Demyelinating Lesion at C1

    
      Re: Demyelinating Lesion at C1
    


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Posted by CCF Neuro MD on June 21, 1997 at 18:40:41:

In Reply to: Demyelinating Lesion at C1 posted by Sandra L Rowe on June 14, 1997 at 15:12:40:

: On Feb.15TH my husband fell about 3 feet from at ladder, and landed on all
  fours.(hands and feet eg. as a baby would crawl.) He was a bit stunned but
  other than that he felt fine. A couple of days latter he noticed numbest and
  tinging in his left hand. Because this sensation was progressive an MRI
  was ordered. The reported results by the Neuro Radiologists(3 had reviewed
  the filmes) were probable tumor. Our Neurologist felt with clinical
  correlation, the lesion was a traumic demyelination as a result of the fall.
  He felt the best cousre of action was to just wait and see how my husband
  did over the next few weeks. During the next week the numbness and tinging
  became progressively sever in his left arm chest and face, he lost some
  fine motor coordination, and his right hand was becoming numb. At this
  point a cerebral MRI was ordered, to look at the possibility of MS. The
  spinal cord and brain showed no other lesions. A repeat MRI was done 12 weeks
  post the fall. This reported the lesion was twice as long and dense,
  (14cm by 5cm)non enhancing (the frist MRI was enhancing)All three neuro radiologist
  reporting probable tumor. We were sent to see the neurosurgeon the following day.
  Because of the location he felt we should wait another 8 weeks and repeat
  the MRI. That a BX. was not an option. That the lesion was not from trauma,
  but a probable primary demyelination lesion, and in the mean time he wanted and LP ordered.
  LP results were as followes:elevated IGG and positive for banding proteins negative
  for malignant cells and myelin material. My husband has since lost the feeling
  in both his legs, and has become a bit clumsy, is unable to touch his nose
  with his eyes closed, has had two hypertensive crisis episode (180/130-120)
  requiring SL Procardia 10mg given in the ER to bring his pressure down to normal
  (120/168). He also developed, what I belive is refered to barber chair
  syndrome, when he tilts his chin toward his chest his back feels like it is
  vibrating. The next scheduled MRI is 7/2/97, in the mean time could point me
  in the right direction to learn more about demyelination diseases. I have
  found very little information on this subject, except for MS.  My husband is 46 year old
  and was in excellent health up until this time. I have my Masters in nursing
  and physiology so I will be able to understand any of the articals you point me in the
  direction of. Please any thoughts, or opinions would be greatly appreciated.
  Sincerely Sandra L Rowe E-Mail ***@**** Phone [phone].  
  
      
    
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Mrs. Rowe:
Your husband's problem is perplexing. A lack of consensus regarding the nature of a spinal cord lesion seen on MRI, along with difficulty correlating it with the history is an uncommon but not rare problem. Overall, the weight of evidence (specially the elevated IgG and oligoclonal bands in CSF, and the absence of Gad enhancement on the follow-up scan) seems to somewhat favor demyelination over an intrinsic cord tumor, although the latter can not be ruled out. I agree completely with the plan of management outlined by your doctors.
Under the term "demyelination" are included a variety of lesser-known conditions other than MS. Post-infectious demyelination, also called acute dissemiated encephalomyelitis (ADEM) or monophasic demyelination, differs from MS in tending to have a one-time "hit" at any single or multiple regions of the CNS white matter (Bradley et al, Neurology in Clinical Practice, 1996, Butterworth-Heinemann; Vinken, Bruyn and Klawans, Handbook of Clinical Neurology, Vol 47, Demyelinating Diseases, Elsevier, 1985). It often occurs after infection or vaccination, and may present as a transverse myelopathy (spinal cord lesion). Devic's disease is another, characterised by a progressive severe myelopathy along with optic nerve affection, but sparing other regions of white matter (Mandler et al, Ann Neurol 34: 162-8, 1993; O'Riordan et al, J Neurol Neurosurg Psych 60: 382-7, 1996). All these disorders are characterized by a somewhat similar pathology and pathogenesis in that inflammation, through a variety of cells and chemical mediators, induces local damage to CNS white matter leading to loss of myelin (insulation). There is some evidence to suggest that minor trauma may disrupt the blood-brain barrier and initiate the inflammatory process in a susceptible individual.
The only suggestions that I have are 1. Evaluation for a systemic disease such as vasculitis, which can mimic demyelination, and in addition can cause hypertension, 2. Checking visual evoked responses to look for evidence of optic nerve affection, and 3.  Considering empirical treatment with corticosteroids. Likely, yourdoctors have already considered these.
This information is provided for general medical educational purposes only. Please consult your physician for diagnostic and treatment options of your specific medical condition.