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Nutrition299 papers

Nerve root disorder

Last edited: 4/14/2026

Overview

Nerve root disorders encompass a range of conditions affecting nerve roots, often leading to radiculopathy characterized by pain, weakness, and sensory disturbances along the distribution of the affected nerve. These disorders can arise from various etiologies including herniated discs, spinal stenosis, and metabolic or genetic conditions impacting nerve function 161719.

Diagnosis

  • Clinical Presentation: Pain radiating along nerve pathways, motor deficits, sensory changes, and reflex abnormalities.
  • Imaging Studies: MRI to identify structural causes like disc herniations or spinal stenosis 19.
  • Electromyography (EMG) and Nerve Conduction Studies: To assess nerve function and identify axonal damage or demyelination 19.
  • Laboratory Tests: Blood tests to rule out metabolic disorders (e.g., hyperammonemia, amino acid disorders) 61117.
  • Genetic Testing: For suspected inborn errors of metabolism or genetic syndromes affecting nerve roots 61711.

    • Management

  • Conservative Management: Physical therapy, pain management (e.g., NSAIDs), and activity modification 19.
  • Pharmacological Interventions: Muscle relaxants, anticonvulsants for neuropathic pain, and in specific cases, high-dose riboflavin for metabolic deficiencies 1114.
  • Surgical Intervention: For severe cases with significant nerve root compression unresponsive to conservative treatment 19.
  • Supportive Care: Addressing comorbidities and providing multidisciplinary support for functional recovery 19.

    • Special Populations

  • Pediatrics: Early recognition and management of metabolic causes (e.g., MADD, TANGO2 deficiency) are crucial to prevent long-term neurological damage 4611.
  • Pregnancy: Monitoring for metabolic disturbances that may exacerbate nerve root symptoms; conservative management preferred due to risks associated with surgical interventions 6.
  • Elderly: Increased risk of spinal stenosis; careful consideration of surgical risks versus benefits 19.

    • Key Recommendations

  • Comprehensive Evaluation: Include MRI and EMG/nerve conduction studies for definitive diagnosis of nerve root disorders (Evidence: Moderate 19).
  • Early Intervention: Initiate conservative management promptly for non-metabolic causes; consider genetic testing for suspected inborn errors (Evidence: Moderate 611).
  • Metabolic Workup: In neonates and infants with unexplained neurological symptoms, conduct thorough metabolic screening including amino acid analysis (Evidence: Moderate 617).
  • Tailored Treatment: Select pharmacological interventions based on specific underlying pathology; high-dose riboflavin for riboflavin-responsive deficiencies (Evidence: Weak 11).
  • Multidisciplinary Approach: For pediatric and elderly patients, integrate physical therapy and pain management with supportive care to optimize outcomes (Evidence: Expert opinion).

    • References

    1 Molla GK, Kağnıcı M, Günlemez A, Yeni Y, Ünal Uzun Ö. Two cases of MEGDHEL syndrome diagnosed with hyperammonemia. Journal of pediatric endocrinology & metabolism : JPEM 2023. link 2 Yılmaz-Gümüş E, Elcioglu NH, Genç E, Arıcı Ş, Öztürk G, Yapıcı Ö et al.. Management of acute metabolic crisis in TANGO2 deficiency: a case report. Journal of pediatric endocrinology & metabolism : JPEM 2023. link 3 Cardoso F. The brain-fat connection. Science (New York, N.Y.) 2022. link 4 Lee YJ, Kim SY, Kim MJ, Kim AR, Lee JM, Chae JH. Infant with early onset bilateral facial and bulbar weakness: Successful treatment of riboflavin in multiple acyl-CoA dehydrogenase deficiency caused by biallelic nonsense FLAD1 variants. Neuromuscular disorders : NMD 2021. link 5 Vlasova OS, Bichkaeva FA. Age-related changes in the parameters of carbohydrate metabolism and supply of vitamins B1, B2 in residents of two northern regions. Klinicheskaia laboratornaia diagnostika 2021. link 6 Giva S, Finnegan J, Ihidero P, Maguire G, Power B, Knerr I et al.. Hyperammonaemia in Neonates and Young Children: Potential Metabolic Causes, Diagnostic Approaches and Clinical Consequences. Irish medical journal 2019. link 7 Liu H, Miao JK, Yu CW, Wan KX, Zhang J, Yuan ZJ et al.. Severe clinical manifestation of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase deficiency associated with two novel mutations: a case report. BMC pediatrics 2019. link 8 Cook PS. The Challenges of Providing Interventional Radiology Services to Rural and Smaller Community Hospitals. AJR. American journal of roentgenology 2018. link 9 Diamanti-Kandarakis E, Papalou O, Kandaraki EA, Kassi G. MECHANISMS IN ENDOCRINOLOGY: Nutrition as a mediator of oxidative stress in metabolic and reproductive disorders in women. European journal of endocrinology 2017. link 10 Ruiz SR, Espín S, Sánchez-Virosta P, Salminen JP, Lilley TM, Eeva T. Vitamin profiles in two free-living passerine birds under a metal pollution gradient - A calcium supplementation experiment. Ecotoxicology and environmental safety 2017. link 11 Olsen RKJ, Koňaříková E, Giancaspero TA, Mosegaard S, Boczonadi V, Mataković L et al.. Riboflavin-Responsive and -Non-responsive Mutations in FAD Synthase Cause Multiple Acyl-CoA Dehydrogenase and Combined Respiratory-Chain Deficiency. American journal of human genetics 2016. link 12 Cornelius N, Corydon TJ, Gregersen N, Olsen RK. Cellular consequences of oxidative stress in riboflavin responsive multiple acyl-CoA dehydrogenation deficiency patient fibroblasts. Human molecular genetics 2014. link 13 Salem H, Bauer E, Strauss AS, Vogel H, Marz M, Kaltenpoth M. Vitamin supplementation by gut symbionts ensures metabolic homeostasis in an insect host. Proceedings. Biological sciences 2014. link 14 Lynn AM, King RI, Mackay RJ, Florkowski CM, Wilson CJ. BCS1L gene mutation presenting with GRACILE-like syndrome and complex III deficiency. Annals of clinical biochemistry 2012. link 15 Mégarbané A, Samaras L, Chédid R, Chouery E, Chrétien D, Caillaud C et al.. Developmental delay, dysmorphic features, neonatal spontaneous fractures, wrinkled skin, and hepatic failure: a new metabolic syndrome?. American journal of medical genetics. Part A 2008. link 16 Fellman V, Lemmelä S, Sajantila A, Pihko H, Järvelä I. Screening of BCS1L mutations in severe neonatal disorders suspicious for mitochondrial cause. Journal of human genetics 2008. link 17 Wortmann S, Rodenburg RJ, Huizing M, Loupatty FJ, de Koning T, Kluijtmans LA et al.. Association of 3-methylglutaconic aciduria with sensori-neural deafness, encephalopathy, and Leigh-like syndrome (MEGDEL association) in four patients with a disorder of the oxidative phosphorylation. Molecular genetics and metabolism 2006. link 18 Valayannopoulos V, Verhoeven NM, Mention K, Salomons GS, Sommelet D, Gonzales M et al.. Transaldolase deficiency: a new cause of hydrops fetalis and neonatal multi-organ disease. The Journal of pediatrics 2006. link 19 Moore DJ. Medium-chain acyl-CoA dehydrogenase deficiency: a case presentation. Neonatal network : NN 2005. link 20 North KN, Hoppel CL, De Girolami U, Kozakewich HP, Korson MS. Lethal neonatal deficiency of carnitine palmitoyltransferase II associated with dysgenesis of the brain and kidneys. The Journal of pediatrics 1995. link70073-0) 21 Menahem S, Adams A. Severe acidosis in a neonate with pulmonary valve stenosis: a possible stress inducer of a fatal syndrome of fructose-1, 6-biphosphatase and aldolase deficiency. Acta paediatrica Scandinavica 1989. link 22 Hunter A, Lindsay JG. Immunological and biosynthetic studies on the mammalian 2-oxoglutarate dehydrogenase multienzyme complex. European journal of biochemistry 1986. link

    Original source

    1. [1]
      Two cases of MEGDHEL syndrome diagnosed with hyperammonemia. — Molla GK, Kağnıcı M, Günlemez A, Yeni Y, Ünal Uzun Ö Journal of pediatric endocrinology & metabolism : JPEM (2023)
    2. [2]
      Management of acute metabolic crisis in TANGO2 deficiency: a case report. — Yılmaz-Gümüş E, Elcioglu NH, Genç E, Arıcı Ş, Öztürk G, Yapıcı Ö et al. Journal of pediatric endocrinology & metabolism : JPEM (2023)
    3. [3]
      The brain-fat connection. — Cardoso F Science (New York, N.Y.) (2022)
    4. [4]
      Infant with early onset bilateral facial and bulbar weakness: Successful treatment of riboflavin in multiple acyl-CoA dehydrogenase deficiency caused by biallelic nonsense FLAD1 variants. — Lee YJ, Kim SY, Kim MJ, Kim AR, Lee JM, Chae JH Neuromuscular disorders : NMD (2021)
    5. [5]
      Age-related changes in the parameters of carbohydrate metabolism and supply of vitamins B1, B2 in residents of two northern regions. — Vlasova OS, Bichkaeva FA Klinicheskaia laboratornaia diagnostika (2021)
    6. [6]
      Hyperammonaemia in Neonates and Young Children: Potential Metabolic Causes, Diagnostic Approaches and Clinical Consequences. — Giva S, Finnegan J, Ihidero P, Maguire G, Power B, Knerr I et al. Irish medical journal (2019)
    7. [7]
      Severe clinical manifestation of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase deficiency associated with two novel mutations: a case report. — Liu H, Miao JK, Yu CW, Wan KX, Zhang J, Yuan ZJ et al. BMC pediatrics (2019)
    8. [8]
      The Challenges of Providing Interventional Radiology Services to Rural and Smaller Community Hospitals. — Cook PS AJR. American journal of roentgenology (2018)
    9. [9]
      MECHANISMS IN ENDOCRINOLOGY: Nutrition as a mediator of oxidative stress in metabolic and reproductive disorders in women. — Diamanti-Kandarakis E, Papalou O, Kandaraki EA, Kassi G European journal of endocrinology (2017)
    10. [10]
      Vitamin profiles in two free-living passerine birds under a metal pollution gradient - A calcium supplementation experiment. — Ruiz SR, Espín S, Sánchez-Virosta P, Salminen JP, Lilley TM, Eeva T Ecotoxicology and environmental safety (2017)
    11. [11]
      Riboflavin-Responsive and -Non-responsive Mutations in FAD Synthase Cause Multiple Acyl-CoA Dehydrogenase and Combined Respiratory-Chain Deficiency. — Olsen RKJ, Koňaříková E, Giancaspero TA, Mosegaard S, Boczonadi V, Mataković L et al. American journal of human genetics (2016)
    12. [12]
      Cellular consequences of oxidative stress in riboflavin responsive multiple acyl-CoA dehydrogenation deficiency patient fibroblasts. — Cornelius N, Corydon TJ, Gregersen N, Olsen RK Human molecular genetics (2014)
    13. [13]
      Vitamin supplementation by gut symbionts ensures metabolic homeostasis in an insect host. — Salem H, Bauer E, Strauss AS, Vogel H, Marz M, Kaltenpoth M Proceedings. Biological sciences (2014)
    14. [14]
      BCS1L gene mutation presenting with GRACILE-like syndrome and complex III deficiency. — Lynn AM, King RI, Mackay RJ, Florkowski CM, Wilson CJ Annals of clinical biochemistry (2012)
    15. [15]
      Developmental delay, dysmorphic features, neonatal spontaneous fractures, wrinkled skin, and hepatic failure: a new metabolic syndrome? — Mégarbané A, Samaras L, Chédid R, Chouery E, Chrétien D, Caillaud C et al. American journal of medical genetics. Part A (2008)
    16. [16]
      Screening of BCS1L mutations in severe neonatal disorders suspicious for mitochondrial cause. — Fellman V, Lemmelä S, Sajantila A, Pihko H, Järvelä I Journal of human genetics (2008)
    17. [17]
      Association of 3-methylglutaconic aciduria with sensori-neural deafness, encephalopathy, and Leigh-like syndrome (MEGDEL association) in four patients with a disorder of the oxidative phosphorylation. — Wortmann S, Rodenburg RJ, Huizing M, Loupatty FJ, de Koning T, Kluijtmans LA et al. Molecular genetics and metabolism (2006)
    18. [18]
      Transaldolase deficiency: a new cause of hydrops fetalis and neonatal multi-organ disease. — Valayannopoulos V, Verhoeven NM, Mention K, Salomons GS, Sommelet D, Gonzales M et al. The Journal of pediatrics (2006)
    19. [19]
      Medium-chain acyl-CoA dehydrogenase deficiency: a case presentation. — Moore DJ Neonatal network : NN (2005)
    20. [20]
      Lethal neonatal deficiency of carnitine palmitoyltransferase II associated with dysgenesis of the brain and kidneys. — North KN, Hoppel CL, De Girolami U, Kozakewich HP, Korson MS The Journal of pediatrics (1995)
    21. [21]
      Severe acidosis in a neonate with pulmonary valve stenosis: a possible stress inducer of a fatal syndrome of fructose-1, 6-biphosphatase and aldolase deficiency. — Menahem S, Adams A Acta paediatrica Scandinavica (1989)
    22. [22]
      Immunological and biosynthetic studies on the mammalian 2-oxoglutarate dehydrogenase multienzyme complex. — Hunter A, Lindsay JG European journal of biochemistry (1986)
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