PubMed · 14811774
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J M VALDES, K WENKEBACH, A SEGURA, A FERRARIS. 1951. [Encephalitis].. https://pubmed.ncbi.nlm.nih.gov/14811774/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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.
In Parkinson's disease (PD), post-mortem examination reveals a loss of dopaminergic (DA) neurons in the substantia nigra (SN) associated with a massive astrogliosis and the presence of activated microglial cells. Similarly, microglial activation has also been reported to be associated with the loss of DA neurons in animal models of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, annonacine and lipopolysaccharide (LPS). Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, raising the possibility that toxic substances released by glial cells could be involved in the propagation of neuronal degeneration. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in PD.