Abrupt Increase In Blood Pressure Research Articles

Blood Pressure Regulation and Hypertension in Obstructive Sleep Apnea Syndrome: A Historical Perspective.

In obstructive sleep apnea syndrome (OSAS), an underlying disease of secondary hypertension, repeated episodes of asphyxia due to obstructive sleep apnea (OSA), followed by arousal, lead to various cardiovascular consequences. Using a canine model of OSAS, it was found that a single load of OSA caused an abrupt increase in blood pressure (BP) (Apnea Surge in seconds), while multiple OSA episodes occurring nightly for 1-3 months led to a sustained elevation of BP during both nighttime and daytime. Epidemiological studies on 24-hour ambulatory BP measurements revealed that some hypertensive patients experienced elevated BP in the early morning (Morning Surge), which could be intensified by OSAS. The resonance of Apnea Surge in seconds and Morning Surge increases the risk of organ damage, triggers the cardiovascular events, and adversely affects the prognosis of hypertensive patients with OSAS.For ameliorating these risks, OSA should be treated with positive airway pressure properly.

Enhanced multiresolution wavelet analysis of cerebrovascular dynamics

The responses of cerebral circulation to an abrupt increase in blood pressure caused by pharmacologically induced hypertension are compared by means of multiresolution wavelet analysis (MWA), which uses standard deviations of expansion coefficients as diagnostic criteria, and an enhanced approach, combining MWA with analysis of long-range power-law correlations in the wavelet domain. We discuss how applying both of these approaches elicits different types of reactions of large blood vessels in the brain and capillary network and show that the use of simple statistical measures limits the information that can be extracted during data processing. Taking into account the correlation features in addition to the width of the probability density is a possible way to improve the characterization of the effects produced by “jumps” in blood pressure.

Sex differences in vascular reactivity in mesenteric arteries from a mouse model of acute intermittent porphyria

Background and aimsAcute intermittent porphyria (AIP) results from a partial deficiency of porphobilinogen deaminase (PBGD). Symptomatic AIP patients, most of whom are women, experience acute attacks characterized by severe abdominal pain and abrupt increases in blood pressure. Here, we characterized the reactivity of mesenteric arteries from male and female AIP mice with ~30% of normal PBGD activity and wild type C57BL/6 mice. MethodsAn acute porphyric attack was induced in AIP mice by treatment with phenobarbital. Vascular responses to K+, phenylephrine (PE), acetylcholine (ACh), and hemin were determined (Wire Multi Myograph). ResultsMaximal contraction to PE was increased in arteries from male and female AIP mice (p < .05) during an induced attack of acute porphyria. Female AIP arteries had increased sensitivity to PE (p < .05) even after nitric oxide (NO) blockade with Nω-nitro-L-arginine methyl ester (L-NAME) (p < .05). Maximal relaxation to ACh was similar in males and females with lower sensitivity in female AIP arteries (p < .05). Hemin induced greater relaxation in AIP arteries in both males and females (p < .05). Summary/conclusionsSex differences in this AIP mouse model include a pro-contractile response in females. These alterations may contribute to the increased blood pressure during an acute attack and provide a novel mechanism of action whereby heme ameliorates the attacks.

362. Transient blindness out off the uterus, reported by Nicolaes Tulp in 1641

Transient blindness, in the setting of (recently) pregnant women is now recognised to be part of the Posterior Reversible Encephalopathy Syndrome (PRES). This term was first coined by Hinchey et al. in 1996 [1]. A pattern is observed of patients who experience headaches, vomiting, confusion, seizures, cortical blindness and other visual abnormalities, that went alongside abrupt increases in blood pressure and impairment of renal function. Interestingly, in former centuries a total blindness related to headache and convulsions, in pregnancy, labour or childbed, being very rare, was noted and described, but information on blood pressure and renal function remains unknown. Exemplary, Nicolaes Tulp, well known from the 1632 Rembrandt’ Anatomy Lesson, a magistrate of the council of Amsterdam, a medical doctor and Praelector anatomiae of the Surgeons Guild, published in 1641 in Latin his Medical observations, of which No. X is titled: Blindness out of the uterus [2]. Tulp described two cases of pregnant women with convulsions, which caused a complete unawareness of delivering their child. The second woman lost her sight completely without any other abnormalities. Both convulsions and blindness were attributed to ‘the blood that with great power and violence went upwards [to the brain]’. The treatment was cupping-glasses on the inner side of both legs, to draw back the blood; and with success: ‘she regained the light in her eyes’. We will compare the rare literature on diagnosis and treatment of transient amaurosis in the last four centuries to actual insights.

Evaluation of the Hemodynamic Response of Intravenous Clonidine versus Ropivacaine Scalp Block to Insertion of Scalp Pins in Neurosurgical Patients.

Background:The application of the skull-pin head-holder, used to stabilize the head during neurosurgical procedures, produces an intense nociceptive stimulus and results in abrupt increases in blood pressure and cerebral blood flow under general anesthesia. Different anesthetic and pharmacologic techniques, including local anesthetics, narcotics, antihypertensives, and deepening of anesthesia with inhalation anesthetics, have been used to blunt this deleterious effect with variable success.Aim:To compare the analgesic and hemodynamic effects of ropivacaine scalp block, and intravenous (IV) clonidine in attenuating the hemodynamic response to the scalp pin insertion in neurosurgical patients.Settings and Design:A comparative two group's clinical study of 64 patients undergoing elective craniotomy in Department of Anaesthesiology, Bangalore Medical College and Research Institute.Methodology:Sixty-four patients were allocated into any one of two groups of 32 patients each, by means of computer-generated randomization: (1) Group S: Patients receiving scalp block with injected ropivacaine 0.25% 30 ml. (2) Group C: Patients receiving 2 μg/kg IV clonidine.Statistical Methods:Descriptive and inferential statistical analysis has been carried out in the present study. Results on continuous measurements are presented on mean ± standard deviation (minimum–maximum) and results on categorical measurements are presented in number (%). Significance is assessed at 5% level of significance.Results:Increase in heart rate and blood pressure during pin insertion was attenuated by clonidine hydrochloride (P < 0.001). The number of patients who required more fentanyl and propofol to stabilize the hypertensive response were more in control group than clonidine group.Conclusion:IV clonidine maximally attenuated the hemodynamic response to application of head pins in a dose of 2 μg/kg compared to ropivacaine scalp block, thus maintaining intracranial pressure for neurosurgical anesthesia.

Clinical features, outcome, and associated factors for posterior reversible encephalopathy in Thai patients with systemic lupus erythematosus: a case-control study.

Posterior reversible encephalopathy syndrome (PRES) in patients with systemic lupus erythematosus (SLE) has been recognized increasingly. This study aimed to determine the prevalence, clinical features, brain imaging findings, outcomes, and associated factors of PRES in Thai SLE patients. SLE patients with PRES were identified from the lupus cohort of Chiang Mai University. Controls were SLE patients with a hospital number close to and actually had SLE diagnosis within 5 years of the case(case:control ratio = 1:4). Of 1,332 SLE patients, 30 episodes of PRES were identified in 24 female SLE patients (prevalence 1.80%). The mean ± SD age at SLE diagnosis and at onset of PRES was 25.02 ± 13.78 and 28.31 ± 12.61years, respectively. Seizure was the most common presenting symptom, as seen in 28 episodes, followed by acute severe headache in 17, alteration of consciousness in 17, nausea and vomiting in 10, blurred vision in 11, and hemiparesis in 3. Abrupt increase in blood pressure and active nephritis were seen in 29 and 26 of the episodes, respectively. Urine protein/creatinine ratio >1.00 (OR 15.72, 95% CI 3.12-79.12, p=0.001) and hemoglobin <10 gm/dL (OR 5.12, 95% CI 1.37-19.15, p=0.015) were associated factors for developing PRES. During the observation period, 7 patients in the PRES group and 8 in the control group died (p=0.015). PRES was uncommon in SLE patients, but associated with a high mortality rate. Active nephritis and anemia were associated factors of PRES in Thai SLE patients.

Hypertensive crisis

Here, we review current concepts on hypertensive crisis (HTN-C) with a focus on epidemiology, causes, pathophysiology and prognosis. We also offer a practical approach to the management of HTN-C. HTN-C is characterized by a severe and abrupt increase in blood pressure (BP) with impending or progressive acute end-organ damage (EOD). HTN-C can be divided into hypertensive emergency (HTN-E) and hypertensive urgency (HTN-U) based on the presence or absence of acute EOD, respectively. Recent retrospective studies have demonstrated that emergency department (ED) referrals from an outpatient clinic or rapid BP-lowering strategies in the ED do not lead to improved outcomes in patients with HTN-U. HTN-C can be a de-novo manifestation or a complication of essential or secondary HTN. The presence of acute EOD is a major poor prognostic indicator in HTN-C. The main objectives of the management of HTN-C are distinction of HTN-E from HTN-U and appropriate risk stratification, prevention or regression of acute EOD due to severely elevated BP, prevention of recurrence of HTN-C with an effective long-term management plan and avoidance of rapid lowering of BP except in some special circumstances. The majority of patients with asymptomatic HTN-U can be safely managed in the outpatient setting without exposing them to the risks of aggressive BP lowering. However, patients with HTN-E require hospitalization, prompt treatment and close monitoring.

High-dose hydroxocobalamin administered after H2S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep

Context. Severe H2S poisoning leads to death by rapid respiratory and cardiac arrest, the latter can occur within seconds or minutes in severe forms of intoxication. Objectives. To determine the time course and the nature of H2S-induced cardiac arrest and the effects of high-dose hydroxocobalamin administered after the end of sulfide exposure. Materials and methods. NaHS was infused in 16 sedated mechanically ventilated sheep to reach concentrations of H2S in the blood, which was previously found to lead to cardiac arrest within minutes following the cessation of H2S exposure. High-dose hydroxocobalamin (5 g) or saline solution was administered intravenously, 1 min after the cessation of NaHS infusion. Results. All animals were still alive at the cessation of H2S exposure. Three animals (18%) presented a cardiac arrest within 90 s and were unable to receive any antidote or vehicle. In the animals that survived long enough to receive either hydroxocobalamin or saline, 71% (5/7) died in the control group by cardiac arrest within 10 min. In all instances, cardiac arrest was the result of a pulseless electrical activity (PEA). In the group that received the antidote, intravenous injection of 5 g of hydroxocobalamin provoked an abrupt increase in blood pressure and blood flow; PEA was prevented in all instances. However, we could not find any evidence for a recovery in oxidative metabolism in the group receiving hydroxocobalamin, as blood lactate remained elevated and even continued to rise after 1 h, despite restored hemodynamics. This, along with an unaltered recovery of H2S kinetics, suggests that hydroxocobalamin did not act through a mechanism of H2S trapping. Conclusion. In this sheep model, there was a high risk for cardiac arrest, by PEA, persisting up to 10 min after H2S exposure. Very high dose of hydroxocobalamin (5 g), injected very early after the cessation of H2S exposure, improved cardiac contractility and prevented PEA.

Molecular Mechanisms of Chronic Intermittent Hypoxia and Hypertension

Obstructive sleep apnea (OSA) is characterized by episodes of repeated airway obstruction resulting in cessation (apnea) or reduction (hypopnea) in airflow during sleep. These events lead to intermittent hypoxia and hypercapnia, sleep fragmentation, and changes in intrathoracic pressure, and are associated with a marked surge in sympathetic activity and an abrupt increase in blood pressure. Blood pressure remains elevated during wakefulness despite the absence of obstructive events resulting in a high prevalence of hypertension in patients with OSA. There is substantial evidence that suggests that chronic intermittent hypoxia (CIH) leads to sustained sympathoexcitation during the day and changes in vasculature resulting in hypertension in patients with OSA. Mechanisms of sympathoexcitation include augmentation of peripheral chemoreflex sensitivity and a direct effect on central sites of sympathetic regulation. Interestingly, the vascular changes that occur with CIH have been ascribed to the same molecules that have been implicated in the augmented sympathetic tone in CIH. This review will discuss the hypothesized molecular mechanisms involved in the development of hypertension with CIH, will build a conceptual model for the development of hypertension following CIH, and will propose a systems biology approach in further elucidating the relationship between CIH and the development of hypertension.

Crosstalk between central pathways of nitric oxide and carbon monoxide in the hypertensive action of cyclosporine

Although the intermediary role of central neurons in the hypertensive and sympathoexcitatory actions of cyclosporine (CSA) has been recognized in previous studies including our own, the underlying mechanism remains obscure. In this study, we tested the hypothesis that central pathways of nitric oxide (NO) and carbon monoxide (CO) modulate the blood pressure (BP) response elicited by CSA in conscious rats. Hemodynamic effects of CSA were evaluated in absence and presence of maneuvers that inhibit or facilitate biosynthesizing enzymes of NO (NOS) or CO (heme oxygenase, HO). CSA (20mg/kg i.v.) produced abrupt increases in BP that peaked in 5min and maintained for at least 45min. The hypertensive effect of CSA disappeared in rats pretreated intracisternally (i.c.) with Nω-nitro-l-arginine methyl ester (L-NAME, nonselective NOS inhibitor), N5-(1-iminoethyl)-l-ornithine (L-NIO, selective eNOS inhibitor), Nω-propyl-l-arginine (NPLA, selective nNOS inhibitor), or 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ, guanylate cyclase inhibitor), suggesting the importance of central eNOS/nNOS/GC cascade in CSA-induced hypertension. L-NAME also abolished the hypotension caused by the sympatholytic drug moxonidine, indicating a tonic sympathoinhibitory action for NO. The inhibition of HO activity by zinc protoporphyrin IX (ZnPP) abrogated the hypertensive action of CSA. The abolition by L-NAME or ZnPP of CSA hypertension was compromised upon simultaneous i.c. exposure to hemin (HO substrate) and l-arginine (NOS substrate), respectively. Together, the interruption of the mutually facilitated NOS/NO and HO/CO pathways and coupled GC/cGMP in central neuronal pools accounts, at least partly, for the hypertensive and perhaps sympathoexcitatory actions of CSA.

M-Atrial Natriuretic Peptide and Nitroglycerin in a Model of Acute Hypertensive Heart Failure: A Comparison of Two cGMP Therapeutics

Systolic hypertension is an increasingly common characteristic among subjects with acute heart failure (HF). Importantly, an abrupt increase in blood pressure (BP) may be the mechanism for acute HF in such subjects often leading to renal as well as myocardial impairment. While the prevalence of hypertension in acute HF is up to 50%, current therapies are limited and there is specifically an unmet need for renal enhancing therapies especially in the setting of hypertension and HF. M-atrial natriuretic peptide (M-ANP) is a novel, designer natriuretic peptide based therapeutic with BP lowering, renal enhancing, and aldosterone inhibiting properties.

Novel Large Animal Model of Acute Experimental Hypertensive Heart Failure

Background: Systolic hypertension especially in women and blacks is increasingly recognized and present in approximately 50% of subjects with acute decompensated heart failure (ADHF). Importantly, an abrupt increase in blood pressure may indeed be the mechanism for ADHF in such subjects. To date there is a lack of a large animal model of ADHF with hypertension to allow detailed characterization of the hemodynamic and neurohumoral phenotype and to test potential therapeutic agents. Objectives: Develop a novel large animal model of pacing induced ADHF and angiotensin II (ANG II) induced hypertension and characterize its cardiorenal and neurohumoral phenotype.

Effects of graded doses of propofol for anesthesia induction on cardiovascular parameters and intraocular pressures in normal dogs

ObjectiveTo determine the effects of graded doses of propofol on cardiovascular parameters and intraocular pressures (IOP) in normal dogs. Study designProspective, randomized, modified Latin square, cross-over experimental study. AnimalsEleven adult random-source dogs weighing 20.2 ± 5.7 kg. MethodsThere were three treatment groups: propofol 8 mg kg−1 intravenous (IV) until loss of jaw tone (Group P), propofol until loss of jaw tone +20% (Group P20), and propofol until loss of jaw tone +50% (Group P50). Atracurium 0.1 mg kg−1 IV was administered in all treatments immediately after the propofol. All dogs received the three treatments in a randomized order, with at least a one week interval between treatments. Direct arterial blood pressure and IOP by applanation tonometry were obtained at baseline, after 5 minutes of pre-oxygenation (before induction), before, and after intubation. Blood gas samples were obtained at baseline, after pre-oxygenation, and before intubation. ResultsThere was no significant difference in IOP readings at any time point among groups. The IOP was significantly higher before intubation versus before induction in all three groups. There was a significantly smaller change in systolic, mean (MAP), and diastolic (DAP) arterial pressures in the P50 group compared with the P group after intubation. There was a significantly smaller change in MAP and DAP in the P50 group compared with the P20 group after intubation. The increase in CO2 from before induction to before intubation was significantly greater in the P50 group than in the P or P20 groups. Conclusions and clinical relevanceGraded doses of propofol did not affect the increase in IOP observed with propofol induction in normal dogs. Higher doses of propofol are of no apparent additional benefit in animals who cannot tolerate an abrupt increase in IOP but may be of benefit in dogs who cannot tolerate an abrupt increase in blood pressure accompanying orotracheal intubation.

The Association of High-Magnitude Cerebral Passivity and Intraventricular Hemorrhage in Premature Infants

The Association of High-Magnitude Cerebral Passivity and Intraventricular Hemorrhage in Premature Infants

Successful re-initiation of calcineurin inhibitors in patients with posterior reversible encephalopathy syndrome (PRES)

18014 Background: Posterior Reversible Encephalopathy Syndrome (PRES) is characterized by headache, altered mental status, seizure or visual loss and is associated with white matter vasogenic edema predominantly affecting the posterior occipital and parietal lobes of the brain. It often occurs after abrupt increases in blood pressure in the background of calcineurin inhibitor therapy. Methods: Retrospective study of 10 patients (pts) diagnosed with PRES while receiving cyclosporine (CSA). Results: Six children, (mean age 10.7 y; range 8–14 y), and 4 adults (mean age 28 y, range 20–35 y) were diagnosed with PRES. Seven had severe aplastic anemia as a primary diagnosis while one pt each had MDS, AML- M4 and Pre B-ALL. Seven had undergone an allogeneic stem cell transplant and all 10 pts were on CSA when PRES occurred. Besides CSA use, potential inciting risk factors for PRES include: concomitant infections (7pts), grade 3–4 GVHD (4 pts), use of ATG (5 pts), high dose steroids (5 pts), meropenem (4 pts) and hypomagnesemia (5 pts). Eight pts experienced seizures and 5 had visual disturbances. The average Mean Arterial Pressure (MAP) when PRES was diagnosed (132 mmHg; range 108–169) was significantly higher than baseline (mean rise 36.94 mmHg; range 12–85). MRI findings of increased T2 fluid attenuated inversion recovery signal predominantly involved the posterior brain regions (8 pts), but atypical findings of global involvement with frontal preponderance were seen in 2 pts. Nine pts required anti-epileptic drugs (AED) acutely; the 8 pts who seized continued AED (single agent levetiracetam in 7/8 pts). Continuous infusional antihypertensives were required for acute BP management in 4 pts; 7 pts required maintenance antihypertensives. CSA was never discontinued in 2 pts and restarted in all pts (median 2 days; range 0–79 days, from diagnosis of PRES to reinitiating CSA) without recurrence of PRES. Conclusions: The “typical” characteristics of specific posterior and white matter involvement is not always observed in PRES. Single agent levetiracetam can effectively prevent recurrent PRES-associated seizures. Prompt BP management and seizure prophylaxis can safely allow for continuing or promptly restarting calcineurin inhibitors critical to pt management. No significant financial relationships to disclose.

Brain Angiotensin and Cardiovascular Reactivity to Negative and Positive Emotional Stress

Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to negative emotional stress is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) has been recognized as an important regulator of cardiovascular reactivity. Apart from threatening events, exposure to appetitive stimuli is capable of inducing a distinct, sympathetically mediated rise in blood pressure in both animals and humans. Recent animal studies employing microinjection of AT1 receptor antagonists directly into hypothalamic and brainstem nuclei indicate that locally released AngII acts to facilitate, through a superoxide-dependent mechanism, the pressor response to negative stress. Conversely, animal studies demonstrated that brain Ang II is less important in the regulation of cardiovascular arousal associated with positively motivated behavior, such as anticipation and consumption of palatable food. Thus, endogenous AngII in the brain appears to control the activation of central pathways primarily associated with the defense response, rather than nonspecifically modulating cardiovascular reactivity regardless of emotional valence (attraction or aversion) of stimuli. These findings may be of clinical importance as they suggest that targeted inhibition of Ang II -superoxide signaling in the brain may selectively reduce blood pressure reactivity to negative emotional stress, without affecting cardiovascular arousal associated with normal daily activities.

Brain superoxide as a key regulator of the cardiovascular response to emotional stress in rabbits

Cardiovascular reactivity, an abrupt increase in blood pressure and heart rate in response to emotional stress, is a risk factor for hypertension and heart disease. Brain angiotensin II (Ang II) type 1 (AT(1)) receptor is increasingly recognized as an important regulator of cardiovascular reactivity. Given that a wide variety of AT(1) receptor signalling pathways exists in neurones, the precise molecular mechanisms that underlie central cardiovascular actions of Ang II during emotional stress are yet to be determined. Growing evidence, however, indicates that reactive oxygen species, and in particular superoxide (.O(2)(-)), are important intracellular messengers of many actions of brain Ang II. In particular, studies employing microinjection of .O(2)(-) scavengers directly into the rostral ventrolateral medulla (RVLM) and dorsomedial hypothalamus of rabbits have shown that the activation of AT(1) receptor-.O(2)(-) signalling is required for full manifestation of the cardiovascular response to emotional stress. This role of .O(2)(-) appears to be highly specific, because .O(2)(-) scavengers in the RVLM do not alter the sympathoexcitatory response to baroreceptor unloading or sciatic nerve stimulation. The subcellular mechanisms for the stress-induced .O(2)(-) production are likely to include the activation of NADPH oxidase and are essentially independent of nitric oxide. This review summarizes current knowledge of redox-sensitive signalling mechanisms in the brain that regulate cardiovascular effects of stress. Additionally, it presents initial evidence that .O(2)(-) may be less important in the activation of central pressor pathways mediating cardiovascular arousal associated with appetitive events, such as food anticipation and feeding.

REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY SYNDROME IN A DOUBLE-LUNG TRANSPLANT PATIENT WHO WAS TREATED WITH TACROLIMUS

INTRODUCTION: Reversible Posterior Leukoencephalopathy (RPL) syndrome is characterized by headache, seizures, visual disturbances, and altered mental functioning. Risk factors include abrupt increases in blood pressure, renal dysfunction, and use of immunosuppressants including calcineurin inhibitors.

Hypertensive Encephalopathy in Cats with Reduced Renal Function

The clinical, hemodynamic, and pathologic features of hypertensive encephalopathy in two cats with reduced renal mass are described. The cats developed a progressive syndrome of lethargy, ataxia, blindness, stupor, and seizures following an abrupt increase in blood pressure associated with a surgical reduction in renal mass. The cats had severe gross brain edema, evidenced by cerebellar changes of caudal coning and cranial displacement over the corpora quadrigemina and cerebral changes of widening and flattening of the gyri. Histologically, interstitial edema was most pronounced in the cerebral white matter. Hypertensive vascular lesions were present as hyaline arteriolosclerosis in one cat and hyperplastic arteriolosclerosis in the other. Rare foci of parenchymal microhemorrhages and necrosis were also observed. Systemic hypertension (especially severe or rapidly developing) accompanied by neurologic signs and the pathologic findings of diffuse brain edema with cerebral arteriolosclerosis are consistent with an etiologic diagnosis of hypertensive encephalopathy.

Tacrolimus-Related Encephalopathy following Allogeneic Stem Cell Transplantation in Children

Tacrolimus is a potent immunosuppressive drug widely used to prevent and treat graft-versus-host disease (GVHD) in stem cell transplantation (SCT). Among 49 patients receiving tacrolimus who underwent SCT from January 2000 to July 2003, 10 patients (20%) developed encephalopathy. The commonly observed symptoms were convulsions and drowsiness, and most patients complained of signal symptoms such as headache, nausea, and cortical blindness before onset. The most common abnormality on neuroimages was high-intensity lesions in white matter on magnetic resonance imaging T2-weighted or fluid-attenuated inversion recovery images. At onset, all patients were receiving treatment for acute GVHD (grade II/III) or extensive chronic GVHD and demonstrated an abrupt increase in blood pressure from baseline levels. The serum tacrolimus concentration was generally within acceptable levels at onset. Symptoms gradually improved in all patients when the blood pressure was lowered with antihypertensive medication, regardless of continued tacrolimus administration following a short-term suspension. The pathogenesis of tacrolimus-related encephalopathy is multifactorial, although refractory GVHD and a sudden increase in blood pressure seem to be major predisposing factors. Because the withdrawal of tacrolimus or switching to less potent anti-GVHD agents usually worsens the GVHD, the administration of tacrolimus should be managed by closely monitoring serum levels and controlling blood pressure.