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

Intracranial hypertension is the final common denominator of morbidity and mortality for diverse neurologic problems, and its proper treatment requires the heuristic application of the available therapeutic alternatives when the clinical situation and patient's prognosis warrants treatment. The initial therapeutic focus for ICP reduction should be control of factors that may aggravate intracranial hypertension such as inappropriate head and body position, elevated body temperature, pain, noxious stimuli, elevated airway pressure, elevated blood pressure, seizures, and hypotonic intravenous fluids. The appropriate conventional therapies (e.g., hyperventilation, osmotic agents, sedatives, barbiturates, and cerebrospinal fluid removal) should be selected based on the details of each individual case. Surgical removal of intracranial mass lesions may be indicated in some circumstances, particularly for intractable intracranial hypertension and progressive, severe brain tissue shifts.
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PMID:Management of intracranial hypertension. 841 24

Sixteen patients were treated with shunting of cerebrospinal fluid (CSF) from the cisterna magna for raised intracranial pressure (15 cases) or CSF leak (one case). There were 11 patients with benign intracranial hypertension, three with craniostenosis, one with chronic meningitis and one with a CSF leak. Cisternal shunting was effective in all cases and obviated the problems of low pressure and sciatica found with lumbar-peritoneal shunts. There were 11 revisions over a total of 31.5 shunt years (i.e. one per 2.9 shunt years). The role of cisternal shunting in neurosurgical practice is discussed.
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PMID:CSF shunting from the cisterna magna: a report of 16 cases. 843 44

To successfully match the treatment to the cause for raised intracranial pressure (ICP) after a severe head injury, it is important to know the underlying mechanism at a given moment for the raised pressure. In particular, it is important to distinguish between active cerebral vasodilation, indicating functional autoregulation, and a passive vascular dilation as the cause for raised ICP. An experimental study was performed in feline models of diffusely raised ICP (n = 6), of active arterial vasodilation caused by arterial hypercarbia (n = 6), and of passive arterial dilation caused by pharmacologically induced arterial hypertension (n = 6) to determine if wave form analysis of ICP can distinguish active from passive arteriolar vasodilation. Pulsatile pressure transmission from the blood pressure pulse to the ICP pulse (cerebrovascular pressure transmission [CVPT]), cerebrovascular resistance, and craniospinal compliance were measured simultaneously at each level of raised ICP, arterial hypercarbia, and arterial hypertension. Arterial hypercarbia, caused by both 5 and 10% inspired CO2 increased low-frequency CVPT, which was followed by an increasingly negative phase shift between the blood pressure and ICP wave form (P < 0.05). Diffusely raised ICP caused by intraventricular infusion of mock cerebrospinal fluid caused increased low-frequency CVPT (P < 0.01) but resulted in no overall change in phase shift, although the sign of the phase shift remained negative. After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). These data demonstrate it may be possible to distinguish active arteriolar vasodilation from a passive loss of autoregulatory vascular tone through simultaneous measurement of the low-frequency CVPT and phase shift. Analysis of the ICP wave form provides information relevant to the management of raised ICP.
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PMID:An experimental study of cerebrovascular resistance, pressure transmission, and craniospinal compliance. 812 65

An idiopathic syndrome of acquired hyperopia with choroidal folds has been characterized. Orbital imaging correlates of this syndrome include flattening of the posterior globe and distention of the perioptic subarachnoid space. The mechanism responsible for the clinical and radiographic findings of this syndrome is undefined. Two patients with unusual presentations of papilledema are reported whose clinical and radiographic findings were otherwise identical to those described in the idiopathic syndrome of acquired hyperopia with choroidal folds. One patient had unilateral disc edema and bilateral choroidal folds. The other patient had bilateral choroidal folds observed 2 years before he developed papilledema in both eyes. Both patients had intracranial hypertension, idiopathic in the first, and related to severe chronic obstructive pulmonary disease and cor pulmonale in the second. A third patient is also described who had typical clinical and orbital imaging findings of idiopathic unilateral acquired hyperopia with choroidal folds. He was also found to have mild intracranial hypertension. Intracranial hypertension can cause acquired hyperopia and choroidal folds and may be the underlying mechanism in some patients with what appears to be idiopathic acquired hyperopia with choroidal folds.
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PMID:Intracranial hypertension and the syndrome of acquired hyperopia with choroidal folds. 857 65

We report a case of diffuse leptomeningeal gliomatosis which spread from the cervical to the sacral spine. A 60-year-old man was admitted with visual disturbance due to papilledema. Magnetic resonance imaging revealed holocord leptomeningeal gliomatosis without a definite intraparenchymal lesion, and the patient's neurological examination was unremarkable except for papilledema. Intracranial hypertension secondary to spinal tumor is well known but unusual, and the mechanism is still unclear. In our case, an elevated protein concentration of cerebrospinal fluid is suggested as the cause of intracranial hypertension.
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PMID:Primary spinal leptomeningeal gliomatosis presenting visual disturbance as the initial symptom: case report. 873 1

The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 +/- 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 +/- 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all < or = 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.
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PMID:Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome. 889 12

Intracranial hypertension is not a definitive diagnosis, but rather a syndrome that may result from a number of neurologic and systemic disorders. Intracranial hypertension refers to prolonged elevation of intracranial pressure, generally above 200 mm H2O. This condition may be recognized by the various clinical signs and symptoms that are manifest in most patients, including headache, papilledema, transient visual obscurations, diplopia, ocular motor disorders, tinnitus, nausea, vomiting, and mental irregularities, as well as dysfunctions of the circulatory and respiratory systems. Thorough medical testing as well as a comprehensive ocular evaluation is indicated in these cases. Intracranial hypertension most commonly results from mass lesions, tension hydrocephalus, and pseudotumor cerebri. Other causes include disorders of venous outflow, such as dural sinus thromboses or arteriovenous malformations, and various encephalopathies. Management for intracranial hypertension may involve medical treatment, drug therapy, or surgical intervention. Typically, diuretics are used initially. Corticosteroids may be used as well, although they are not the first choice for treatment. Cerebrospinal fluid shunting procedures may be necessary if medical treatment fails. Optic nerve sheath decompression may also be attempted when chronic papilledema threatens visual function. It is important that the primary care optometrist recognize the manifestations of intracranial hypertension in order to make necessary referrals for management of the underlying etiologies.
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PMID:Intracranial hypertension. 897 12

In children with craniosynostosis, raised intracranial pressure (ICP) and upper airway obstruction (UAO) are both common features. However, potential interactions between UAO and ICP during sleep are poorly understood. The aim of the present study was to compare the levels of ICP during sleep between a group of patients with syndromic craniosynostosis (with facial involvement and consequent UAO) and a group of control patients with isolated unicoronal synostosis (with no facial involvement and normal upper airways). Polygraphic cardiorespiratory sleep studies with continuous monitoring of ICP were performed during unsedated sleep in 13 children with syndromic craniosynostosis and 7 control patients with isolated unicoronal synostosis only. In the syndromic group, UAO was present in 11 out of 13 patients, with 8 out of 13 having frank obstructive sleep apnoea. In contrast, none of the control patients showed signs of UAO during sleep. There was no evidence of central apnoeas in any of the patients studied. Clinical histories taken from parents tended to underestimate the severity of the respiratory problems. Elevated ICP was seen in 10 of the 13 syndromic patients, with borderline raised ICP in the remaining three cases. In contrast, raised ICP was seen in only 3 of the 7 control patients, with borderline raised levels in 2 of the 7. For both patient groups, ICP was higher during active sleep compared to quiet sleep. Multiple regression analysis showed that ICP during active sleep was dependent upon disease severity (unicoronal/ multiple synostosis) and to the baseline ICP level during quiet sleep. Both raised ICP and airway obstruction were more apparent during active sleep. There was a significant correlation between severity of UAO and increased ICP in active sleep. We conclude that obstructive respiratory problems are frequent in the syndromic patients, and can be severe in a large proportion of cases; intracranial hypertension is also frequent in this group. Further studies are required to investigate the possibility of a causal relationship between upper airway obstruction and raised intracranial pressure.
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PMID:Upper airway obstruction and raised intracranial pressure in children with craniosynostosis. 904 34

Head elevation is a conventional nursing intervention used to control raised intracranial pressure and avoid complications in patients with neurotrauma or other conditions requiring management of intracranial hemodynamics. This therapy, however, provides a particular dilemma for health care providers. While elevating the head of the bed does decrease intracranial pressure, it may put some patients at risk for intracranial hypertension and cerebral ischemia due to decreases in cerebral perfusion pressure. This article analyzes research on head positioning that provides individual outcome measurements versus group means in adult patients with various conditions. The risk/benefit method of analysis used in this review revealed that in addition to only monitoring and controlling for ICP, we must also monitor and control CPP with a greater emphasis on this particular measurement. This analysis also revealed that optimal head positioning to manage intracranial hemodynamics should be decided upon on an individual basis using both ICP and CPP measurements.
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PMID:Management of intracranial hemodynamics in the adult: a research analysis of head positioning and recommendations for clinical practice and future research. 906 53

Two patients with meningoradiculitis associated with HIV presented with symptoms and signs of intracranial hypertension. In the patients described, the raised intracranial pressure resolved after lumbar puncture. After exclusion of opportunistic infection, such patients may be managed with therapeutic lumbar puncture alone.
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PMID:Intracranial hypertension and HIV associated meningoradiculitis. 912 Apr 63


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