ABSTRACT
PURPOSE: To report an unusual case of idiopathic hypertrophic spinal pachymeningitis (IHSP) with a review of relevant literature and to discuss the etiology, clinical features, imaging, treatment and prognosis of IHSP. METHODS: The case of a 44-year-old woman is reported. MEDLINE was used to search relevant literatures written in English since 2004. RESULTS: The patient suffered from progressive mild thoracic backache followed by truncal and lower extremity weakness, numbness and urinary retention. The diagnosis was confirmed by magnetic resonance (MR) imaging and histopathologic examination. Although she received corticosteroid therapy and decompressive surgery, the patient suffered a rapid relapse probably because of the withdrawal of postoperative steroid therapy. CONCLUSIONS: IHSP is a rare disease characterized by inflammatory hypertrophy of the dura mater without identifiable cause and featured clinical progress of radiculalgia to myelopathy. It is a diagnosis of exclusion. In our view, surgical decompression with postoperative steroid therapy may be optimal. Furthermore,we speculated that increased levels of protein and cell count in cerebrospinal fluid (CSF) might be positively related to the disease progression. High inflammatory signs or CSF protein and cell levels before surgery or postoperative residual lesions are possible reasons of poor prognosis in patients with IHSP.
Subject(s)
Meningitis/diagnosis , Adult , Back Pain/etiology , Combined Modality Therapy , Decompression, Surgical/methods , Dura Mater/pathology , Female , Glucocorticoids/therapeutic use , Humans , Hypertrophy/complications , Hypertrophy/diagnosis , Hypertrophy/therapy , Hypesthesia/etiology , Magnetic Resonance Imaging , Meningitis/complications , Meningitis/therapy , Prognosis , Rare Diseases/pathology , RecurrenceABSTRACT
The Golgi apparatus (GA), an intermediate organelle of the cell inner membrane system, plays a key role in protein glycosylation and secretion. In recent years, this organelle has been found to act as a vital intracellular Ca(2+) store because different Ca (2+) regulators, such as the inositol-1,4,5-triphosphate receptor, sarco/endoplasmic reticulum Ca(2+) -ATPase and secretory pathway Ca 2+ -ATPase, were demonstrated to localize on their membrane. The mechanisms involved in Ca(2+) release and uptake in the GA have now been established.Here, based on careful backward looking on compartments and patterns in GA Ca (2+) regulation, we review neurological diseases related to GA calcium remodeling and propose a modified cytosolic Ca(2+) adjustment model, in which GA acts as part of the panel point.
