Multiple sclerosis
<p>From: <a href="http://austinpublishinggroup.com/physical-medicine/fulltext/pmr-v2-id1052.php">Progressive Myalgic Encephalomyelitis (ME) or A New Disease? A Case Report</a> </p>
<p>Of particular interest are the MS-like symptoms. This aspect of ME has been largely overlooked despite the work of the renowned MS specialist Charles Poser [11]. In one article, he compared and contrasted the two disorders and noted that individuals with MS are more likely to demonstrate signs of disease such as nystagmus, cerebellar incoordination, ataxia, spasticity, hyperreflexia, abnormal plantar responses and sensory disturbances, principally of vibration and position senses. He emphasized that like MS; ‘chronic post viral fatigue syndrome’ is associated with post-exertional worsening, paresthesiae and dizziness. However, in his view, the parasthesiae tend to be of a different type: in the latter, they often have a burning, painful component and a migratory characteristic. "Such sensory complaints are unusual in MS." Moreover, any lesions found on MRI are periventricular in location, rather than the cortex. Also of significance is that individuals with postviral syndrome rarely have specific complaints such as diplopia, incoordination and true gait ataxia, nor do they exhibit abnormalities such as nystagmus, sustained clonus or Babinski signs.</p>
<p>According to Poser, the similarities between the two disorders have undoubtedly resulted in misdiagnosis as well as inappropriate treatment. Indeed, he estimated that in his practice, 22% of 366 referrals with presumed MS actually fulfilled the criteria for, and probably had CFS [12].</p>
<p>Although there is growing interest in the structure and function of the brain in patients with CFS, the findings on MRI have been equivocal and difficult to interpret. One reason is the changing concept of the illness, which began as a post-infectious syndrome and is now hard to differentiate from neurasthenia [13]. In one of the older studies, Schwartz et al. evaluated 16 individuals with strictlydefined CFS and found abnormalities in 8 [14]. They reported that the most frequent abnormal findings were small foci of increased T2 signal in white matter involving the centrum semiovale, the corona radiata, the internal capsule, the periventricular region or the sub cortical white matter (U fibres). The cortex was of normal signal intensity in all cases. However, other studies have reported different results [15-18]. As a review concluded, perhaps the most consistent findings in CFS are a decline in grey matter volume and enlargement of the ventricular volume [18].</p>
<p>The lack of knowledge relating to progressive ME means that our understanding of this condition is extremely limited. Without studying this subgroup, it is possible that the findings from the research on CFS or ME/CFS may not applicable to these patients and that certain interventions could have significant adverse effects. It is also important to consider whether the history described above represents a progression of ME or a novel disease, resembling both ME and MS.</p>
<p>Of particular interest are the MS-like symptoms. This aspect of ME has been largely overlooked despite the work of the renowned MS specialist Charles Poser [11]. In one article, he compared and contrasted the two disorders and noted that individuals with MS are more likely to demonstrate signs of disease such as nystagmus, cerebellar incoordination, ataxia, spasticity, hyperreflexia, abnormal plantar responses and sensory disturbances, principally of vibration and position senses. He emphasized that like MS; ‘chronic post viral fatigue syndrome’ is associated with post-exertional worsening, paresthesiae and dizziness. However, in his view, the parasthesiae tend to be of a different type: in the latter, they often have a burning, painful component and a migratory characteristic. "Such sensory complaints are unusual in MS." Moreover, any lesions found on MRI are periventricular in location, rather than the cortex. Also of significance is that individuals with postviral syndrome rarely have specific complaints such as diplopia, incoordination and true gait ataxia, nor do they exhibit abnormalities such as nystagmus, sustained clonus or Babinski signs.</p>
<p>According to Poser, the similarities between the two disorders have undoubtedly resulted in misdiagnosis as well as inappropriate treatment. Indeed, he estimated that in his practice, 22% of 366 referrals with presumed MS actually fulfilled the criteria for, and probably had CFS [12].</p>
<p>Although there is growing interest in the structure and function of the brain in patients with CFS, the findings on MRI have been equivocal and difficult to interpret. One reason is the changing concept of the illness, which began as a post-infectious syndrome and is now hard to differentiate from neurasthenia [13]. In one of the older studies, Schwartz et al. evaluated 16 individuals with strictlydefined CFS and found abnormalities in 8 [14]. They reported that the most frequent abnormal findings were small foci of increased T2 signal in white matter involving the centrum semiovale, the corona radiata, the internal capsule, the periventricular region or the sub cortical white matter (U fibres). The cortex was of normal signal intensity in all cases. However, other studies have reported different results [15-18]. As a review concluded, perhaps the most consistent findings in CFS are a decline in grey matter volume and enlargement of the ventricular volume [18].</p>
<p>The lack of knowledge relating to progressive ME means that our understanding of this condition is extremely limited. Without studying this subgroup, it is possible that the findings from the research on CFS or ME/CFS may not applicable to these patients and that certain interventions could have significant adverse effects. It is also important to consider whether the history described above represents a progression of ME or a novel disease, resembling both ME and MS.</p>