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At least 19 recordsLinked to original sources
PubMed2002

A new classification and a synergetical pattern in intracranial hypertension.

Intracranial hypertension develops from the initial cerebral effect of increased intracranial pressure and becomes symptomatical; then it acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increases in intracranial pressure (ICP) can be compensated and the ICH disease is in its acute form, equivalent to a decompensated ICH syndrome. Based on the etiopathogenesis of intracranial hypertension, a new classification is proposed: parenchymatous intracranial hypertension with an intrinsic cerebral cause; vascular intracranial hypertension, which has its etiology in disorders of the cerebral blood circulation; and essential or idiopathic intracranial hypertension, the former pseudotumor cerebri, an incomplete ICH syndrome. A synergetical pattern of the ICH is based on the relation between ICP and the period of high-pressure action: the critical pressure--time fluctuation causes the autoregulation of the cerebral blood flow to decrease or determines the brain herniation. The decompensation is a state of instability and appears when the intrinsic ratio of pressure--time fluctuation is changed: the high ICP lasts longer than the corresponding normal ICP, or the ICP is higher than the one that normally lasts the same period of time.

Cerebrovascular Circulation↗
PubMed1998

[Intracranial hypertension].

Intracranial hypertension is a serious consequence of the impaired intracranial volume homeostasis. It can be encountered in practically all fields of clinical praxis. The article reviews bibliographic data of the mechanisms of the intracranial hypertension development: Intracranial expansion, Brain edema, Hemodynamic brain edema, Liquor accumulation--hydrocephalus. A pathophysiological approach to the hypotheses of edema and brain swelling is stressed. Outlines of the modern diagnostics and therapy of the intracranial hypertension are presented.

Humans↗
PubMed1996

Intracranial hypertension.

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.

Combined Modality Therapy↗
PubMed1983

[Intracranial hypertension].

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.

Brain Neoplasms↗
PubMed1994

Glomus jugulare tumors masquerading as benign intracranial hypertension.

Intracranial hypertension has been reported as a complication of massive glomus jugulare tumors with intracranial extension. We describe a patient with papilledema, failing vision, and a diagnosis of benign intracranial hypertension with bilateral glomus jugulare tumors that went undetected for 2 years. There was no evidence of intracranial invasion by the tumors to explain the elevation of intracranial pressure. Embolization followed by surgical removal of the left tumor resulted in stabilization of the neurologic condition and preservation of the lower cranial nerves, including intact hearing. The likely mechanism of intracranial hypertension in this case is an impairment of cerebrospinal fluid absorption. This unusual presentation should be recognized to avoid delayed diagnosis and treatment. Furthermore, intracranial hypertension is not always associated with massive intracranial tumor involvement, as had been previously proposed.

Adult↗
PubMed1993

Management of intracranial hypertension.

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.

Brain↗
PubMed1982

Effect of labetalol on intracranial pressure in dogs with and without intracranial hypertension.

Intracranial pressure measurements and ventricular volume pressure response curves were made during induced hypotension with labetalol, a combined alpha- and beta-adrenoceptor antagonist, in dogs without (group I) and with (group II) intracranial hypertension. The administration of 600 mg labetalol resulted in a percentage decrease of mean systemic arterial blood pressure (MAP) of 27% (+/- 10%) in group I, and 32% (+/- 9%) in group II from control values without changes in intracranial pressure and the ventricular volume pressure response curve. Larger decreases in MAP were not possible, even with a dose 3 times that clinically recommended. Labetalol may be a safe hypotensive agent to supplement neurolept analgesia, but it is not the drug of choice to induce deliberate hypotension.

Animals↗
PubMed1997

[The internal environment and intracranial hypertension].

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.

Acidosis, Lactic↗
PubMed1983

Furosemide and mannitol in the treatment of acute experimental intracranial hypertension.

Intracranial hypertension was induced in dogs and a small number of baboons by the inflation of epidural balloons. The resulting increased intracranial pressure (ICP) was treated with standard clinical doses of furosemide (0.7 mg/kg), "mini" doses of mannitol (0.75 g/kg), or both agents in combination. Mannitol consistently and rapidly reduced ICP in all animals. When results were averaged, furosemide used alone caused a slow reduction in ICP, but the results were variable in individual animals--with ICP actually increased in some. When furosemide and mannitol were given together, the ICP fell rapidly and remained low for considerably longer than after either agent alone.

Animals↗
PubMed1997

[Slow pressure waves during intracranial hypertension].

Intracranial pressure waves include fast waves (pulse and respiration) and slow waves. Only the latter are considered here. Since the definition of three wave types in the pioneering works of Janny (1950) and Lundberg (1960), their study of frequential characteristics shows they are included in a spectrum where three contiguous frequency bands are individualised: the B wave band (BW) between 8 x 10(-3) Hz and 50 x 10(-3) Hz; the Infra B band (IB) below 8 x 10(-3) Hz; and the Ultra B band (UB) beyond 50 x 10(-3) Hz to 200 x 10(-3) Hz. The origin of these waves is vascular and some may be physiological. They are probably generated by central neuro-pacemakers and/or cyclic phenomena of cerebral autoregulation. They are linked with slow peripheral arterial pressure waves, with biological rhythms and with biomechanics and vasomotricity in the craniospinal enclosure. They are pathological for the slowest (IB), particularly if they are plateau waves, but the physiologic-pathologic boundary is not yet established for each type of slow waves. They can cause severe consequences if they result in major cerebral perfusion pressure changes, and if they induce or worsen herniations.

Biomechanical Phenomena↗
PubMed2003

Differential diagnosis of patients with intracranial sinus venous thrombosis related isolated intracranial hypertension from those with idiopathic intracranial hypertension.

In patients presenting with intracranial hypertension without hydrocephalus, mass lesions, and with normal cerebrospinal fluid (CSF) composition (pseudotumor cerebri syndrome), the diagnosis of intracranial sinus venous thrombosis (ISVT) has crucial etiological, therapeutic and prognostic implications. Utilizing two well-defined groups of pseudotumor cerebri patients, one with magnetic resonance imaging (MRI) or angiography confirmed ISVT (17 patients) and the other in whom ISVT has been excluded (idiopathic intracranial hypertension [IIH], 27 patients), we investigated the characteristics that might be helpful in distinguishing them. No clinical or auxiliary findings differed between the ISVT and IIH groups except for female gender and lower CSF protein level, which were significantly associated with the latter. While the syndrome pseudotumor cerebri could be due to multiple causes including ISVT, the term IIH should be restricted for patients with isolated intracranial hypertension attributable to no other neurological or systemic disease. Since CT frequently misses ISVT, patients with pseudotumor cerebri syndrome should undergo MRI and MR venography before being labeled as IIH. We conclude that Modified Dandy's Diagnostic Criteria of pseudotumor cerebri, formulated prior to MRI era, can no longer be applied for the diagnosis of IIH.

Adolescent↗
PubMed1989

Alteration of intracranial pressure, cerebral blood flow, autoregulation and carbondioxide-reactivity by hypotensive agents in baboons with intracranial hypertension.

Intracranial pressure (ICP) was recorded by epidural transducer and cisterna magna catheter, and regional cerebral blood flow (rCBF) using the intraarterial Xenon 133-technique were measured in baboons with normal and during increased ICP provoked by an inflatable balloon positioned subdurally. Arterial blood pressure was altered by controlled infusion of Sodium-nitroprusside (SNP), Nitroglycerine (NG) or Trimetaphan (TMP) with the aim of reducing blood pressure by about 20%. During exflated balloon SNP provoked an increase of ICP which was more prominent than with NG and TMP. During increased ICP (due to inflation of the balloon) again SNP led to a higher further increase of ICP than both NG and TMP. rCBF rose during the state of normal ICP when SNP was infused. This was not observed with infusion of NG or TMP. When ICP was increased again by inflation of the balloon all 3 substances reduced rCBF, indicating damage to the autoregulation. CO2-reactivity as measured by induced hyperventilation with reduction of arterial CO2-tension was affected by all 3 substances thus indicating impairment of vasoconstriction during increase of ICP and simultaneous decrease of blood pressure. However, this impairment of physiological vasoconstriction was more prominent with SNP than with NG and TMP. The results indicate that all 3 substances should be used with care to reduce blood pressure during surgery or under intensive care condition, particularly in patients with increased ICP.

Animals↗
PubMed1988

Treatment of systemic hypertension and intracranial hypertension in cases of brain hemorrhage.

We studied the effects of nifedipine, chlorpromazine, reserpine, furosemide, and thiopental on the mean arterial blood pressure, mean intracranial pressure, and cerebral perfusion pressure in 38 patients with increased intracranial pressure resulting from either hemorrhagic cerebrovascular disease or systemic hypertension. These agents are widely used in neurosurgical practice for the treatment of systemic hypertension. Patients were assigned to two groups on the basis of their mean intracranial pressure. Group I comprised 20 patients with a mean intracranial pressure of 20-40 mm Hg (moderately increased ICP group), and Group II consisted of 18 patients with a mean intracranial pressure of greater than 40 mm Hg (severely increased ICP group). Nifedipine, chlorpromazine, and reserpine reduced mean arterial blood pressure by 18-20% in both groups (p less than 0.05 in each). In Group I these agents raised mean intracranial pressure by 10-35% and decreased cerebral perfusion pressure by 20-32% (p less than 0.05 for both), but in Group II these changes were more marked: mean intracranial pressure increased 38-64% and cerebral perfusion pressure decreased 40-54% (p less than 0.01 for both). Furosemide did not significantly reduce mean arterial blood pressure but slightly reduced mean intracranial pressure in each group. Thiopental reduced both mean arterial blood pressure and intracranial pressure in both groups. The effect on intracranial pressure was pronounced in Group II, in which mean arterial blood pressure fell by 18% (p less than 0.05) and mean intracranial pressure decreased 50% (p less than 0.01), whereas in Group I mean arterial blood pressure was reduced by 16% and mean intracranial pressure dropped 23% (p less than 0.05 in each).(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1981

Benign intracranial hypertension vs. intracranial arteriovenous malformation: a possible CT dilemma.

A nine-year-old boy, presenting only with signs of increased ICP, underwent computerized tomography. This examination demonstrated no abnormalities in the precontrast scan. Following C. E., it showed scattered areas of blood-like density in both hemispheres, as well as a presumedly abnormal vessel in the left occipital region and dilated vein of Galen, sinus rectus, and tentorial veins. The presumptive diagnosis of left occipital AVM was not confirmed by angiography, which also ruled out obstructions of the intracranial sinuses. The possible mechanism responsible for this atypical CT picture is briefly discussed in the light of pertinent literature. It is suggested that careful consideration should be given to the indications for angiography in similar cases, in the presence of a "hypervascular" aspect of the postcontrast CT scan, particularly if a considerable amount of contrast medium has been used.

Cerebral Angiography↗
PubMed2001

Langerhans' cell histiocytosis presenting as intracranial hypertension.

Benign intracranial hypertension is known to be associated with obesity, endocrine abnormalities, various medications, and cerebral venous sinus thrombosis. We report a patient presenting with headaches and vomiting attributed to benign intracranial hypertension. The diagnostic work-up revealed Langerhans' cell histiocytosis of the occipital bone. There was no evidence for cerebral vein thrombosis by cranial computed tomography scan, Doppler ultrasonography, planar and single photon emission computed tomography technetium 99m-labelled red blood cell scintigraphy, and magnetic resonance angiography. Excision of the occipital bone lesion and a short course of acetazolamide and prednisone were curative. We hypothesize that cytokines secreted by the tumor were responsible for the development of intracranial hypertension.

Child↗