes and GH deficiency display intermediate patterns—functional improvement is GSC Advanced Research and Reviews, 2025, 25(02), 244–262 252 common, but residual neuropathy or cognitive slowness may persist. These data highlight that the window for complete neuromuscular recovery is narrowest in infancy and early childhood, underscoring the clinical value of rapid diagnosis and treatment. Table 4 Pediatric–Adult Differences in Neuromuscular Manifestations of Endocrine Disorders (Frequency, Severity, Duration, Reversibility) Endocrine Disorder (with Ref.) Frequency (Children vs Adults) Severity (Children vs Adults) Duration (Children vs Adults) Reversibility (Children vs Adults) Mechanistic Notes Congenital Adrenal Hyperplasia (46,51) Higher crisis frequency in infancy/early childhood vs lower in adults Acute weakness more severe in salt-wasting infants; adults milder Episodic in children (crises); adults chronic androgen/GC effects Good with early steroids and electrolyte correction; adults variable Salt loss + cortisol deficiency → impaired perfusion and excitability Hypopituitarism (multiple axes) (47) Diagnosed more often in childhood via growth failure vs less frequent in adults Greater motor delay and hypotonia in children; adults fatigue predominant Chronic without replacement in both; developmental window critical in children Better muscular recovery with early multi-axis replacement in children; adults slower Deficits in GH/TSH/ACTH amplify pediatric motor and cognitive impact Endocrine Myopathies (overview) (48,52) Broader spectrum in children; adults more classic phenotypes Children: hypotonia/delay; adults: proximal weakness Children often subacute; adults chronic Children more reversible if treated early; adults partial Pediatric plasticity and lower cumulative exposure favor recovery Diabetes Mellitus (Type 1/2) (49) Neuropathy less frequent in children vs common in adults Children: subtle small fiber/autonomic signs; adults more severe Shorter duration in children; adults’ decades-long Partial in children with tight control; adults limited reversal Hyperglycemia/variability → oxidative stress, microvascular injury Recurrent Hypoglycemia / Hyperinsulinism (50) More frequent in infants/young children vs rare in adults Children: seizures, neuroglycopenia; adults: milder neuro symptoms Acute episodes in children may cluster; adults sporadic Better with prompt stabilization in children; residual deficits if prolonged Energy failure injures developing WM and synapses Cushing’s Syndrome / Hypercortisolism (55,53) Rarer in children; iatrogenic more common across ages Children: marked proximal myopathy; adults: severe but more insidious Months–years in both; pediatric growth delay adds burden Muscular: partial; cognition: partial children improve more if short exposure GC excess → proteolysis, mitochondrial dysfunction; hippocampal injury Thyrotoxic Periodic Paralysis (56) Adolescents > younger children; Children: dramatic episodic flaccid paralysis; Episodic in both; trigger-linked Excellent with euthyroidism and K+; β-adrenergic ↑Na⁺/K⁺-ATPase → intracellular K⁺ shift GSC Advanced Research and Reviews, 2025, 25(02), 244–262 259 Authors’ Contributions ATS conceptualized the study, designed the review framework, and supervised manuscript preparation. 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