Whole body magnetic resonance imaging in the diagnosis of Parsonage Turner syndrome

Purpose: To describe magnetic resonance imaging (MRI) findings in patients with suspected Parsonage Turner syndrome and to emphasize the value of an additional whole body MR scan to improve specificity of this diagnosis.

Material and Methods: Three patients with proven Parsonage Turner syndrome referred for conventional MRI of the shoulder girdle and additional whole body turboSTIR MRI were included for study.

Results: In each case, imaging revealed edema in the muscles of the shoulder girdle. Whole body turboSTIR MRI scan confirmed localized unilateral changes in each case improving specificity and confidence in the diagnosis of Parsonage Turner syndrome in each case.

Conclusion: Whole body turboSTIR MR imaging is a useful diagnostic tool in the evaluation of patients with suspected Parsonage Turner syndrome. Inclusion of the brain, neck, brachial plexus, and extremity musculature at whole body imaging allows differentiation from polymyositis and elimination of additional causes of shoulder girdle pain and weakness including gross lesions in the brain, neck, and brachial plexus by a single non-invasive study.     

Rapid, painless unilateral vision loss in a 37-year-old healthy woman

A 37-year-old woman experienced painless, progressive vision loss to no light perception in the left eye over the course of 3 days. The right eye was unaffected. On examination, the only other abnormal finding was a +4 left afferent pupillary defect. She was initially diagnosed with retrobulbar optic neuritis and admitted for treatment with intravenous methylprednisolone. Neuro-imaging revealed a large right anterior cerebral artery aneurysm that crossed the midline to compress the left optic nerve. The aneurysm was treated with coil embolization, which was technically successful but which did not lead to significant improvement in vision.     

Transfer of myelin-specific cells deviated in vitro towards IL-4 production ameliorates ongoing experimental allergic neuritis

A causal role of IL-4 (Th2) production for recovery in experimental allergic neuritis (EAN) was indicated by experiments where Th1-like autoreactive cell populations, taken from the induction phase of the disease, were deviated to extensive secretion of IL-4 in a selective fashion, by ex vivo stimulation with autoantigen in the presence of IL-4. The deviated cells were adoptively transferred to EAN rats at a time just prior to the onset of clinical signs. This treatment ameliorated EAN compared with sham treatment. This therapeutic approach, with generation of autoreactive IL-4-secreting cells ex vivo followed by subsequent adoptive transfer, may become a new selective treatment of organ-specific autoimmune diseases since, in contrast to previous attempts, it is done in a physiological and technically easy way.     

Inflammation and proinflammatory cytokine production,but no demyelination of facial nerves,in experimental autoimmune neuritis in Lewis rats

Experimental autoimmune neuritis (EAN) is a CD4⁺ T cell-mediated, inflammatory demyelinating disease of the peripheral nervous system (PNS) that serves as a model for Guillain–Barré syndrome (GBS) in humans. The facial nerve paralysis is relatively commonly found in GBS patients. Here, EAN was established in Lewis rats by immunization with P2 peptide 57–81, a purified component of peripheral nerve myelin, and Freund's complete adjuvant (FCA). To study whether the facial nerves are involved in the pathogenic process during the EAN course, we observed the clinical and pathological changes as well as cytokine production in facial nerves on Day 14 postimmunization (p.i.), i.e. at height of clinical EAN. As a result, all rats immunized with P2 peptide 57–81 developed severe EAN on Day 14 p.i., but none of the rats manifested clinical signs of facial nerve paralysis. Additionally, only mild inflammatory cell infiltration and proinflammatory cytokine, interferon-γ (IFN-γ) and tumour necrosis factor (TNF-) production as well as devoid demyelination were seen in facial nerves of the EAN rats. On the contrary, severe inflammation and demyelination as well as upregulated IFN-γ and TNF- production were observed in sciatic nerves of the same EAN rats. The underlying mechanism for the difference of the local manifestation of the disease process of EAN remains to be resolved.     

Asymptomatic visual loss in multiple sclerosis

Visual disturbances are common in multiple sclerosis (MS) and often a result of acute demyelinating optic neuropathy. Careful examination of MS patients, who have never suffered optic neuritis, may also reveal asymptomatic visual loss. This type of silent disease activity was investigated by computerised resolution perimetry, which has the potential to reflect the percentage of functional retino-cortical neural channels. The time of onset and the evolution of asymptomatic visual loss was investigated. One approach was to retrospectively select patients who never had suffered acute optic neuritis from a closely monitored MS population and re-examine them again. Sixteen patients were identified and vision was evaluated during a period of 5.5–9 years of follow-up and compared with that in 14 healthy controls. The mean channel percentage of the MS group was 89 ± 19 % (SD) on entry into the study, compared with 110 ± 15 % (SD) of controls (p < 0.003). At termination of the study the mean percentage was essentially unchanged both in MS patients (87 ± 21 %, SD) and controls (110 ± 19 %, SD). The second approach was to test a group of 7 patients with MS or strongly suspected MS, with the same method, in close connection with their first clinical exacerbation. All cases lacked visual symptoms and none had previously had acute visual loss. Again, virtually all performed subnormally in the vision tests, and to the same degree as in the first group of patients. Results were compared with those obtained from 25 MS patients who had experienced one or more attacks of optic neuritis. Compared with controls the loss of functional retino-cortical neural channels was 20 % in patients without a previous history of optic neuritis and 30 % in patients who previously had experienced optic neuritis. We conclude that asymptomatic visual loss seems to be a universal feature of MS and has a substantial impact on the visual pathways, that it is present already at the time of clinical onset of the disease, and that any progression thereafter is slow enough to elude detection during several years of follow-up. Received: 28 June 2000, Received in revised form: 7 March 2001, Accepted: 23 April 2001     

特发性(脱髓鞘性)视神经炎的流行病学、诊断及治疗的展望

特发性视神经炎是一种神经眼科的常见疾病,严重威胁视力。目前其病因不明,治疗上方法众多,疗效不一。本文回顾近年来特发性视神经炎的流行病学、病因及治疗进展,为进一步阐明该疾病的发病规律、寻找病因、明确诊断、探索有效治疗方案提供有益的线索。     

视神经炎发展为多发性硬化的危险因素分析

目的:分析视神经炎发展为多发性硬化(multiple sclerosis,MS)的危险因素。方法:对比分析6例发展为MS的视神经炎患者和其余45例视神经炎患者的临床资料,寻找视神经炎发展为多发硬化的危险因素。结果:发展为MS的视神经炎复发率比其他视神经炎高(P<0.01),眼球周围疼痛较其他视神经炎多见,但无统计学意义(P=0.18)。性别、年龄、单侧或双侧发病、视力下降程度、视盘水肿等方面均未见明显差异。血沉高于正常的视神经炎患者较血沉正常的患者更不易发展为MS(P<0.05)。结论:对于复发的、存在眼球周围疼痛的视神经炎患者要重点关注其发展为MS的可能。视神经炎患者应常规行血沉检查。最好以头颅MRI检查替代头颅CT检查,条件允许时检查脊髓MRI。     

Radiology of the orbital apex

The orbital apex, formed by the superior orbital fissure and optic canal, is the cross-road between the orbit and the intracranial structures. Pathological processes may extend intracranially via the superior orbital fissure and vice versa. In addition to intrinsic soft tissue lesions, various pathological processes may involve the surrounding osseous anatomy. Malignant lesions arising from adjacent structures or from haematogeneous metastasis may also infiltrate this region.     

猴失神经手指神经植入后感觉终器的溃变与再生

目的：观察猴失神经手指感觉神经植入后感觉终器溃变与再生情况。方法：用猴手失神经模型,神经植入后在第１,３,５,８,１２ｍｏ分别取材进行电镜观察。结果：游离神经末梢其再生过程是;神经植入３ｏｍ真皮层出现新生的神经轴突,５ｍｏ时有髓和无髓纤维的数量明显增加,髓鞘增厚结构更加清晰８ｍｏ～１２ｍｏ再生轴突;成这正常水平,Ｍｅｒｋｅｌ细胞（１）感觉神经的植入能骺细胞溃变的发生。９２）感觉神经的植入ｅｒｋｅｌ