Many researches that discourse the treatment of prolactinomas with dopamine agonists (DA) provide data about pituitary tumor apoplexy of some prolactinomas. Therefore, DA are listed as risk factors for apoplexy of prolactinomas. The authors wish to explore the percentage (frequency) of pituitary tumor apoplexy during the treatment of prolactinomas with DA. From June 2011 to February 2012, we sought electronic databases and found 2169 articles and 71 book chapters relevant to DA. Only seven articles have been included into systematic review and from 4 articles we extracted numerical data that showed percentage of pituitary tumor apoplexy. One hundred and fifty-seven patients treated with DA were included in four studies. Results showed the following percentage of apoplexy during the treatment of prolactinomas with DA (apoplexy/therapy ratio): 1/84(1,19%), 13/29(44,83%), 1/15(6,67%) and 1/29(3,45%). One result stands out from the other (13/29-44,83%) because of retrospective search for pituitary hemorrhage by MRI imaging of sellar region and some of the patients were without clinical signs of apoplexy. Median and mean age of included patients was usually over 30 years. Pituitary tumor apoplexy appeared more frequently in macroprolactinomas than in microprolactinomas and also within a year and a half since the beginning of treatment with DA. Conclusively, clinically manifested pituitary tumor apoplexy appears in relatively small percentage of prolactinomas treated with DA. We were also concluded that apoplexy appears asymptomatic and because of that and because of more frequently appearing in macroprolactinomas, there are recommendations for performing MRI imaging of sellar region more often in patients with macroprolactinomas than in patients with microprolactinomas who are treated with DA.
The capacity of the cerebrovasculature to buffer changes in blood pressure (BP) is crucial to prevent stroke, the incidence of which is three- to fourfold elevated after spinal cord injury (SCI). Disruption of descending sympathetic pathways within the spinal cord due to cervical SCI may result in impaired cerebrovascular buffering. Only linear analyses of cerebrovascular buffering of BP, such as transfer function, have been used in SCI research. This approach does not account for inherent nonlinearity and nonstationarity components of cerebrovascular regulation, often depends on perturbations of BP to increase the statistical power, and does not account for the influence of arterial CO tension. Here, we used a nonlinear and nonstationary analysis approach termed wavelet decomposition analysis (WDA), which recently identified novel sympathetic influences on cerebrovascular buffering of BP occurring in the ultra-low-frequency range (ULF; 0.02-0.03Hz). WDA does not require BP perturbations and can account for influences of CO tension. Supine resting beat-by-beat BP (Finometer), middle cerebral artery blood velocity (transcranial Doppler), and end-tidal CO tension were recorded in cervical SCI ( n = 14) and uninjured ( n = 16) individuals. WDA revealed that cerebral blood flow more closely follows changes in BP in the ULF range ( P = 0.0021, Cohen's d = 0.89), which may be interpreted as an impairment in cerebrovascular buffering of BP. This persisted after accounting for CO. Transfer function metrics were not different in the ULF range, but phase was reduced at 0.07-0.2 Hz ( P = 0.03, Cohen's d = 0.31). Sympathetically mediated cerebrovascular buffering of BP is impaired after SCI, and WDA is a powerful strategy for evaluating cerebrovascular buffering in clinical populations.
Study design Experimental study. Objectives Compromised cerebrovascular function likely contributes to elevated neurological risk in spinal cord injury (SCI). Passive heating offers many cardiovascular and neurological health benefits; therefore, we aimed to determine the effects of an acute bout of heating on cerebrovascular function in chronic SCI. Methods Persons with cervical SCI (n = 15) and uninjured controls (CON; n = 15) completed 60 min of lower limb hot water immersion (40°C). Assessments of middle cerebral (MCA) and posterior cerebral artery (PCA) velocities, pulsatilities, and neurovascular coupling (NVC) were performed using transcranial Doppler ultrasound. Duplex ultrasonography was used to index cerebral blood flow via the internal carotid artery (ICA), and carotid-femoral pulse-wave velocity (PWV) was measured using tonometry. The NVC response was quantified as the peak hyperemic value during 30-s cycles of visual stimulation. Results Mean arterial pressure changed differentially with heating [mean (standard deviation); SCI: +6(14) mmHg, CON: −8(12) mmHg; P = 0.01]. There were no differences in any intracranial artery measures (all P > 0.05), except for small (~10%) increases in MCA conductance in CON after heating vs. SCI (interaction P = 0.006). Resting ICA flow was greater in SCI vs. CON (P = 0.03) but did not change with heating in either group (interaction P = 0.34). There were also no between-group differences in the NVC response (ΔPCA conductance) pre-[SCI: 29(19)% vs. CON: 30(9)%] or post-heating [SCI 30(9)% vs. 25(9)%; interaction P = 0.22]. Conclusions Mild acute heating does not impair or improve cerebrovascular function in SCI or CON. Thus, further study of the effects of chronic heating interventions are warranted.
Clinical guidelines for bladder management after SCI recommend avoiding the Credé maneuver due to potential complications such as hernia or bruising. This current case report demonstrates the additional risk of inducing AD and dangerously high BP elevation.
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