Background and Purpose-Stroke during pregnancy is an emerging concern. Although females undergo many physiological, endocrine, and neurological alterations during pregnancy, the consequences of such changes on outcome after stroke are unclear. It is predicted that increases in steroid hormones observed during pregnancy may confer protective effects against the neurological and pathological sequelae of stroke. Methods-We therefore investigated behavioral and histological consequences of a global cerebral ischemia (2-vessel occlusion; 2VO), and how these outcomes correlated with pregnancy-related changes in hormones in Sprague-Dawley rats. Results-After the 2VO, pregnant rats exhibited poorer memory in a contextual fear conditioning test of learning and memory than sham-treated controls, whereas nonpregnant rats did not. They also showed enhanced CA1 hippocampal neuronal injury. This susceptibility to damage is despite significant pregnancy-associated hypothermia and is probably not associated with alterations in 17-estradiol or corticosterone levels. Conclusion-These findings are the first to show enhanced neuronal damage in pregnant animals after global cerebral ischemia. They also suggest that the mechanism may be independent of changes in estrogen, corticosterone, and body temperature. (Stroke. 2008;39:975-982.)
Postnatal hippocampal neurogenesis has been demonstrated to affect learning and memory in numerous ways. Several studies have now demonstrated that increased neurogenesis can induce forgetting of memories acquired prior to the manipulation of neurogenesis and, as a result of this forgetting can also facilitate new learning. However, the mechanisms mediating neurogenesis-induced forgetting are not well understood. Here, we used a subregion-based analysis of the immediate early gene c-Fos as well as in vivo fiber photometry to determine changes in activity corresponding with neurogenesis induced forgetting. We found that increasing neurogenesis led to reduced CA1 activity during context memory retrieval. We also demonstrate here that perineuronal net expression in areas CA1 is bidirectionally altered by the levels or activity of postnatally generated neurons in the dentate gyrus. These results suggest that neurogenesis may induce forgetting by disrupting perineuronal nets in CA1 which may otherwise protect memories from degradation.
Idiopathic hypertrophic spinal pachymeningitis (IHSP) is a comparatively rare disease characterized by hypertrophic inflammation of the dura mater and clinical symptoms that progress from local pain to myelopathy. We report a case of IHSP followed up for 20 years in a 46-year-old man. Expansive laminoplasty was performed in 1991, and this case has been previously reported by a co-author. After 17 years, the patient's gait disturbance returned. Physical examination and imaging confirmed IHSP that had developed into syringomyelia at the T2-L1 conus level. This case was diagnosed as adhesive spinal arachnoiditis due to pachymeningitis caused by syringomyelia. T1-T4 laminectomy, a syringo-subarachnoid shunt (S-S shunt), and L2-L3 laminectomy were performed. The patient again developed dysesthesia and gait disturbance 3 years after the second operation. Most reports of IHSP have limited their focus to short-term follow-up after initial treatment with no long-term results. At present, there are only five reports referring to long-term results of greater than 5 years. All but one case needed additional surgery. To the best of our knowledge, this is the first case in which syringomyelia occurred in a patient with IHSP. It is important to note that syringomyelia may be a cause of symptom recrudescence during long-term follow-up in IHSP patients.
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