Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 8787  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  » Next article
  » Previous article 
  » Table of Contents
  
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (187 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

 
  In this Article
 »  Abstract
 »  Materials and Me...
 »  Results
 »  Discussion
 »  Conclusion
 »  Acknowledgment
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    Viewed12735    
    Printed245    
    Emailed6    
    PDF Downloaded919    
    Comments [Add]    
    Cited by others 34    

Recommend this journal

 


 
ORIGINAL ARTICLE
Year : 2008  |  Volume : 56  |  Issue : 1  |  Page : 22-26

Imaging features in Hirayama disease


1 Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India

Date of Acceptance24-Oct-2007

Correspondence Address:
Arun K Gupta
Department of Radiology, SCTIMST, Trivandrum - 695 011, Kerala
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.39307

Rights and Permissions

 » Abstract 

Purpose: To evaluate the MR findings in clinically suspected cases of Hirayama disease. Materials and Methods: The pre and post contrast neutral and flexion position cervical MR images of eight patients of clinically suspected Hirayama disease were evaluated for the following findings: localized lower cervical cord atrophy, asymmetric cord flattening, abnormal cervical curvature, loss of attachment between the posterior dural sac and subjacent lamina, anterior shifting of the posterior wall of the cervical dural canal and enhancing epidural component with flow voids. The distribution of the above features in our patient population was noted and correlated with their clinical presentation and electromyography findings. Observations: Although lower cervical cord atrophy was noted in all eight cases of suspected Hirayama disease, the rest of the findings were variably distributed with asymmetric cord flattening, abnormal cervical curvature, anterior shifting of the posterior wall of the cervical dural canal and enhancing epidural component seen in six out of eight (75%) cases. An additional finding of thoracic extension of the enhancing epidural component was also noted in five out of eight cases. Conclusion: Dynamic post contrast MRI evaluation of cervicothoracic spine is an accurate method for the diagnosis of Hirayama disease.


Keywords: Dynamic magnetic resonance imaging, Hirayama disease, monomelic amyotrophy


How to cite this article:
Sonwalkar HA, Shah RS, Khan FK, Gupta AK, Bodhey NK, Vottath S, Purkayastha S. Imaging features in Hirayama disease. Neurol India 2008;56:22-6

How to cite this URL:
Sonwalkar HA, Shah RS, Khan FK, Gupta AK, Bodhey NK, Vottath S, Purkayastha S. Imaging features in Hirayama disease. Neurol India [serial online] 2008 [cited 2019 Aug 17];56:22-6. Available from: http://www.neurologyindia.com/text.asp?2008/56/1/22/39307


Juvenile muscular atrophy of the distal upper limb [Hirayama disease] is a rare disease affecting primarily young men in the second to third decades. [1],[2] Hirayama disease, juvenile muscular atrophy of the distal upper extremity, is also known as monomelic amyotrophy, [3] benign focal amyotroph, [4] juvenile muscular atrophy of a unilateral upper extremity [5] and juvenile asymmetric segmental spinal muscular atrophy. [6] Hirayama disease differs from the known types of motor neuron diseases because of its nonprogressive behavior and pathologic findings of focal ischemic changes in the anterior horn of the lower cervical cord. [2],[7] Various magnetic resonance imaging (MRI) features have been described in the literature for the diagnosis of this entity. The present study summarizes these different MRI findings and evaluates their distribution among the studied patient population.


 » Materials and Methods Top


Eight patients with clinical suspicion of Hirayama disease were evaluated with MR imaging. The pre and post contrast MR imaging was done in neutral and flexion position of cervical spine and imaging findings were correlated with their neurological presentation, disease course and electromyography findings. All the patients evaluated were males between 11-24 years of age with the mean age of 18.5 years. The criteria for patient selection were weakness and wasting predominantly in C7, C8 and T1 myotomes in one upper limb or asymmetrically in both upper limbs, insidious onset in teens or early twenties, initial fast progression for one to three years followed by arrest of disease or relatively benign course, irregular coarse tremors in the fingers of the affected hand[s], mild transient worsening of symptoms on exposure to cold, electromyography evidence of chronic denervation in the clinically or subclinically affected muscles and absence of objective sensory loss. [1] Electrophysiological study included nerve conduction study (NCS) and electromyography (EMG). Motor conduction studies were done in median and ulnar nerves (and radial in few cases) of both upper limbs and peroneal and tibial nerves of one lower limb. Sensory conductions were studied from median, ulnar and sural nerves of corresponding limbs. Needle EMG studies were done in muscles of C7 - T1 myotomes including the cervical paraspinals.

The MR imaging was done on a superconducting 1.5-T system (Signa, GE Medical Systems, Milwaukee, Wisconsin). The neutral-position MR protocol included transverse and sagittal T1-weighted (spin echo, repetition time msec/echo time msec of 500-600/15-20), transverse T2*-weighted (gradient-echo, 400-500/15-20, flip angle of 20°-30°) MR imaging and sagittal T2-weighted MR imaging (fast spin echo, 3000-3500/90-140 [effective]). The flexion MR imaging protocol consisted of sagittal T1-weighted (500-600/15-20) and T2-weighted (4,000/85-99, matrix size of 256 × 256) MR imaging and transverse T2*-weighted MR imaging (400-500/15-20, flip angle of 20°-30°, matrix size of 256 × 192) with approximately 30-40° neck flexion by using an indigenous positioning sponge. Post gadolinium transverse and sagittal T1 weighted images in flexion and extension were obtained in all cases. Section thickness was 4 mm with 1-mm gap for both sagittal and transverse MR imaging with all sequences. Lower cervical cord was defined as the cord between C4 and C7. The following features were evaluated: localized lower cervical cord atrophy, asymmetric cord flattening, abnormal cervical curvature, loss of attachment between the posterior dural sac and subjacent lamina, anterior shifting of the posterior wall of the cervical dural canal and enhancing epidural component with flow voids. An additional feature detected was the thoracic extension of the enhancing epidural component. Localized cord atrophy was defined as a decrease in cord size in comparison with the normal cord above and that below the affected level confirmed on axial images.

Asymmetric cord flattening was evaluated on transverse MR images. To avoid confusion with cord compression due to adjacent spurs or herniated disks, cord flattening was defined as flattening without a narrowed or obliterated adjacent subarachnoid space. An elliptic spinal cord was considered normal, a pear-shaped spinal cord was considered asymmetric cord flattening and a triangular spinal cord was considered symmetric cord flattening. Cervical curvature was classified according to the principles suggested by Guigui et al. [8] and Batzdorf and Batzdorff. [9] Cervical curvature was measured according to the relationship of the dorsal aspect of the vertebral bodies C3 through C6 to a line drawn from the dorsocaudal aspect of the vertebral body C2 to the dorsocaudal aspect of the vertebral body C7. By definition, normal lordotic cervical curvature is curvature in which no part of the dorsal aspect of the vertebral bodies C3 through C6 crosses the line from C2 through C7. An abnormal [straight or kyphotic] curvature is curvature in which part or all of the dorsal aspects of the vertebral bodies C3 through C6 meet or cross through the line from C2 through C7 [Figure - 1]. For evaluating the loss of attachment between the posterior dural sac and subjacent lamina, the lamina was defined as the part of vertebra between junctions of laminae medially and laterally by a tangential line along the medial aspect of the pedicle. This was divided equally into three parts. More than 33.3% loss of attachment between the posterior dural sac and subjacent lamina was considered significant. [10] On flexion studies, anterior displacement of dural sac and appearance of enhancing epidural component posterior to the thecal sac, which disappeared on neutral position, was noted.


 » Results Top


Clinical features

All the patients were male with mean age of 18.5 years (range 11-24) years at the time of clinical examination. The duration of illness at the time of clinical examination and electrophysiology study was three to 12 months in seven patients and 48 months in the eighth (patient no. 4). Major symptoms included hand wasting (8/8), grip weakness (6/8), tremulousness of fingers (4/8). The patient who presented after four years of illness also had forearm wasting, weakness and dysaesthesia. On clinical examination, all the patients had pure motor, asymmetrical, upper limb, lower motor neuron type of involvement [Table - 1]. None of the patients had any neck pain or radicular symptoms.

Electrophysiology

Nerve conduction study and EMG were done in all the patients within a week of the clinical examination. In addition, somatosensory evoked potentials (SSEP) were studied in one patient. Ulnar compound muscle action potential (CMAP) was reduced in six patients while median and radial in one each. Distal latencies and F-wave latencies were variably affected. Conduction velocities were normal in all nerves. Sensory conduction study was absolutely normal in all the patients. Median SSEP done in one patient was normal. All the eight patients showed denervation changes (fibrillations, positive sharp waves, large amplitude potentials but no polyphasics or fasciculations) mainly in C8-T1 muscles. Cervical paraspinal EMG was done in six patients and all were normal [Table - 2].

Imaging findings [Table - 3]

All eight cases of suspected Hirayama disease showed lower cervical cord atrophy with asymmetry noted in six of eight cases [Figure - 2]. These six cases were also showing other findings like abnormal cervical curvature, anterior shifting of the posterior wall of the cervical dural canal and enhancing epidural component. The thickness of the enhancing epidural component was, however, variable ranging from 1.5 to 6 mm. No relation was found between the duration of illness and thickness of the epidural component. An additional finding of thoracic extension of the enhancing epidural component was also noted in five cases. Abnormally prominent posterior epidural flow voids were noted in four cases. Loss of attachment between the posterior dural sac and subjacent lamina was noted in four of these cases [Figure - 3].

Follow-up

Follow-up was available in six patients. One patient (patient no. 5) was initially evaluated in June 1996 when clinical and electrophysiology features were suggestive of Hirayama's disease but MRI (no dynamic study done) was negative. Repeat examination after eight years (September 2004) showed mild progression (increased wasting and reflex loss). Repeat MRI done was suggestive of Hirayama's disease in the dynamic study. The other five patients had last follow-up after four to 11 months of presentation (four using cervical collar, including patient no.3 whose MRI is negative). All the five had static course clinically.


 » Discussion Top


The pathogenesis of this entity is debated. An assumption of imbalanced growth between the patient's vertebral column and spinal canal contents has been suggested. [6],[11],[12] This imbalanced growth will cause disproportional length between the patient's vertebral column and the spinal canal contents causing a tight dural sac and anterior displacement of posterior dural wall when the neck is flexed. The different growth rates between male and female patients have been proposed to be the factor related to the male preponderance of Hirayama disease by Toma et al. [13] The incidence of atopic disorders and levels of serum IgE and mite antigen-specific IgE were also found to be higher in patients with Hirayama disease than in the general population suggesting that atopy may be a contributing factor for Hirayama disease. [14]

In a normal spine, the spinal dura mater is a loose sheath that is anchored in the vertebral canal by the nerve roots and by its attachment to the periosteum in two places: one at the foramen magnum and the dorsal surfaces of C2 and C3 and the other at the coccyx. Normally, the slack of the dura mater can compensate for the increased length in flexion. In patients with Hirayama disease, however, the tight dural sac can result in separation of the posterior dural sac from its subjacent lamina and various degrees of abnormal cervical curvature (straight or kyphotic). On neck flexion, the tight dural sac cannot compensate for the increased length of the posterior wall, which causes anterior shifting of the posterior dural wall and consequent compression of the cord against the posterior margin of adjacent vertebral bodies. This compression may cause microcirculatory disturbances in the territory of the anterior spinal artery in the lower cervical spinal cord. [1],[7] The chronic circulatory disturbance resulting from repeated or sustained flexion of the neck may produce gliosis and localized cord atrophy at the lower cervical region. [15] Different pathophysiological mechanisms have been proposed for the venous engorgement seen on flexion studies. Firstly, the negative pressure in the posterior spinal canal resulting from anterior shifting of the dural canal is thought to increase the flow to the posterior internal vertebral venous plexus causing their prominence. Second, the posture of neck flexion decreases the venous drainage of the jugular veins, impeding the venous return of internal vertebral venous plexus causing their prominence and engorgement. [16] Finally, the compressed anterior internal vertebral venous plexus caused by anterior displacement of the dural canal increases the burden of the posterior internal vertebral venous plexus leading to its distension. [17] The extensions of posterior epidural enhancement in the thoracic region found in our cases suggest that jugular vein compression, as a cause of prominence of the epidural venous plexus is less likely.

The various MR imaging features described in Hirayama disease are as follows: localized lower cervical cord atrophy, asymmetric cord flattening, parenchymal signal changes in lower cervical cord, abnormal cervical curvature, loss of attachment between the posterior dural sac and subjacent lamina, anterior shifting of the posterior wall of the cervical dural canal, enhancing epidural component in lower cervical and thoracic region and prominent posterior epidural flow voids suggestive of dilated epidural venous plexus. The findings reported more frequently are asymmetrical/symmetrical atrophy of lower cervical cord, prominence and enhancement of posterior epidural venous plexus on flexion studies and anterior shifting of posterior dural sac on flexion. Loss of attachment between the posterior dural sac and subjacent lamina on neutral position, anterior shifting of the posterior wall of the cervical dural canal, enhancing epidural component in the lower cervical and thoracic region and prominent posterior epidural flow voids suggestive of dilated epidural venous plexus on flexion studies are reported as highly suggestive for the diagnosis of Hirayama disease. [1],[6],[10],[12],[15],[17]

Early diagnosis and therapeutic intervention in the form of cervical collar therapy to prevent neck flexion may minimize the functional disability of the young patients. This induces a premature arrest of disease progression and is more beneficial in those cases with shorter duration of illness. Since the progressive stage is expected to cease in a few years, application of a cervical collar for three to four years generally has been advocated. [18] In selected patients, encouraging results have also been obtained with surgical intervention, which involves mainly cervical decompression and/or fusion with or without duraplasty. [19]


 » Conclusion Top


Dynamic post contrast MRI evaluation of cervicothoracic spine is a helpful method in arriving at the correct diagnosis of Hirayama disease and should be an essential part of the protocol in cases with high suspicion of motor neuron disease.


 » Acknowledgment Top


Authors wish to thank the Director, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India for providing the facilities and for the kind permission to present this report.

 
 » References Top

1.Hirayama K. Non-progressive juvenile spinal muscular atrophy of the distal upper limb [Hirayama's disease]. In: De Jong JM, Handbook of clinical neurology. Vol 15. Elsevier: Amsterdam, the Netherlands; 1991. p. 107-20.  Back to cited text no. 1    
2.Hirayama K, Toyokura Y, Tsubaki T. Juvenile muscular atrophy of unilateral upper extremity: A new clinical entity. Psychiatr Neurol Jpn 1959;61:2190-7.  Back to cited text no. 2    
3.Gourie Devi M, Suresh TG, Shankar SK. Monomelic amyotrophy. Arch Neurol 1984;41:388-94.  Back to cited text no. 3    
4.Biondi A, Dormont D, Weitzner I Jr, Bouche P, Chaine P, Bories J. MR imaging of the cervical cord in juvenile amyotrophy of distal upper extremity. AJNR Am J Neuroradiol 1989;10:263-8.  Back to cited text no. 4  [PUBMED]  
5.Kohno M, Takahashi H, Yagishita A, Tanabe H. "Disproportion theory" of the cervical spine and spinal cord in patients with juvenile cervical flexion myelopathy: A study comparing cervical magnetic resonance images with those of normal controls. Surg Neurol 1998;50:421-30.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Pradhan S, Gupta RK. Magnetic resonance imaging in juvenile asymmetric segmental spinal muscular atrophy. J Neurol Sci 1997;146:133-8.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Hirayama K, Tomonaga M, Kitano K, Yamada T, Kojima S, Arai K. Focal cervical poliopathy causing juvenile muscular atrophy of distal upper extremity: A pathological study. J Neurol Neurosurg Psychiatry 1987;50:285-90.  Back to cited text no. 7  [PUBMED]  
8.Guigui P, Benoist M, Deburge A. Spinal deformity and instability after multilevel cervical laminectomy for spondylotic myelopathy. Spine 1998;23:440-7.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Batzdorf U, Batzdorff A. Analysis of cervical spine curvature in patients with cervical spondylosis. Neurosurgery 1988;22:827-36.  Back to cited text no. 9  [PUBMED]  
10.Chi-Jen Chen, Hui-Ling Hsu, Ying-Chi Tseng, Rong-Kuo Lyu, Chiung-Mei Chen, Ying-Chih Huang, et al. Hirayama flexion myelopathy: Neutral-position MR imaging findings-importance of loss of attachment. Radiology 2004;231:39-44.  Back to cited text no. 10    
11.Kikuchi S, Tashiro K, Kitagawa K, Iwasaki Y, Abe H. A mechanism of juvenile muscular atrophy localized in the hand and forearm (Hirayama's disease): Flexion myelopathy with tight dural canal in flexion. Rinsho Shinkeigaku 1987;27:412-9.  Back to cited text no. 11    
12.Mukai E, Sobue I, Muto T, Takahashi A, Goto S. Abnormal radiological findings on juvenile-type distal and segmental muscular atrophy of upper extremities. Rinsho Shinkeigaku 1985;25:620-6.  Back to cited text no. 12  [PUBMED]  
13.Toma S, Shiozawa Z. Amyotrophic cervical myelopathy in adolescence. J Neurol Neurosurg Psychiatry 1995;58:56-64.  Back to cited text no. 13  [PUBMED]  
14.Kira J, Ochi H. Juvenile muscular atrophy of the distal upper limb (Hirayama disease) associated with atopy. J Neurol Neurosurg Psychiatry 2001;70:798-801.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Schroder R, Keller E, Flacke S, Schmidt S, Pohl C, Klockgether T, et al. MRI findings in Hirayama's disease: Flexion-induced cervical myelopathy or intrinsic motor neuron disease? J Neurol 1999;246:1069-74.  Back to cited text no. 15    
16.Mukai E, Matsuo T, Muto T, Takahashi A, Sobue I. Magnetic resonance imaging of juvenile-type distal and segmental muscular atrophy of upper extremities. Clin Neurol (Tokyo) 1987:27:99-107.  Back to cited text no. 16    
17.Chi-Jen Chen, Chiung-Mei Chen, Chia-Lun Wu, Long-Sun Ro, Sien-Tsong Chen, Tsong-Hai Lee. Hirayama disease: MR diagnosis. AJNR Am J Neuroradiol 1998;19:365-8.  Back to cited text no. 17    
18.Tokumaru Y, Hirayama K. Cervical collar therapy for juvenile muscular atrophy of distal upper extremity [Hirayama disease]: Results from 38 cases. Rinsho Shinkeigaku 2001;41:173-8.  Back to cited text no. 18  [PUBMED]  
19.Kohno M, Takahashi H, Ide K, Yamakawa K, Saitoh T, Inoue K. Surgical treatment for patients with cervical flexion myelopathy. J Neurosurg 1999;91:33-42.  Back to cited text no. 19  [PUBMED]  


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3]

This article has been cited by
1 Hirayama disease: Study of clinical, electrophysiological & radiological characteristics at tertiary care centre from north-west India
Maulik Panchal,Chandramohan Sharma,Anjani kumar Sharma
Indian Journal of Medical Specialities. 2018; 9(1): 20
[Pubmed] | [DOI]
2 Benign focal amyotrophy
P. Cintas
Revue Neurologique. 2017; 173(5): 338
[Pubmed] | [DOI]
3 Progressive myoclonic tremor mimicking functional tremor in Hirayama disease
Do-Young Kwon,Jinhee Kim,HoKyong Yoon,Moon Ho Park
Acta Neurologica Belgica. 2017;
[Pubmed] | [DOI]
4 Correlations of clinical, neuroimaging, and electrophysiological features in Hirayama disease
Ming-Feng Liao,Hong-Shiu Chang,Kuo-Hsuan Chang,Long-Sun Ro,Chun-Che Chu,Hung-Chou Kuo,Rong-Kuo Lyu
Medicine. 2016; 95(28): e4210
[Pubmed] | [DOI]
5 Hirayama Disease: A Rare Disease with Unusual Features
S. Anuradha,Vanlalmalsawmdawngliana Fanai
Case Reports in Neurological Medicine. 2016; 2016: 1
[Pubmed] | [DOI]
6 The Abnormalities in Neuro-Imaging and Somatosensory Evoked Potentials in Hirayama Disease
Jin-Sung Park,Sang-Hoon Lee
Korean Journal of Clinical Neurophysiology. 2015; 17(1): 38
[Pubmed] | [DOI]
7 Monomelic amyotrophy: Clinical profile and natural history of 279 cases seen over 35 years (1976–2010)
Atchayaram Nalini,Mandavilli Gourie-Devi,Kandavel Thennarasu,Aravinda Hanumanthapura Ramalingaiah
Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration. 2014; : 1
[Pubmed] | [DOI]
8 Electrophysiological differences between Hirayama disease, amyotrophic lateral sclerosis and cervical spondylotic amyotrophy
Xiang Jin,Jian-Yuan Jiang,Fei-Zhou Lu,Xin-Lei Xia,Li-Xun Wang,Chao-Jun Zheng
BMC Musculoskeletal Disorders. 2014; 15(1): 349
[Pubmed] | [DOI]
9 Hirayama Disease in Children From Mainland of China
Guang Yang,Xiaosu Yang,Ming Zhang,Yi Yang,Bo Xiao,Guoliang Li,De Yang,Xiaoyi Wang
Journal of Child Neurology. 2014; 29(4): 509
[Pubmed] | [DOI]
10 Nosology of Juvenile Muscular Atrophy of Distal Upper Extremity: From Monomelic Amyotrophy to Hirayama Disease—Indian Perspective
Kaukab Maqbool Hassan,Hirdesh Sahni
BioMed Research International. 2013; 2013: 1
[Pubmed] | [DOI]
11 “Sand-watch” spinal cord: a case of inferior cervical spinal cord atrophy
Peter Bede,Ronan Walsh,Andrew J. Fagan,Orla Hardiman
Journal of Neurology. 2013;
[Pubmed] | [DOI]
12 Hirayama disease in unilateral and bilateral forms-3 case reports
Shruti Thakur,R.G. Sood,Anupam Jhobta,Dinesh Sharma,Sushma Makhaik,Neeti Aggarwal,Charu S. Thakur
The Egyptian Journal of Radiology and Nuclear Medicine. 2013; 44(2): 291
[Pubmed] | [DOI]
13 Efficacy of anterior cervical decompression and fusion procedures for monomelic amyotrophy treatment: a prospective randomized controlled trial
Feizhou Lu,Hongli Wang,Jianyuan Jiang,Wenjun Chen,Xin Ma,Xiaosheng Ma,Xinlei Xia,Lixun Wang
Journal of Neurosurgery: Spine. 2013; 19(4): 412
[Pubmed] | [DOI]
14 Hirayama disease is a pure spinal motor neuron disorder—a combined DTI and transcranial magnetic stimulation study
Kai Boelmans,Jörn Kaufmann,Sophie Schmelzer,Stefan Vielhaber,Malte Kornhuber,Alexander Münchau,Stephan Zierz,Charly Gaul
Journal of Neurology. 2013; 260(2): 540
[Pubmed] | [DOI]
15 Hirayama disease in unilateral and bilateral forms-3 case reports
Thakur, S. and Sood, R.G. and Jhobta, A. and Sharma, D. and Makhaik, S. and Aggarwal, N. and Thakur, C.S.
Egyptian Journal of Radiology and Nuclear Medicine. 2013; 44(2): 291-295
[Pubmed]
16 Hirayama disease is a pure spinal motor neuron disorder - A combined DTI and transcranial magnetic stimulation study
Boelmans, K. and Kaufmann, J. and Schmelzer, S. and Vielhaber, S. and Kornhuber, M. and Münchau, A. and Zierz, S. and Gaul, C.
Journal of Neurology. 2013; 260(2): 540-548
[Pubmed]
17 Authorsæ Reply in response to the correspondence about the article "hirayama disease in children from North America" Published in journal of child neurology Dec 2011 issue
Ghosh, P.S. and Moodley, M. and Friedman, N.R. and Rothner, A.D. and Ghosh, D.
Journal of Child Neurology. 2012; 27(6): 817-818
[Pubmed]
18 Clinical and radiological profile of Hirayama disease: A flexion myelopathy due to tight cervical dural canal amenable to collar therapy
Hassan, K.M. and Sahni, H. and Jha, A.
Annals of Indian Academy of Neurology. 2012; 15(2): 106-112
[Pubmed]
19 How does the neck flexion affect the cervical MRI features of Hirayama disease?
Chao Hou, Hongbin Han, Xiaohong Yang, Xiaojuan Xu, Hui Gao, Dongsheng Fan, Yu Fu, Yu Sun, Bo Liu
Neurological Sciences. 2012;
[VIEW] | [DOI]
20 Authors’ Reply in Response to the Correspondence About the Article “Hirayama Disease in Children From North America” Published in Journal of Child Neurology Dec 2011 Issue
Partha S. Ghosh,Manikum Moodley,Neil R. Friedman,A. David Rothner,Debabrata Ghosh
Journal of Child Neurology. 2012; 27(6): 817
[Pubmed] | [DOI]
21 Hirayama Disease in Children From North America
Partha S. Ghosh,Manikum Moodley,Neil R. Friedman,A. David Rothner,Debabrata Ghosh
Journal of Child Neurology. 2011; 26(12): 1542
[Pubmed] | [DOI]
22 Waterskier’s Hirayama syndrome
Arun L. W. Bokde, Peter Bede, Susan C. Byrne, Marwa Elamin, Ronan J. Walsh, Orla Hardiman
Journal of Neurology. 2011;
[VIEW] | [DOI]
23 Hirayama disease in children from North America
Ghosh, P.S. and Moodley, M. and Friedman, N.R. and Rothner, A.D. and Ghosh, D.
Journal of Child Neurology. 2011; 26(12): 1542-1547
[Pubmed]
24 Waterskieræs Hirayama syndrome
Bede, P. and Bokde, A.L.W. and Byrne, S.C. and Elamin, M. and Walsh, R.J. and Hardiman, O.
Journal of Neurology. 2011; 258(11): 2078-2079
[Pubmed]
25 Teaching neuroImages: Anterior horn cell hyperintensity in Hirayama disease
Desai, J.A. and Melanson, M.
Neurology. 2011; 77(12)
[Pubmed]
26 Role of dynamic MRI study in Hirayama disease
Parihar, A. and Khurana, N. and Aga, P. and Singh, R. and Garg, R.K.
Annals of Indian Academy of Neurology. 2011; 14(2): 138-139
[Pubmed]
27 Angiographically proven cervical venous engorgement: A possible concurrent cause in the pathophysiology of Hirayamaæs myelopathy
Ciceri, E.F. and Chiapparini, L. and Erbetta, A. and Longhi, L. and Cicardi, B. and Milani, N. and Solero, C.L. and Savoiardo, M.
Neurological Sciences. 2010; 31(6): 845-848
[Pubmed]
28 MRI features of Hirayama disease at different cervical flexion angles
Gao, H. and Han, H.-B. and Xu, X.-J. and Hou, C. and He, Q.-Y. and Fan, D.-S. and Fu, Y. and Sun, Y.
Chinese Journal of Radiology. 2010; 44(6): 653-656
[Pubmed]
29 Forward shifting of posterior dural sac during flexion cervical magnetic resonance imaging in Hirayama disease: An initial study on normal subjects compared to patients with Hirayama disease
Vincent Lai, Yiu Chung Wong, Wai Lun Poon, Ming Keung Yuen, Yat Pang Fu, Oi Wah Wong
European Journal of Radiology. 2010;
[VIEW] | [DOI]
30 Pediatric Hirayama Disease
Hosokawa, T., Fujieda, M., Wakiguchi, H., Oosaki, Y.
Pediatric Neurology. 2010; 43(2): 151-153
[Pubmed]
31 MRI findings in Hirayama disease
Raval, M., Kumari, R., Dung Dung, A., Guglani, B., Gupta, N., Gupta, R.
Indian Journal of Radiology and Imaging. 2010; 20(4): 245-249
[Pubmed]
32 Pediatric Hirayama Disease
Takatoshi Hosokawa,Mikiya Fujieda,Hiroshi Wakiguchi,Yasushi Oosaki
Pediatric Neurology. 2010; 43(2): 151
[Pubmed] | [DOI]
33 Angiographically proven cervical venous engorgement: a possible concurrent cause in the pathophysiology of Hirayama’s myelopathy
Elisa F. Ciceri,Luisa Chiapparini,Alessandra Erbetta,Laura Longhi,Benedetta Cicardi,Nicoletta Milani,Carlo Lazzaro Solero,Mario Savoiardo
Neurological Sciences. 2010; 31(6): 845
[Pubmed] | [DOI]
34 Bilaterally symmetric form of Hirayama disease
Pradhan, S.
Neurology. 2009; 72(24): 2083-2089
[Pubmed]



 

Top
Print this article  Email this article
Previous article Next article
Online since 20th March '04
Published by Wolters Kluwer - Medknow