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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pure motor stroke is the commonest lacunar syndrome, but it may be associated with nonlacunar mechanisms of infarction. Pure motor brachiofacial weakness has been considered as a partial syndrome depending on a lacunar mechanism. We studied the correlations between stroke type, topography of infarction and etiology in 22 patients with pure motor brachiofacial weakness who were consecutively admitted to our stroke unit during a 10-year period. Seventeen patients had a small deep infarct, 4 had a cortical infarct in the superficial MCA territory and 1 had no specific lesion. The part of the cardiovascular risk factors was about 36% for smoking, 13% for diabetes mellitus, 60% for dyslipidemia and 40% for heart disease. Hypertension was present in 75% of our cases. None of the patients had a large artery stenosis on Doppler ultrasonography. We concluded that brachiofacial pure motor stroke is not always correlated to lacunar infarcts and may be due to a cortical infarct. MRI should be performed when brain CT is normal because of the implications it may have in management and therapy.
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PMID:Brachiofacial pure motor stroke. 1143 77

Thirty years after its first description metabolic suppressive therapy is still controversial in patients with intractable intracranial hypertension. In this study high dose propofol was used to induce metabolic suppression. The effects on intracranial pressure (ICP) and the cerebral metabolic rates for oxygen and glucose (CMRO2 and CMRGlc) are reported. A total of 28 studies were performed on 14 head injured patients. A Xenon133 cerebral blood flow (CBF) and a CO2-reactivity (CO2R) test were performed prior to induction of metabolic suppression. The following parameters were continuously monitored: EEG, etCO2, SjvO2, ICP, MAP and bilateral MCA flow velocity (VMCA). PCO2 was obtained before and during propofol-induced EEG burst-suppression in arterial and jugular-venous blood. CMRO2, CMRGlc and Metabolic Ratio (MR = CMRO2/CMRGlc) were calculated. MR < 0.6 was defined as relative hyperglycolysis. ICP decreased by 24.1 +/- 29.0% during burst-suppression. Arterial, jugular-venous and etCO2 also decreased. Multiple regression analysis revealed that CO2 was the strongest predictor for ICP. Lower baseline ICP and normal CO2 reactivity were predictors for normal metabolic suppression reactivity. In studies with normal metabolic ratio, ICP reduction was associated with a reduction in CMRO2. In studies with hyperglycolysis, ICP reduction was poor but CMRGlc decreased significantly. In conclusion, intact CO2R, normal or only moderately elevated ICP and normal MR are predictive of ICP reduction with high dose propofol after head injury.
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PMID:Metabolic suppressive therapy as a treatment for intracranial hypertension--why it works and when it fails. 1216 59

The indexes of auxiliary laboratory diagnosis, including plasma norepinephine (NE) levels, plasma epinephrine (E) levels, mean blood flow velocity of the middle cerebral artery (MCA-Vm) and systolic blood flow velocity of the middle cerebral artery (MCA-Vs), were observed in patients with the syndrome of hyperactivity liver-yang. The results indicated that the levels of the 4 indexes were significantly higher in the patients with the syndrome of hyperactivity liver-yang than those in the controls. In hypertension patients with the syndrome of hyperactivity liver-yang, there was a positive correlation between symptomatic scores of the syndrome of hyperactivity liver-yang and diastolic pressure (Pd), plasma NE and E levels. The symptoms ameliorated, and the levels of the 4 indexes decreased correspondingly in 3 weeks after the treatment of Qianyangfang (a traditional Chinese herb).
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PMID:[Further study on the indexes of auxiliary laboratory diagnosis in the syndrome of hyperactivity of liver-yang]. 1257 3

A 25-year-old woman (gravida 1, para 0) who had no history indicating the toxemia of pregnancy developed hypertension and severe throbbing headache after the delivery of her first child by the cesarean section. Generalized tonic-clonic seizure ensued 5 days after the delivery, after which she did not fully regain her consciousness. Her head T2-weighted and FLAIR MRIs showed areas of multiple high intensities in the basal ganglia and cerebral white matter. Her cerebral MRA revealed the segmental stenosis and irregular wall of the major vessels, in particular of the right MCA trunk. Three weeks later, these abnormalities in the neuroimages disappeared and she was free of any symptoms. The history disclosed that obstetricians had used methylergometrine maleate for uterine contraction after delivery and then sumatriptan for her throbbing headache. We speculate that these vasoconstrictive agents might have induced the postpartum cerebral angiopathy. Postpartum cerebral angiopathy may be distinct from reversible posterior leukoencephalopathy in that the abnormalities are not restricted to the posterior lobes and that the vascular changes are apparent on neuroimagings. However, this entity might have a common underlying physiology, which is the abnormally elevated blood pressure that occurs in the setting of early postpartum period. Caution should be exercised when vasoconstrictives are to be used in postpartum period.
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PMID:[Postpartum cerebral angiopathy--a case report the vasculopathy associated with co-administration of two vasoconstrictives, methylergometrine maleate and sumatriptan]. 1519 57

The authors investigated the effects of phenylephrine-induced hypertension on the development of cerebral edema and neuronal dysfunction during focal cerebral ischemia. Mean arterial pressure was increased by 25-30 mm Hg immediately after middle cerebral artery occlusion (MCAO) in anesthetized rats. The increase was maintained for 3 h, at which time the brains were harvested and sectioned along coronal planes spanning the distribution of the MCA. The specific gravity (SG) was determined in specimens of cortex and subcortex. Brain sections adjacent to those used for SG measurement were incubated in 2,3,5-triphenyltetrazolium (TTC). There was edema formation in both groupsipsilateral to MCAO. However, in some regions, there was less edema accumulation in the induced hypertension group than in normotensive control animals. In adjacent regions, the area of reduced or absent TTC staining was also significantly less in the induced hypertension group. The data indicate that, in this model, induced hypertension established soon after the onset of ischemia can serve to reduce the area of histochemically detectable neuronal dysfunction, and that not only is edema formation not aggravated, but it is actually reduced.
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PMID:The influence of phenylephrine-induced hypertension during focal cerebral ischemia on the formation of brain edema. 1581 77

Nontraumatic arterial dissection of the anterior cerebral artery (NAD-ACA) is a relatively rare disease entity, although case reports have recently been increased. We treated 6 patients suffering from NAD-ACA from January 1996 to December 2003, and the neuroradiological findings together with the clinical courses were reviewed. There were 3 males and 3 females with a mean age of 57.7-year-old, ranging from 41 to 65. Five patients had a past history of hypertension and one diabetes mellitus. At the onset, all patients presented with clinical manifestations of cerebral ischemia. Among them, all exhibited contralateral hemiparesis with greater weakness of the lower extremity, and two patients exhibited headache. Initial angiography revealed the pearl and string sign in four patients and string sign, tapered occlusion in each one. Follow-up angiographies revealed sequential changes in all patients; four improved and two progressed. Main anatomic site of the lesion was as follows; five in the A2 and one in the A1 portion, in addition, one patient was complicated by saccular aneurysm, one by PCA dissection, and two had with saccular aneurysm contralateral ACA & MCA and VA dissection each other. Four patients were treated conservatively by intravenous administration of argatroban, one by intravenous administration of Dextrane and one by anti-platelet agent in the acute stage. All patients were treated by anti-platelet agents in the chronic stage. Good recovery was achieved in five patients, but one who suffered from severe subarachnoid hemorrhage in the chronic stage died. Our experience suggests that hypertension and/or the succeeding abnormal structural changes in the arterial wall may contribute to the occurrence of this disease. NAD-ACA showing clinical manifestations of cerebral ischemia could result in a relatively good prognosis; however, attention should be paid to patients treated conservatively with a very closed follow-up angiography to prevent a possibility of severe hemorrhage.
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PMID:[Nontraumatic arterial dissection of the anterior cerebral artery: six cases report]. 1602 47

Improving models of human stroke by the use of aged animals has been advocated; however the commonly used rat middle cerebral artery thread-occlusion model has produced suboptimal stroke induction and excess mortality in aged rats. We report the development of a modified method for silicone-coating the tip of occluding threads which produces a malleable silicone-coated tip which is firmly bonded and of highly consistent diameter, and overcomes problems of thread insertion through the narrowed carotid canal found in aged animals. Comparison of stroke outcomes and mortality were made between these threads and heat-treated poly-L-lysine coated threads. The rate of successful stroke induction in aged rats was significantly improved (from 14% to 86%). Similarly, mortality fell from 21-31% to 3-7% or less in both young and old rats with or without diabetes and hypertension. An occluding thread tip diameter of 0.35-0.38 mm was optimal for induction of mid-sized strokes in both young and old rats. This method of thread manufacture overcomes problems of inconsistency of diameter and bonding of the silicone-coated tip, and these threads produce significant improvements in stroke induction by MCA occlusion, particularly in aged animals and those with co-morbidities.
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PMID:Modification of the method of thread manufacture improves stroke induction rate and reduces mortality after thread-occlusion of the middle cerebral artery in young or aged rats. 1651 79

Maintaining cerebrovascular function is a priority for reducing damage following acute ischemic events such as stroke, and under chronic stress in diseases such as hypertension. Ischemic episodes lead to endothelial cell damage, deleterious inflammatory responses, and altered neuronal and astrocyte regulation of vascular function. These, in turn, can lead to impaired cerebral blood flow and compromised blood-brain barrier function, promoting microvascular collapse, edema, hemorrhagic transformation, and worsened neurological recovery. Multiple studies demonstrate that protein kinase C (PKC), a widely expressed serine/threonine kinase, is involved in mediating arterial tone and microvascular function. However, there is no clear understanding about the role of individual PKC isozymes. We show that intraperitoneal injection of deltaV1-1-TAT(47-57) (0.2 mg/kg in 1 mL), an isozyme-specific peptide inhibitor of deltaPKC, improved microvascular pathology, increased the number of patent microvessels by 92% compared to control-treated animals, and increased cerebral blood flow by 26% following acute focal ischemia induced by middle cerebral artery occlusion in normotensive rats. In addition, acute delivery of deltaV1-1-TAT(47-57) in hypertensive Dahl rats increased cerebral blood flow by 12%, and sustained delivery deltaV1-1-TAT(47-57) (5 uL/h, 1 mM), reduced infarct size by 25% following an acute stroke induced by MCA occlusion for 90 min. Together, these findings demonstrate that deltaPKC is an important therapeutic target for protection of microvascular structure and function under both acute and chronic conditions of cerebrovascular stress.
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PMID:DeltaPKC mediates microcerebrovascular dysfunction in acute ischemia and in chronic hypertensive stress in vivo. 1735 Jun 2

Spontaneous intracranial artery dissection (SIAD), leading to occlusion or stenosis of arterial lumen is a frequent but less studied cause of ischemic stroke especially in young adults. We studied 17 patients (10 men, 7 women, mean age 27.5 +/- 8.5 years) with SIAD. All the patients have undergone magnetic resonance imaging of the head, magnetic resonance angiography (MRA) (in 16 patients--follow-up MRA), 1 patient--conventional cerebral angiography. SIAD was located in the middle cerebral artery (MCA, 14 patients); posterior cerebral artery (PCA, 2 patients) and basilar artery (BA, 1 patient). Fifteen patients (88%) with SIAD developed ischemic stroke, 2 patients (12%)--a transient ischemic attack (TIA). The appearance of the local brain ischemia symptoms was combined with headache in 93% cases. The course of ischemic stroke was favorable in most cases with complete or good functional recovery in 66% of patients. A fatal outcome was observed in 1 patient (7%) with massive brain infarct. The initial cerebral angiography carried out in most cases (76%) within 3 weeks after the disease onset revealed occlusion (71%) or stenosis (29%) of corresponding cerebral arteries (MCA, PCA, BA). The last cerebral angiography conducted in 90% cases 4,5 months or later showed positive dynamics--appearance or improvement of the blood flow in these arteries--in 82% patients. The factors provoking SIAD were alcohol, contraceptive drugs and less frequent recent infection. None of patients had atherosclerosis, vasculitis or arterial hypertension. Clinical manifestations of connective tissue weakness were in 71% of patients, hypotension--65%, mitral valve prolapse--46%. In conclusion, SIAD is one of the causes of ischemic stroke and TIA in young adults and characteristic clinical manifestations and follow-up MRA have a great diagnostic importance. The development of SIAD appears to be related to weakness of connective tissue of arterial wall.
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PMID:[Spontaneous intramural intracranial artery dissection and ischemic stroke]. 1819 22

Cortical ischemic stroke affecting the precentral "hand knob" area is a rare but well known stroke entity. To date, little is known about the underlying stroke mechanisms and the prognosis. Twenty-nine patients admitted to our service between 2003 and 2007 were included in the study on the basis of an acute ischemic infarct of the cortical "hand knob" area confirmed by diffusion-weighted magnetic resonance imaging with contralateral hand paresis. For all patients clinical, epidemiological as well as imaging data at the time point of admission were analysed retrospectively and follow-up data on all patients was obtained. The majority (n = 21/72%) had an isolated infarct of the cortical "hand knob" area. In 23 (79%) patients it was a first ever stroke. Ten patients (34%) had ipsilateral extracranial stenosis of the internal carotid artery (ICA), whereas potential cardiac embolic sources were less frequent (n = 4/14%). No patient exhibited ipsilateral MCA stenosis. All but two patients (93%) had marked atherosclerotic alterations of the ICA. Hypertension was the most prevalent vascular risk factor (n = 23/79%). At follow-up (mean 25.0 months, range 0.4-47.4 months) no patient had died and only one (3%) experienced a recurrent stroke. The majority of patients (79%) reported improvement of hand paresis, 17 (59%) were asymptomatic (modified Rankin score = 0). Only one patient was significantly disabled due to a recurrent stroke. In conclusion, ischemic infarcts affecting the cortical "hand knob" area are frequently associated with atherosclerotic changes of the carotid artery, suggesting an arterio-arterial thrombembolic stroke mechanism. It mostly reflects first ever ischemic stroke, and follow-up data suggest a rather benign course.
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PMID:Ischemic stroke of the cortical "hand knob" area: stroke mechanisms and prognosis. 1935 29


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