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Journal articles on the topic 'Anterior horn cell disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Ryan, Monique M., Claire M. Cooke-Yarborough, Peter G. Procopis, and Robert A. Ouvrier. "Anterior horn cell disease and olivopontocerebellar hypoplasia." Pediatric Neurology 23, no. 2 (2000): 180–84. http://dx.doi.org/10.1016/s0887-8994(00)00166-1.

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2

Vuopala, Katri, Jaakko Ignatius, and Riitta Herva. "Lethal arthrogryposis with anterior horn cell disease." Human Pathology 26, no. 1 (1995): 12–19. http://dx.doi.org/10.1016/0046-8177(95)90109-4.

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3

Gaitanis, John N., Hugh J. McMillan, Allan Wu, and Basil T. Darras. "Electrophysiologic Evidence for Anterior Horn Cell Disease in Amyoplasia." Pediatric Neurology 43, no. 2 (2010): 142–47. http://dx.doi.org/10.1016/j.pediatrneurol.2010.03.018.

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4

Desai, J. A., and M. Melanson. "Teaching NeuroImages: Anterior horn cell hyperintensity in Hirayama disease." Neurology 77, no. 12 (2011): e73-e73. http://dx.doi.org/10.1212/wnl.0b013e31822f02d0.

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5

Görgen-Pauly, Ute, Jürgen Sperner, Irwin Reiss, Hans-Björn Gehl, and Erich Reusche. "Familial pontocerebellar hypoplasia type I with anterior horn cell disease." European Journal of Paediatric Neurology 3, no. 1 (1999): 33–38. http://dx.doi.org/10.1053/ejpn.1999.0177.

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6

Torne, Krupa, and Neeta Sutay. "A rare presentation of anterior horn cell disease in children." European Journal of Paediatric Neurology 21 (June 2017): e109. http://dx.doi.org/10.1016/j.ejpn.2017.04.941.

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7

Corbett, Joel, Stephen Walsh, Sandeep Bhuta, and Arman Sabet. "105 Snake eyes in the thoracic spine." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 6 (2018): A41.3—A42. http://dx.doi.org/10.1136/jnnp-2018-anzan.104.

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IntroductionBilateral anterior horn cell hyperintensity on spinal imaging (‘snake eyes’ sign) is seen in pathologies including cervical spondylosis, spinal cord infarction and Hirayama’s disease. Below is the first report of lower limb monomelic amyotrophy (MMA) with thoracic spine snake eyes sign. We present a case report of lower limb MMA with bilateral anterior horn hyperintensity, and literature review of cases with this clinico-radiologic presentation.CaseA 47 year old man presented with an 11 year history of asymmetric, progressive, proximal right lower limb weakness and wasting followin

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8

de Carvalho, M., and M. Swash. "Fasciculation-cramp syndrome preceding anterior horn cell disease: an intermediate syndrome?" Journal of Neurology, Neurosurgery & Psychiatry 82, no. 4 (2010): 459–61. http://dx.doi.org/10.1136/jnnp.2009.194019.

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9

Wongworawat, Yan Chen, Yin Allison Liu, Ravi Raghavan, et al. "Aggressive FUS-Mutant Motor Neuron Disease Without Profound Spinal Cord Pathology." Journal of Neuropathology & Experimental Neurology 79, no. 4 (2020): 365–69. http://dx.doi.org/10.1093/jnen/nlaa011.

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Abstract A 29-year-old man presented with rapidly progressive severe neck weakness, asymmetrical bilateral upper extremity weakness, bulbar dysfunction, profound muscle wasting, and weight loss. Within 1 year, his speech became unintelligible, he became gastrostomy- and tracheostomy/ventilator-dependent, and wheelchair bound. Electrophysiology suggested motor neuron disease. Whole exome sequencing revealed a heterozygous pathogenic variant in the fused in sarcoma gene (FUS), c.1574C&gt;T,p. R525L, consistent with autosomal dominant amyotrophic lateral sclerosis. Autopsy revealed extensive

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10

Pisharam, N. Thekkootu, T. Solomon, and R. Sharma. "Anterior horn cell and encephalopathic variant of Fabry's disease — The neuro-Fabry." Journal of the Neurological Sciences 333 (October 2013): e455-e456. http://dx.doi.org/10.1016/j.jns.2013.07.1626.

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11

Wilmshurst, Jo M., Robert Surtees, Tim Cox, and Richard O. Robinson. "Cerebellar ataxia, anterior horn cell disease, learning difficulties, and dystonia: a new syndrome." Developmental Medicine & Child Neurology 42, no. 11 (2000): 775–79. http://dx.doi.org/10.1017/s0012162200001432.

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12

Wilmshurst, Jo M., Robert Surtees, Tim Cox, and Richard O. Robinson. "Cerebellar ataxia, anterior horn cell disease, learning difficulties, and dystonia: a new syndrome." Developmental Medicine & Child Neurology 42, no. 11 (2007): 775–79. http://dx.doi.org/10.1111/j.1469-8749.2000.tb00042.x.

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13

MITSUMOTO, HIROSHI, and ANITA L. BOGGS. "Vacuolated Anterior Horn Cells in Wobbler Mouse Motor Neuron Disease." Journal of Neuropathology and Experimental Neurology 46, no. 2 (1987): 214–22. http://dx.doi.org/10.1097/00005072-198703000-00008.

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14

Leigh, P. N., B. H. Anderton, A. Dodson, J. M. Gallo, M. Swash, and D. M. Power. "Ubiquitin deposits in anterior horn cells in motor neurone disease." Neuroscience Letters 93, no. 2-3 (1988): 197–203. http://dx.doi.org/10.1016/0304-3940(88)90081-x.

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15

Yamanouchi, Yoko, Hideo Yamanouchi, and Laurence E. Becker. "Synaptic alterations of anterior horn cells in Werdnig-Hoffmann disease." Pediatric Neurology 15, no. 1 (1996): 32–35. http://dx.doi.org/10.1016/0887-8994(96)00123-3.

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16

Tejada, J., L. E. Hernandez-Echebarria, J. F. Fernandez-Lopez, et al. "Acute anterior horn cell disease resembling poliomyelitis as a manifestation of respiratory syncytial virus infection." Journal of Neurology, Neurosurgery & Psychiatry 60, no. 1 (1996): 106–7. http://dx.doi.org/10.1136/jnnp.60.1.106-a.

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17

Lee, John-Ih, Stephan Macht, Philipp Albrecht, Hans-Peter Hartung, and Norbert Goebels. "Brachial amyotrophic diparesis associated with anti-Hu positive anterior horn cell disease and autonomic disorder." Journal of Neurology 260, no. 1 (2012): 301–2. http://dx.doi.org/10.1007/s00415-012-6711-3.

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18

Nanda, Satyan, Rahul Handa, Rajiv Anand, et al. "Curious case of steroid responsive diffuse anterior horn cell disease associated with COVID-19 infection." Neurological Sciences 42, no. 8 (2021): 3415–17. http://dx.doi.org/10.1007/s10072-021-05163-9.

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19

MitsumotO, H., and A. L. Boggs. "NEURONAL FUNCTION OF VACUOLATED ANTERIOR HORN CELLS IN WOBBLER MOTOR NEURON DISEASE." Journal of Neuropathology and Experimental Neurology 44, no. 3 (1985): 327. http://dx.doi.org/10.1097/00005072-198505000-00069.

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20

Mizusawa, Hidehiro, Haruomi Nakamura, Ikuro Wakayama, Shu-Hui C. Yen, and Asao Hirano. "Skein-like inclusions in the anterior horn cells in motor neuron disease." Journal of the Neurological Sciences 105, no. 1 (1991): 14–21. http://dx.doi.org/10.1016/0022-510x(91)90112-k.

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21

Edmundson, Christyn, and Shawn Bird. "Acute Manifestations of Neuromuscular Disease." Seminars in Neurology 39, no. 01 (2019): 115–24. http://dx.doi.org/10.1055/s-0038-1676838.

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AbstractNeuromuscular emergencies may be defined as disorders or exacerbation of diseases of the peripheral nervous system that are rapidly progressive and potentially life-threatening. Such disorders can affect any level of the peripheral nervous system, from the muscle to the anterior horn cell. While their clinical manifestations may vary, severe morbidity and mortality is most frequently the result of neuromuscular respiratory failure. Some disorders, such as Guillain–Barré syndrome, provide the additional threat of severe, and potentially irreversible, nerve loss. Others, such as rhabdomy

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22

Picheca, Christopher, Vignan Yogendrakumar, James I. Brooks, Carlos Torres, Elizabeth Pringle, and Jocelyn Zwicker. "Polio-Like Manifestation of Powassan Virus Infection with Anterior Horn Cell Involvement, Canada." Emerging Infectious Diseases 25, no. 8 (2019): 1609–11. http://dx.doi.org/10.3201/eid2508.190399.

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23

Winder, Toni R., and Roland N. Auer. "Sensory Neuron Degeneration in Familial Kugelberg-Welander Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 16, no. 1 (1989): 67–70. http://dx.doi.org/10.1017/s0317167100028535.

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ABSTRACT:A 53 year old man developed symptoms of motor neuron disease in childhood. There was a family history of a similar disorder and it was felt to represent a form of Kugelberg-Welander disease. In addition to the motor deficits, sensory abnormalities in his legs were documented during life. Autopsy revealed anterior horn cell loss throughout the length of the spinal cord, with preservation of the phrenic nucleus. The lumbar dorsal root ganglia showed active degeneration of sensory neurons, with nuclear changes exceeding cytoplasmic ones. The fasciculus gracilis showed Wallerian degenerat

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24

SWASH, M., M. LEADER, A. BROWN, and K. W. SWETTENHAM. "FOCAL LOSS OF ANTERIOR HORN CELLS IN THE CERVICAL CORD IN MOTOR NEURON DISEASE." Brain 109, no. 5 (1986): 939–52. http://dx.doi.org/10.1093/brain/109.5.939.

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25

Hader, Walter J., Bohdan Rozdilsky, and Cheranada P. Nair. "The Concurrence of Multiple Sclerosis and Amyotrophic Lateral Sclerosis." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, no. 1 (1986): 66–69. http://dx.doi.org/10.1017/s0317167100035824.

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ABSTRACT:We report the clinical and pathological findings of the unusual combination of two idiopathic central nervous system diseases, multiple sclerosis and amyotrophic lateral sclerosis in a 56 year old physician with a twenty-seven year history of a disease initially characterized by relapses and remissions, followed by an eight year quiescent period. During the last year of life there was rapid deterioration with development of generalized weakness, atrophy, weight loss and fasciculations of body and tongue, and associated difficulty with swallowing and sudden respiratory failure. The aut

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26

Struck, Aaron F., Shahriar Salamat, and Andrew J. Waclawik. "Motor Neuron Disease With Selective Degeneration of Anterior Horn Cells Associated With Non-Hodgkin Lymphoma." Journal of Clinical Neuromuscular Disease 16, no. 2 (2014): 83–89. http://dx.doi.org/10.1097/cnd.0000000000000056.

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27

Sasaki, Shoichi, and Makoto Iwata. "Ultrastructural Study of the Synapses of Central Chromatolytic Anterior Horn Cells in Motor Neuron Disease." Journal of Neuropathology & Experimental Neurology 55, no. 8 (1996): 932–39. http://dx.doi.org/10.1097/00005072-199608000-00009.

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28

Vuopala, K., P. Makela-Bengs, A. Suomalainen, R. Herva, J. Leisti, and L. Peltonen. "Lethal congenital contracture syndrome (LCCS), a fetal anterior horn cell disease, is not linked to the SMA 5q locus." Journal of Medical Genetics 32, no. 1 (1995): 36–38. http://dx.doi.org/10.1136/jmg.32.1.36.

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29

Joshi, Tapan, Daniel Becker, and Janet M. Dean. "Poster 288: Anterior Horn Cell Disease Secondary to West Nile Virus Mimicking Transverse Myelitis in Pediatric Population: A Case Report." PM&R 1 (September 2009): S229. http://dx.doi.org/10.1016/j.pmrj.2009.08.311.

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30

Eisen, Andrew, and Donald Calne. "Amyotrophic Lateral Sclerosis, Parkinson’s Disease and Alzheimer’s Disease: Phylogenetic Disorders of the Human Neocortex Sharing Many Characteristics." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, S1 (1992): 117–23. http://dx.doi.org/10.1017/s0317167100041482.

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ABSTRACT:Features common to amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD) and Alzheimer’s disease (AD) are reviewed. Shared epidemiological aspects include an increasing frequency which is proportional for each disease. We draw attention to geographic non-uniform distribution which, for ALS and PD, correlates positively with latitude. Clinical and pathological overlap occurs in the same patients, and in members of the same family. A high early morning plasma cysteine/sulphate ratio possibly related to the development of proteinacious inclusions, as well as ubiquinated neuronal

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31

Ono, Seiitsu, Kazuyuki Hara, Hiroshi Sasaki, Isamu Sugano, and Koichi Nagao. "Degeneration of anterior horn cell in neuronal type of Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy type II): A Golgi study." Acta Neuropathologica 85, no. 6 (1993): 596–601. http://dx.doi.org/10.1007/bf00334668.

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32

Auer, Roland N., Robert B. Bell, and Mary Anne Lee. "Neuropathy with Onion Bulb Formations and Pure Motor Manifestations." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 16, no. 2 (1989): 194–97. http://dx.doi.org/10.1017/s0317167100028894.

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ABSTRACT:A thirty-eight-year-old man presented with a six year history of symptoms resembling an anterior horn cell disorder. There was progressive upper extremity wasting and weakness in the absence of sensory complaints. Electrophysiologic abnormalities were confined to motor nerve conduction and indicated a demyelinating process involving the brachial plexus and major proximal upper extremity nerve trucks bilaterally. Biopsy of the proximal right ulnar nerve revealed changes suggesting a chronic demyelinating process, and onion-bulb formations were present. Immunohistochemical staining for

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33

Vogt, Matthew R., Peter F. Wright, William F. Hickey, Kelli L. Boyd, and James E. Crowe. "#16: Enterovirus D68 Visualized in the Anterior Horn of the Spinal Cord of a Pediatric Patient with Flaccid Paralysis." Journal of the Pediatric Infectious Diseases Society 10, Supplement_2 (2021): S8. http://dx.doi.org/10.1093/jpids/piab031.015.

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Abstract Background Acute flaccid myelitis (AFM) is a polio-like paralyzing illness of children. AFM incidence is increasing during every other year outbreaks that occur in the United States simultaneously with outbreaks of enterovirus D68 (EV-D68) infection. Demonstrating that EV-D68 directly causes AFM has been challenging due to rare detection of the virus in the cerebrospinal fluid (CSF) of patients despite frequent detection at nonsterile sites. Murine studies have shown that EV-D68 can infect spinal cord anterior horn motor neurons and cause paralysis, similar to poliovirus. However, a k

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34

Cantó-Santos, Judith, Josep M. Grau-Junyent, and Glòria Garrabou. "The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases." Antioxidants 9, no. 10 (2020): 964. http://dx.doi.org/10.3390/antiox9100964.

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Neuromuscular diseases (NMDs) are a heterogeneous group of acquired or inherited rare disorders caused by injury or dysfunction of the anterior horn cells of the spinal cord (lower motor neurons), peripheral nerves, neuromuscular junctions, or skeletal muscles leading to muscle weakness and waste. Unfortunately, most of them entail serious or even fatal consequences. The prevalence rates among NMDs range between 1 and 10 per 100,000 population, but their rarity and diversity pose difficulties for healthcare and research. Some molecular hallmarks are being explored to elucidate the mechanisms t

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35

Nates, J. L., D. J. Cooper, B. Day, and D. V. Tuxen. "Acute Weakness Syndromes in Critically Ill Patients—A Reappraisal." Anaesthesia and Intensive Care 25, no. 5 (1997): 502–13. http://dx.doi.org/10.1177/0310057x9702500509.

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Over the last twenty years, increasing numbers of critically ill, mechanically ventilated patients who develop acute profound muscle weakness have been described. These acute weakness syndromes have not been well understood and they have been given many names including: acute steroid myopathy, acute quadriplegic myopathy, the floppy person syndrome, critical illness polyneuropathy, critical illness polyneuromyopathy, and prolonged neurogenic weakness. Many of these “syndromes” either overlap or represent the same disease process in different patients. Many have been incompletely diagnosed. Dur

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36

Burton, Jodie M., Ralph Z. Kern, William Halliday, et al. "Neurological Manifestations of West Nile Virus Infection." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 31, no. 2 (2004): 185–93. http://dx.doi.org/10.1017/s0317167100053828.

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AbstractBackground:Over the past four years, West Nile virus (WNV) has become a significant health issue in North America. In 2002, WNV infection made its first appearance in the human population in Canada.Methods:Patients who presented to the University Health Network and Mount Sinai Hospital in Toronto with neurological disease attributed to WNV infection were identified and followed by the neurology service. Clinical features and results of laboratory, electrodiagnostic, radiological and pathological studies are presented.Results:In August and September 2002, 26 patients were admitted with

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37

Vogt, Matthew R., Peter Wright, William Hickey, James E. Crowe, and Kelli Boyd. "1408. Enterovirus D68 RNA Visualized in the Anterior Horn of the Spinal Cord of a Pediatric Patient with Flaccid Paralysis." Open Forum Infectious Diseases 7, Supplement_1 (2020): S712. http://dx.doi.org/10.1093/ofid/ofaa439.1590.

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Abstract Background Acute flaccid myelitis (AFM) is a polio-like paralyzing illness of children. AFM incidence is increasing during every other year outbreaks that occur in the United States simultaneously with outbreaks of enterovirus D68 (EV-D68) infection. Demonstrating that EV-D68 directly causes AFM has been challenging due to rare detection of the virus in the cerebrospinal fluid (CSF) of patients despite frequent detection at nonsterile sites. Murine studies have shown that EV-D68 can infect spinal cord anterior horn motor neurons and cause paralysis, similar to poliovirus. However, a k

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38

Matsumoto, Sadayuki, Satoshi Goto, Hirofumi Kusaka, et al. "Ubiquitin-positive inclusion in anterior horn cells in subgroups of motor neuron diseases: A comparative study of adult-onset amyotrophic lateral sclerosis, juvenile amyotrophic lateral sclerosis and werdnig-hoffmann disease." Journal of the Neurological Sciences 115, no. 2 (1993): 208–13. http://dx.doi.org/10.1016/0022-510x(93)90226-o.

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39

Islam, M. "P72 Riluzole causing pancytopenia: a clinically important rarity." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 3 (2019): e41.1-e41. http://dx.doi.org/10.1136/jnnp-2019-abn.132.

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DesignCase Report: An 83-year-old lady, was admitted with progressive speech and swallowing difficulty and wasting of small muscles of hand for 3 months. EMG revealed widespread anterior horn cell disease. With a diagnosis of MND, She was started on Riluzole 50 mg, LFT and FBC were normal before and 2 days after 1 st dose and the dose increased to a recommended dose of 50 mg twice a day. While waiting for PEG tube insertion, within 7 days, FBC showed a significant drop in Hb of 23 g/L ( from 125 to 102 g/L), Platelet dropped to 150×x10^9/L from 208 × 10^9/L, leucopenica ( 2.4 × 10^9/L) without

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40

Chowdhury, Rajib Nayan, Md Enayet Hussain, Md Nahidul Islam, et al. "An audit of patients referred for nerve conduction study in a tertiary care hospital in Bangladesh." Journal of Dhaka Medical College 23, no. 1 (2015): 102–8. http://dx.doi.org/10.3329/jdmc.v23i1.22703.

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Background: To examine the pattern and burden of neurologic disorders at electrophysiology lab of a tertiary care centre. Methodology: This retrospective chart review was carried out from the records and notes of electrophysiology lab in National Institute of Neurosciences and Hospital (NINS) from January to December 2013. A total of 1372 patients were evaluated with nerve conduction study (NCS) and electromyography (EMG) during this period. Result: Majority of the patients (67.6%) presented after forty with a mean age at presentation of 48.11±17.3 years. The male patients (55.2%) predominated

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41

van Os, Nienke J. H., Anke Hensiek, Judith van Gaalen, et al. "Trajectories of motor abnormalities in milder phenotypes of ataxia telangiectasia." Neurology 92, no. 1 (2018): e19-e29. http://dx.doi.org/10.1212/wnl.0000000000006700.

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ObjectiveTo describe and classify the neurologic trajectories in patients with mild neurologic forms of ataxia telangiectasia (A-T) from the Dutch A-T cohort, combined with patients reported in the literature.MethodsClinical, genetic, and laboratory data of 14 patients with mild neurologic phenotypes of A-T from the Dutch cohort were analyzed and combined with corresponding data from the literature. A mild neurologic phenotype was defined by a later onset, nonataxia presenting or dominant feature, or slower progression compared to the classic A-T phenotype. Neurologic trajectories were classif

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42

Pedroso, José Luiz, Wladimir Bocca Vieira de Resende Pinto, Paulo Victor Sgobbi de Souza, Carolina Andriotti, João Norberto Stavale, and Orlando G. P. Barsottini. "Anterior horn degeneration in Machado-Joseph disease." Journal of the Neurological Sciences 368 (September 2016): 290–91. http://dx.doi.org/10.1016/j.jns.2016.07.037.

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43

Hoogers, S. E., P. W. Wirtz, and H. Koppen. "Subacute anterior horn disease caused by neuroborreliosis." Neurological Sciences 34, no. 6 (2012): 1019–20. http://dx.doi.org/10.1007/s10072-012-1168-9.

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44

Turner, B. "Superficial siderosis associated with anterior horn cell dysfunction." Journal of Neurology, Neurosurgery & Psychiatry 72, no. 2 (2002): 274a—275. http://dx.doi.org/10.1136/jnnp.72.2.274-a.

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45

Larsen, R., S. Ashwal, and N. Peckham. "Incontinentia pigmenti: Association with anterior horn cell degeneration." Neurology 37, no. 3 (1987): 446. http://dx.doi.org/10.1212/wnl.37.3.446.

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46

Ertekin, Cumhur, Nilgun Arac, Safiye Bilgin, Hakan Ediboglu, and Mustafa Ertas. "Subclinical Anterior Horn Cell Involvement in Juvenile Myoclonic Epilepsy." Epilepsia 35, no. 2 (1994): 322–27. http://dx.doi.org/10.1111/j.1528-1157.1994.tb02438.x.

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47

Ikemoto, Akito, Asao Hirano, Sadayuki Matsumoto, Ichiro Akiguchi, and Jun Kimura. "Synaptophysin expression in the anterior horn of Werdnig-Hoffmann disease." Journal of the Neurological Sciences 136, no. 1-2 (1996): 94–100. http://dx.doi.org/10.1016/0022-510x(95)00297-f.

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48

Vernino, Steven. "PARANEOPLASTIC DISORDERS AFFECTING THE NEUROMUSCULAR JUNCTION OR ANTERIOR HORN CELL." CONTINUUM: Lifelong Learning in Neurology 15 (February 2009): 132–46. http://dx.doi.org/10.1212/01.con.0000300011.79845.eb.

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49

Zernicke, R. F., A. C. Vailas, S. R. Shaw, R. A. Bogey, T. J. Hart, and J. Matsuda. "Heterogeneous mechanical response of rat knee menisci to thermomechanical stress." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 1 (1986): R65—R70. http://dx.doi.org/10.1152/ajpregu.1986.250.1.r65.

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Thermodilatometric, dynamic thermomechanical, and light-microscopic analyses were done on the anterior and posterior regions of the rat knee menisci to correlate regional differences in morphology and extracellular matrix composition with regional mechanical behavior. Following the administration of a general anesthetic, menisci were excised from 12 young female Sprague-Dawley rats. During thermodilatometric and thermomechanical testing, tissue temperature was increased at a constant rate of 3.5 degrees C/min from 30 to 100 degrees C. Light microscopy revealed regional differences in cell dens

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50

Chen, Peng, Pengzhou Huang, Yuxiang Ren, Guanwei Jiang, Wentao Zhang, and Xintao Zhang. "Anomalous insertion of the anterior horn of the medial meniscus combined with anterior horn hypertrophy and a synovial cyst: case report and literature review." Journal of International Medical Research 49, no. 2 (2021): 030006052098153. http://dx.doi.org/10.1177/0300060520981538.

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Objective To gain a greater understanding of anomalous insertions of the anterior horn of the medial meniscus through evaluation of a rare case and a review of the existing literature on medial meniscus malformations. Methods This report describes a 26-year-old man with an anomalous insertion of the anterior horn of the medial meniscus combined with symptomatic hypertrophy of the anterior horn and a synovial cyst. We also conducted a review of the existing literature on medial meniscus malformations using five major scholarly literature databases and search engines. Results The literature revi

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