idiopathic intracranial hypertension

(redirected from meningitis serosa)

pseu·do·tu·mor ce·re·bri

a disorder most commonly seen in obese young women, characterized clinically by headache, blurred vision, and visual obscurations resulting from increased intracranial hypertension; on clinical examination, papilledema is detected but on neuroimaging studies there is no evidence of an intracranial mass lesion and the ventricles are either of normal size or small; if untreated, occasionally results in permanent visual loss; of an unknown cause.
Farlex Partner Medical Dictionary © Farlex 2012

idiopathic intracranial hypertension

A neurological disorder characterised by an idiopathic increase in intracranial pressure in the absence of organic disease; it is more common in young women, especially if obese.
Clinical findings
Headache, nausea, vomiting, pulsatile tinnitus, double vision and other visual symptoms; with time, swelling of the optic disc and blindness.
Brain scan and a lumbar puncture to exclude organic disease.

Acetazolamide, or surgery to relieve the pressure.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.


(hi?per-ten'shon ) [ hyper- + tension],


In adults, a condition in which the blood pressure (BP) is higher than 140 mm Hg systolic or 90 mm Hg diastolic on three separate readings recorded several weeks apart. Hypertension is one of the major risk factors for coronary artery disease, heart failure, stroke, peripheral vascular disease, kidney failure, and retinopathy. It affects about 50 million people in the U.S. Considerable research has shown that controlling HTN increases longevity and helps prevent cardiovascular illnesses. Synonym: high blood pressure See: blood pressurehypertensive (hi?per-ten'siv), adjective

All systems for categorizing high BP are somewhat arbitrary, but the current consensus is that normal BPs are < 120 mm Hg systolic and < 80 mm Hg diastolic. Borderline high BPs (prehypertension) are between 120 and 139 mm Hg systolic and 80 to 89 mm Hg diastolic. Patients with BP readings between 140/90 and 160/100 mm Hg are said to have stage 1 HTN.

Stage 2 HTN is a pressure from 160/100 to 179/109 mm Hg. Stage 3 HTN begins at 180/110 mm Hg and has no upper limit. At each stage of HTN, from prehypertensive levels through the three stages of HTN, the risks of strokes, heart attacks, and kidney failure increase. See: table

Hypertension in children has been defined as BP above the 95th percentile for age, height, and weight. As many as 28% of children have secondary HTN compared to 1% to 5% in adults.


Hypertension results from many different conditions, some curable and others treatable. Curable forms of HTN (secondary HTN), which are relatively rare, may be caused by coarctation of the aorta, pheochromocytoma, renal artery stenosis, primary aldosteronism, and Cushing's syndrome. Excess alcohol consumption (more than two drinks daily) is a common cause of high BP; abstinence or drinking in moderation effectively lowers BP in these cases. Aortic valve stenosis, pregnancy, obesity, and the use of certain drugs (such as cocaine, amphetamines, steroids, or erythropoietin) also may lead to hypertension. Usually, however, the cause is unknown; then high BP is categorized as primary, essential, or idiopathic. Primary hypertension may result from the body's resistance to the action of insulin, hyperactivity of the sympathetic nervous system, hyperactivity of the renin-angiotensin-aldosterone system, or endothelial dysfunction.


Hypertension is usually a silent (asymptomatic) disease in the first few decades of its course. Because most patients are symptom-free until complications arise, they may have difficulty taking seriously a condition from which they perceive no immediate danger. Occasionally, patients with HTN report headache. When complications result from high BPs, patients mention symptoms referable to the affected organs.


If HTN is newly diagnosed, routine studies should be done on the patient to establish a baseline for treatment. In addition to a thorough patient history, assessment for risk factors, and physical examination, these studies include an ECG, urinalysis, serum potassium and calcium levels, blood urea nitrogen, fasting glucose level, and cholesterol profile, including triglycerides. The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC) guidelines to reduce cardiovascular disease complications recommends a target blood pressure of less than 140/90; 130/80 for patients with diabetes mellitus or renal disease. Because HTN has been identified as a growing concern among children, the JNC recommends regular BP checks beginning at age 3. Lifestyle modifications that lower BP include dietary sodium restriction to about 2 g/day, made possible by avoiding salted food such as ham, potato chips, and processed foods and by not adding salt to food at the table; maintaining a healthy weight (a body mass index above 24.9 can elevate BP); eating lower-calorie foods; restricting total cholesterol and saturated fat intake; quitting smoking; limiting alcohol intake (to about one drink daily); and participating in a program of regular exercise. When lifestyle modifications fail over the course of several months to control BP naturally, medications should be used. Drug therapy for stage 1 HTN includes low-dose thiazide diuretics for most patients, although angiotensin converting enzyme (ACE) inhibitors, beta blockers, calcium channel blockers or a combination of these may be prescribed. For stage 2 HTN, two-drug combinations are prescribed for most patients, usually a thiazide-type diuretic along with a beta blocker, ACE inhibitors, angiotensin receptor blockers, alpha blockers, or centrally active alpha blocking agents. If a woman develops HTN during pregnancy, treatment should be with methyldopa, a beta blocker, or a vasodilator, as these drugs provide the least risk to the fetus. See: table pregnancy-induced hypertension

Patient care

Blood pressure should be checked at every health care visit, and patients should be informed of their BP reading and its meaning. Positive lifestyle changes should be encouraged. Adherence to medical regimens is also emphasized, and patients are advised to inform their health care providers of any side effects of therapy that they experience because these can often be managed with dosage adjustment or a change in medication. The technique of home BP monitoring is taught to receptive patients. Pressures should be measured and recorded for both arms, unless there is a medical prohibition for one arm, indicating which arm was used for each reading.

accelerated hypertension

A significant increase in BP, with some evidence of vascular damage on funduscopic examination of the retina. Prompt treatment is indicated to prevent organ damage. See: malignant hypertension

benign intracranial hypertension

Pseudotumor cerebri.

chronic thromboembolic pulmonary hypertension

Abbreviation: CTEPH
Pulmonary HTN that results from the migration of blood clots (usually from the lower extremities) into the lungs. Elevated BP in the lungs gradually overloads the right ventricle and causes right-sided heart failure.


Symptoms usually include shortness of breath, esp. during exercise.


The disease, when identified, may be treated with surgical removal of blood clots.

cuff-inflation hypertension

A marked increase in BP in association with inflation of the sphygmomanometer cuff. This does not represent true hypertension.

drug-resistant hypertension

Resistant hypertension.

essential hypertension

Hypertension that develops without apparent cause. Synonym: primaryhypertension

gestational hypertension

High BP developing after 20 weeks of pregnancy. It may be mild; it often resolves after delivery, and it usually does not produce proteinuria or other features of preeclampsia.

Goldblatt hypertension

See: Goldblatt, Harry

idiopathic intracranial hypertension

Pseudotumor cerebri.

intra-abdominal hypertension

Abbreviation: IAH
An increase in measured abdominal pressures, from a normal of 0 mm Hg to levels between 15 and 20 mm Hg. It may occur in patients with multiple traumatic injuries to the abdomen or with intraperitoneal diseases, e.g., severe pancreatitis. It is associated with the development of abdominal compartment syndrome, shock, and multiple organ failure.

intracranial hypertension

Abbreviation: ICH
An increase in the pressure inside the skull from any cause such as a tumor, hydrocephalus, intracranial hemorrhage, trauma, infection, or interference with the venous flow from the brain. See: hydrocephalus


Patients with intracranial HTN should not undergo a lumbar puncture or any other procedure that decreases the cerebrospinal fluid pressure in the vertebral canal.

malignant hypertension

A form of HTN that progresses rapidly, accompanied by severe vascular damage. It may be life-threatening or cause stroke, encephalopathy, cardiac ischemia, or renal failure.

masked hypertension

Elevated BP that is not identified during professional evaluations in the office but only during ambulatory home blood pressure monitoring.

ocular hypertension

Increased intraocular pressure, typically exceeding 21 mm Hg. This condition, present in glaucoma, may predispose affected persons to optic nerve damage and visual field loss.

permissive hypertension

The temporary ignoring of the treatment of elevated blood pressures in patients with acute stroke or transient ischemic attack (TIA).


In these conditions the rapid lowering of blood pressure to normal ranges (< 140/90 mm Hg) may worsen neurological deficits.

portal hypertension

Hypertension in the portal vein caused by an obstruction of the flow of blood through the liver. It is found in diseases such as cirrhosis, in which it is responsible for ascites, splenomegaly, and the formation of varices.

pregnancy-induced hypertension

Abbreviation: PIH
High blood pressure, proteinuria, and edema occurring during pregnancy. Diagnostic criteria include an increase of 30 mm Hg systolic or 15 mm Hg diastolic over the baseline pressure for the individual woman (or readings of 140/90) on two assessments with at least a 6-hr interval between measures; edema; and proteinuria of at least 300 mg/24 hr. PIH occurs most commonly in the late second trimester or last trimester, but it may manifest earlier in women with molar pregnancies. It is potentially life-threatening and may worsen rapidly and, if untreated, develop into eclampsia. See: eclampsia; HELLP syndrome; preeclampsia


The cause of PIH is unknown, but there are several major contributing theories: vasoconstriction and vasospasm, and a possible imbalance between prostaglandins, prostacyclin, and thromboxane A2. The incidence is higher among adolescent and older primigravidas, diabetics, and women with pre-exisitng vascular problems or multiple pregnancies. Geographical, ethnic, racial, familial, low socioeconomic, nutritional, and immunological factors may contribute to PIH. Characteristic complaints include sudden weight gain, severe frontal headaches, and visual disturbances. Indications of increasing severity include complaints of epigastric or abdominal pain; generalized, presacral, and facial edema; oliguria; and hyperreflexia.

The treatment consists of bedrest, a high-protein diet, and medications including mild sedatives, antihypertensives, and intravenous anticoagulants if indicated. Complications are HELLP syndrome (hemolysis, elevated liver enzymes and low platelets) and eclampsia (the convulsive form of PIH).

Patient care

To enable the woman to actively participate in her health maintenance, reduce the potential for development of PIH, and facilitate early diagnosis and treatment, the health care provider should emphasize the importance of regular prenatal visits and good prenatal nutrition. Signs to report promptly are identified with the patient: sudden weight gain, swelling of the hands and face, headache, pitting edema of the ankles and legs, and reduced urine output.

At each prenatal visit, the pregnant woman's BP is monitored. The patient also is assessed for albuminuria; weekly weight gain of more than 3 lb (1.36 kg) in the second trimester or more than 1 lb (0.45 kg) in the third trimester; and generalized edema, esp. of the face and hands, and pitting edema of the ankles and legs. Protein intake is monitored to ensure adequate maternal serum protein levels, normal oncotic pressure, limitation of edema formation, and normal fetal development.

As preeclampsia progresses, the woman may complain of headaches, blurred vision or other visual disturbances, epigastric pain or heartburn, chest pressure, irritability, emotional tension, and decreased fetal activity. The patient is assessed for hyperreflexia of the deep tendon reflexes and clonus, and, if preeclampsia worsens, for oliguria. The goals of treatment are to stop progress of the condition and to ensure survival of the fetus and the mother's health.

Hospitalization may be necessary if the patient exhibits signs of moderate to severe preeclampsia and has failed to respond to home management. Intravenous magnesium sulfate may be given, first as a bolus and continued as a maintenance dose, until the severity of the disease decreases. If magnesium sulfate is used, the patient must be assessed frequently for the presence of deep tendon reflexes, respirations over 12 per minute, hourly urine output, and signs and symptoms of magnesium toxicity. Calcium gluconate, if needed, is the antidote for magnesium sulfate.

The clinical status of mother and fetus is continually evaluated; maternal vital signs and fetal heart rate are monitored. The patient is assessed for impending labor, and fetal and maternal responses to labor contractions are evaluated. The obstetrician is notified of any change in the patient's or the fetus' condition. Emergency care is provided during convulsions; prescribed medications are administered as directed, and patient and fetal response are evaluated. Careful monitoring of the administration of magnesium sulfate, intake and output, and the woman's response to the medication are necessary. Health care providers should be esp. alert for signs of toxicity, e.g., an absence of patellar reflexes (hyporeflexia), flushing, and muscle flaccidity.

Psychological support and assistance to develop effective coping strategies are provided to both patient and family, who are to be prepared for possible premature delivery. Cesarean birth or oxytocin induction may be required. Although infants of mothers with PIH are usually small for gestational age, they sometimes fare better than other premature infants of similar weight because they have developed adaptive ventilatory and other responses to intrauterine stress.

primary hypertension

Essential hypertension.

pulmonary hypertension

Hypertension in the pulmonary arteries (above 25 to 30 mm Hg). Primary pulmonary hypertension is a rare familial illness in which small pulmonary arteries become blocked as a result of abnormalities in the structure of blood vessels in the lung. Secondary pulmonary hypertension is an elevation in pulmonary artery pressure as a result of left ventricular failure, blood clots in the pulmonary arteries, or chronic lung diseases.

rebound hypertension

Hypertension after withdrawal of an antihypertensive drug.

renal hypertension

1. Hypertension produced by kidney disease. It is caused by alteration in the renal regulation of sodium and fluids or by alteration in renal secretion of vasoconstrictors, which alter the tone of systemic or local arterioles.
2. Hypertension produced experimentally by constriction of renal arteries. It is due to a humoral substance (renin) produced in an ischemic kidney.

renovascular hypertension

Hypertension that is caused by decreased blood flow through one or both renal arteries and that normalizes after angioplasty or surgery to open the affected artery. It is an uncommon but surgically treatable form of high blood pressure.

resistant hypertension

Hypertension that does not normalize with the use of a diuretic medication plus optimal doses of two additional antihypertensive drugs.
Synonym: drug-resistant hypertension.

venous hypertension

Hypertension in the legs of patients with venous insufficiency. Its hallmark is pain in the legs when the patient is standing or sitting and dangling his legs but not when lying down.

white coat hypertension

A colloquial term for an episode of hypertension when the reading is taken by a health care professional. It is attributed to anxiety over medical examination procedures or fear of possible findings.
*Not taking antihypertensive drugs and not acutely ill. When systolic and diastolic BPs fall into different categories, the higher category should be selected to classify the person's BP status. For example, 160/92 mm Hg should be classified as stage 2 HTN, and 174/120 mm Hg should be classified as stage 3 HTN. Isolated systolic HTN is defined as systolic BP of 140 mm Hg or greater and diastolic BP below 90 mm Hg and staged appropriately (e.g., 170/82 mm Hg is defined as stage 2 isolated systolic HTN). In addition to classifying stages of HTN on the basis of average BP levels, clinicians should specify presence or absence of target organ disease and additional risk factors. This specificity is important for risk classification and treatment. † Optimal blood pressure with respect to cardiovascular risk is below 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance. ‡ Based on the average of two or more readings taken after a period of rest and using the correct techniques at each of two or more visits after an initial screening. SOURCE: Adapted from the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High BP, NIH publication No. 98-4080, November 1997, and other sources.
CategorySystolic (mm Hg)Diastolic (mm Hg)
Stage 1140–159or90–99
Stage 2160–179or100–109
Stage 3= 180or= 110
InterventionApproximate Decrease (in mm Hg)
Weight loss (20 pounds)5 - 10
Dietary approaches to stop hypertension (DASH) diet8 - 14
Regular exercise4 - 9
Reducing sodium intake2 - 8
Limiting alcohol intake to one or two drinks a day2 - 4
Medical Dictionary, © 2009 Farlex and Partners
References in periodicals archive ?
INTRODUCTION: Idiopathic intracranial hypertension (IIH) was first described by Quincke under the name 'meningitis serosa' in 1897.
(1.) Quincke H (1897) [Uber meningitis serosa und verwandete Zustande.] Deutsche Zeitschrift fur Nervenheilkunde, 9, 140-68.