Benign perimesencephalic hemorrhage occurring after previous aneurysmal subarachnoid hemorrhage: a case report

<p>Abstract</p> <p>Introduction</p> <p>Both aneurysmal subarachnoid hemorrhage and benign perimesencephalic hemorrhage are well-described causes of spontaneous subarachnoid hemorrhage that arise as a result of different pathologic processes. To the best of the authors' knowledge, there have been no reports of both vascular pathologies occurring in the same individual.</p> <p>Case presentation</p> <p>A 51-year-old Caucasian woman with a history of aneurysmal subarachnoid hemorrhage presented five years after her initial treatment with ictal headache, meningismus, nausea and emesis similar to her previous bleeding event. Computed tomographic imaging revealed perimesencephalic bleeding remote from her previously coiled anterior communicating artery aneurysm. Both immediate and delayed diagnostic angiography revealed no residual filling of the previously coiled aneurysm and no other vascular anomalies, consistent with benign perimesencephalic hemorrhage. The patient had an uneventful hospital course and was discharged to home in good condition.</p> <p>Conclusions</p> <p>This report for the first time identifies benign perimesencephalic hemorrhage occurring in the setting of previous aneurysmal subarachnoid hemorrhage. The presence of a previously treated aneurysm can complicate the process of diagnosing benign perimesencephalic hemorrhage. Fortunately, in this case, the previously treated anterior communicating artery aneurysm was remote from the perimesencephalic hemorrhage and could be ruled out as a source. The patient's prior aneurysmal subarachnoid hemorrhage did not worsen the anticipated good outcome associated with benign perimesencephalic hemorrhage.</p

Functional outcome and quality of life 5 and 12.5 years after aneurysmal subarachnoid haemorrhage

Patients who recover from aneurysmal subarachnoid haemorrhage (SAH) often remain disabled or have persisting symptoms with a reduced quality of life (QoL). We assessed functional outcome and QoL 5 and 12.5 years after SAH. In a consecutive series of 64 patients with mean age at SAH of 51 years, initial outcome assessments had been performed at 4 and 18 months after SAH. At the initial and current outcome assessments, functional outcome was measured with the modified Rankin Scale (mRS) and QoL with the SF-36 and a visual analogue scale (VAS). We studied the change in outcome measurements over time. We used the non-parametric Wilcoxon test to compare differences in mRS grades and calculated differences with corresponding 95% confidence intervals in the domain scores of the SF-36 and the VAS. After 5 years, seven patients had died and five patients had missing data. Compared with the 4-month follow-up, the mRS had improved in 29 of the 52 patients, remained similar in 19 patients. The overall QoL (SF-36 domains and VAS score) was better. At 12.5 years an additional six patients had died. Compared to the 4-month study, 25 of the 46 remaining patients had improved mRS, 12 had remained the same and in nine patients the mRS had worsened. Between the 5 and the 12.5 years follow-up, the improvement in mRS had decreased but patients reported overall a better QoL. Among long-time survivors, QoL may improve more than a decade after SAH

A liver fibrosis cocktail? Psoriasis, methotrexate and genetic hemochromatosis

BACKGROUND: Pathologists are often faced with the dilemma of whether to recommend continuation of methotrexate therapy for psoriasis within the context of an existing pro-fibrogenic risk factor, in this instance, patients with genetic hemochromatosis. CASE PRESENTATIONS: We describe our experience with two male psoriatic patients (A and B) on long term methotrexate therapy (cumulative dose A = 1.56 gms and B = 7.88 gms) with hetero- (A) and homozygous (B) genetic hemochromatosis. These patients liver function were monitored with routine biochemical profiling; apart from mild perivenular fibrosis in one patient (B), significant liver fibrosis was not identified in either patient with multiple interval percutaneous liver biopsies; in the latter instance this patient (B) had an additional risk factor of partiality to alcohol. CONCLUSION: We conclude that methotrexate therapy is relatively safe in patients with genetic hemochromatosis, with no other risk factor, but caution that the risk of fibrosis be monitored, preferably by non-invasive techniques, or by liver biopsy

Spermatogonial Stem Cell Niche and Spermatogonial Stem Cell Transplantation in Zebrafish

Background Spermatogonial stem cells (SSCs) are the foundation of spermatogenesis, and reside within a specific microenvironment in the testes called “niche” which regulates stem cell properties, such as, self-renewal, pluripotency, quiescence and their ability to differentiate. Methodology/Principal Findings Here, we introduce zebrafish as a new model for the study of SSCs in vertebrates. Using 5′-bromo-2′-deoxyuridine (BrdU), we identified long term BrdU-retaining germ cells, type A undifferentiated spermatogonia as putative stem cells in zebrafish testes. Similar to rodents, these cells were preferentially located near the interstitium, suggesting that the SSC niche is related to interstitial elements and might be conserved across vertebrates. This localization was also confirmed by analyzing the topographical distribution of type A undifferentiated spermatogonia in normal, vasa::egfp and fli::egfp zebrafish testes. In the latter one, the topographical arrangement suggested that the vasculature is important for the SSC niche, perhaps as a supplier of nutrients, oxygen and/or signaling molecules. We also developed an SSC transplantation technique for both male and female recipients as an assay to evaluate the presence, biological activity, and plasticity of the SSC candidates in zebrafish. Conclusions/Significance We demonstrated donor-derived spermato- and oogenesis in male and female recipients, respectively, indicating the stemness of type A undifferentiated spermatogonia and their plasticity when placed into an environment different from their original niche. Similar to other vertebrates, the transplantation efficiency was low. This might be attributed to the testicular microenvironment created after busulfan depletion in the recipients, which may have caused an imbalance between factors regulating self-renewal or differentiation of the transplanted SSCs

UVA/UVA1 phototherapy and PUVA photochemotherapy in connective tissue diseases and related disorders: a research based review

BACKGROUND: Broad-band UVA, long-wave UVA1 and PUVA treatment have been described as an alternative/adjunct therapeutic option in a number of inflammatory and malignant skin diseases. Nevertheless, controlled studies investigating the efficacy of UVA irradiation in connective tissue diseases and related disorders are rare. METHODS: Searching the PubMed database the current article systematically reviews established and innovative therapeutic approaches of broad-band UVA irradiation, UVA1 phototherapy and PUVA photochemotherapy in a variety of different connective tissue disorders. RESULTS: Potential pathways include immunomodulation of inflammation, induction of collagenases and initiation of apoptosis. Even though holding the risk of carcinogenesis, photoaging or UV-induced exacerbation, UVA phototherapy seems to exhibit a tolerable risk/benefit ratio at least in systemic sclerosis, localized scleroderma, extragenital lichen sclerosus et atrophicus, sclerodermoid graft-versus-host disease, lupus erythematosus and a number of sclerotic rarities. CONCLUSIONS: Based on the data retrieved from the literature, therapeutic UVA exposure seems to be effective in connective tissue diseases and related disorders. However, more controlled investigations are needed in order to establish a clear-cut catalogue of indications

Subarachnoid haemorrhage and the life after

Of all stroke patients 5% has a subarachnoid haemorrhage (SAH); a bleed in the space between the brain and the skull that contains blood vessels that supply the brain. Every year 9 per 100.000 patients have an SAH and half the patients are younger than 55 years old. In most instances (80%) the cause of the bleeding is a ruptured aneurysm and in 10% a perimesencephalic nonaneurysmal haemorrhage (PMH). Patients with a PMH have a good short term outcome. The cause of a PMH is probably a venous source. Aneurysmal SAH has a poor outcome: 35% dies in the first 4 weeks after the haemorrhage and 20% remains dependent for activities of daily life. Life expectancy is reduced after aneurysmal SAH, probably from an excess of other heart and vessel diseases. Chapter 2 describes the supplemental value of scrutinising the history of relatives to detect SAH and heart and vessel diseases in 1290 first degree and 3588 second degree relatives of a consecutively collected cohort of 163 patients with SAH. Almost half of the families with a positive history for SAH in a first or second degree relative would have been gone undetected without the information provided by scrutinising all individual relatives. In Chapter 3 we studied the feasibility of follow-up through e-mail in patients discharged after SAH. E-mail follow-up was easy to perform, comfortable for the patient or relative and less time-consuming than follow-up by telephone. However, only 60% of all included patients had an e-mail address and 21% of those patients changed once or more the e-mail address. In Chapter 4 we describe a long-term follow-up study to assess life expectancy in 160 patients with a PMH with a total number of patients-years of 1213. At time of follow-up (range 1 – 23 years) 149 patients were still alive. Patients with PMH have no excess in mortality compared with the general population. In Chapter 5 we studied anosmia after PMH. The presumed causes of anosmia after a ruptured aneurysmal SAH are the sudden intracranial arterial pressure or the presence of blood in itself. It is unknown whether anosmia can develop after a PMH. Nine of 148 included patients had noticed a loss of smell already during the clinical course. Two patients reported a complete recovery after 8 to 12 weeks. We found no relation between anosmia and risk factors such as age, sex or hydrocephalus. Chapter 6 describes long-term outcome of 92 patients discharged to a nursing home after SAH. After 2 years 28 (30%) of these patients were discharged home or to another facility and forty-four patients (43%) lived longer than 5 years. Chapter 7 is a continuation of a former study of quality of life 4 and 18 months after SAH. In that cohort of patients there was improvement of functional outcome measured in modified Rankin scale and quality of life measured in SF-36 and a VAS score. Overall there was still an improvement in quality of life, while functional outcome worsened between 5 and 12.5 years