PubMed · 14777539
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F TOBEL. 1950. [Encephalitis as a compressive process].. https://doi.org/10.1007/bf00574916
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The pathogenesis and development of lesions in multiple sclerosis (MS) are still unexplained and are the subject of some controversy. On the basis of histopathological analysis of a small set of MS cases, a recently published study postulates primary oligodendroglial damage as the initiator of MS lesions, with infiltration of leukocytes into the central nervous system (CNS) as a secondary phenomenon. In this paper we outline the current controversial discussion and different concepts of lesion development in MS. We conclude that demyelination can result from different pathogenic mechanisms, with either primary autoimmune inflammation or primary oligodendroglial damage and a secondary inflammatory reaction. Lesions can be divided into four subtypes (patterns I-IV) on the basis of histopathological characteristics, which supports the idea that MS lesions develop in different ways. These new aspects may have major implications for treatment. However, except in a few specific forms, most MS patients cannot currently be assigned to one of these lesion subtypes by means of clinical and paraclinical parameters. Without this, individual treatments tailored to the pathogenesis will not be possible.
The case of inflammatory vasculopathy and encephalopathy caused by treatment with tacrolimus is reported. This 49-year-old woman developed progressive gait ataxia and right-sided hemiparesis after 7 years of tacrolimus therapy for focal sclerosing glomerulonephritis. MRI presented multifocal cerebral lesions with contrast enhancement. Oligoclonal banding was positive. When the treatment with tacrolimus was stopped, the clinical symptoms resolved completely and the MRI findings improved with corticoid monotherapy.
We report on a 48 year old female patient who acquired a bacterial meningoencephalitis as a result of a cervical myelography. Examination of the cerebrospinal fluid (CSF) revealed 309 cells per microliter and Streptococcus acidominimus was isolated as the infectious agent. Cranial MRI demonstrated disseminated lesions predominantly in the pontine and medullary brain stem as well as in thalamic nuclei. The patient developed a crossed central neuropathic pain syndrome. Neurological examination showed mechanic allodynia and hyperpathy along the left-sided extremities as well as right-sided neuropathic facial pain. On the MRI a dorsolateral medullary lesion on the right side, in the territory of the posterior inferior cerebellar artery was found. The localization of the lesion is suggestive of involvement of the spinal trigeminal tract or nucleus and the spinothalamic tract that would explain the neuropathic pain syndrome.A combination of gabapentine and amitriptyline reduced the pain markedly whereas opioids failed to provide sufficient analgesia.