Overview: lateral position of cerebrospinal fluid pressure measurement of the average adult over 1.96kPa ( quite 200mmH2O), the intracranial pressure is increased. intracranial hypertension syndrome (intracranial hypertension) is caused by a variety of cranial contents of the total volume increase, or congenital malformations caused by the small cranial capacity, the increased intracranial pressure and beyond the scope of their compensation, then the emergence of a common nerve system syndrome, also known as intracranial hypertension (increased intracranial pressure).
common cause of increased intracranial pressure due to:
4. intracranial inflammation, such as all kinds of encephalitis, meningitis, septicemia.
8. congenital anomalies, such as the aqueduct of the malformation, basilar invagination and congenital malformations of cerebellar tonsillar herniation, can cause CSF flow obstruction, and thus secondary hydrocephalus and increased intracranial pressure; narrow cranial disease, due to the cranial cavity is small, limiting the normal development of the brain, increased intracranial pressure often occur.
(B) the pathogenesis
1. increased intracranial pressure caused by the mechanism in the following areas:
(2) increased intracranial blood volume, a variety of causes accumulation of carbon dioxide in the blood or hypercapnia, make cerebral vasodilation, cerebral blood flow increased dramatically; hypothalamus , saddle, or brain stem injury, can lead to cerebral vascular regulation center of the disorders, cerebral vascular reactivity to expand, so that cerebral blood flow increased dramatically.
(3) too much cerebrospinal fluid, is seen in hydrocephalus.
(4) intracranial space-occupying lesions, an additional increase in the cranial contents, in addition to lesions of the cranial cavity itself occupies a certain volume, it can also cause lesions around the brain edema or cerebrospinal fluid circulation pathway obstruction, leading to increased intracranial pressure.
(1) systemic blood pressure response: When the brain loss of autoregulation of blood vessels, in order to maintain the required blood flow, the body through the autonomic nervous system reflex, so that systemic peripheral vasoconstriction, blood pressure, cardiac output increased to improve cerebral perfusion pressure, accompanied by respiratory rhythm slow, deep breathing to increase. This kind of elevated arterial pressure, accompanied by heart rate, stroke volume increased and respiratory rhythm slowed to deepen the triple response, known as systemic vascular pressure reaction or cushing (Cushing) of the three main symptoms. More common in acute brain injury or acute intracranial hypertension patients.
(2) the relationship between intracranial pressure and volume: Langfitt, et al (1965) the animal experiments show that, due to the compensatory role of the cranial contents, outside the presence of pathological factors not necessarily lead to changes in intracranial pressure, intracranial pressure and intracranial contents volume does not increase the number of linear relations, but an exponential relationship. This relationship can also be used brain plasticity (plasticity) and compliance (compliance) to represent. Plasticity within the soft tissue from the cranial cavity of plasticity and flexibility, is the unit volume change produced by pressure changes, with △ P / △ V said. compliance on behalf of the compensatory function of the volume within the cranial cavity, is the unit change in intracranial pressure produced by volume changes, with △ V / △ P said. increase in cranial volume of the contents of the early, there is enough room for adjustment, that is, compliance (compensatory) strong; cranial contents increase in volume later, less and less room for adjustment, disease resistance encountered in the expansion getting bigger, so a sharp increase in intracranial pressure. By checking compliance and plasticity, helps determine the severity of intracranial hypertension. Clinical use is as follows: ventricular drainage or lumbar cerebrospinal fluid when the release of 1ml, if the pressure drop is still very little description of the compensatory period, if the pressure drops more than 0.39kPa (3mmHg), then prompt intracranial pressure / volume curve has exceeded the critical point that compensatory function has been exhausted.
(3) herniation: especially intracranial space-occupying intracranial lesions and injuries, increased intracranial pressure caused by the uneven, often the brain tissue pressure shift position, part of the brain tissue through the cracks of certain anatomical parts of the shift to a lower pressure when the hernia is (brain herniation). This is the most fatal intracranial emergencies.[Sign]
early symptoms of intracranial hypertension syndrome, what?
intracranial hypertension syndrome is a gradual process of development, the clinical manifestations of varying severity. Typical syndrome of intracranial hypertension, including increased intracranial pressure due to their clinical manifestations, and the cause of increased intracranial pressure caused due to defects in the nervous system.
common symptoms and signs:
2. vomiting for vomiting.
4. abducens nerve palsy with diplopia due to abducens nerve to go line up at the base of the skull, intracranial pressure arise when vulnerable to unilateral or bilateral paralysis and diplopia, no location significance.
(2) respiratory: acute intracranial hypertension, the initial breathing deep and slow, to the medulla oblongata failure, to shallow breathing, slow and irregular breathing or sighing respiration , and finally to a sudden stop.
(4) sense: because of high intracranial pressure and cerebral edema, cerebral cortex and brain stem reticular formation ischemia, hypoxia, can cause varying degrees of consciousness. chronic high intracranial pressure may first appear restless, then drowsiness to coma. High intracranial pressure and disturbance of consciousness is not necessarily proportional, depending on the site may be, such as the hypothalamus or brain stem contusion consciousness tumor can be very heavy, not very high intracranial pressure.
main clinical manifestations of the "three main symptoms": headache; nausea and vomiting; retinal optic disc edema. Other common manifestations of consciousness, vision loss, double vision, convulsions, and decorticate rigidity. Some can be expressed as mood swings, easy anger, or crying, or feeling indifferent, unresponsive, slow movements and thinking of psychiatric symptoms.
in infant patients, headache symptoms often not obvious, often appear scalp vein engorgement, the head increases, the expansion fontanelle, suture separation, increased anterior fontanelle tension or uplift. head of percussion was "broken pot sound" (Macewn sign).
of chronic intracranial hypertension syndrome, skull x-ray can be found in the sella, saddle back, and especially before and after clinoid bone destruction or absorption; skull diffuse sparse thin; brain increase and deepen the back pressure trace; 15 children before the age of visible suture widened and separated, the younger the more common. Those caused by intracranial mass, but also shows the shift of pineal calcification of normal, pathological calcification, partial skull growth or damage, auditory canal, and other abnormal brain changes in the hole.
electronic and computer tomography (CT) or magnetic resonance imaging (MRI) can be found in intracranial space-occupying lesions, diagnosis, and these two safe and easy and accurate inspection and reliable. For those who have objective signs of increased intracranial pressure or neurological examination with positive findings or clinically highly suspected in patients with increased intracranial pressure, should be early CT or MRI.
for patients with increased intracranial pressure, lumbar puncture to promote the risk of brain herniation, lumbar puncture should be banned or carefully done. If necessary, should be given to dehydration after lumbar puncture manometry is properly sealed. lumbar puncture should also strengthen dehydration and close observation.
typical intracranial hypertension syndrome with headache, vomiting, and optic disc edema, such as performance, particularly in the most objective optic disc edema, according to the signs, the diagnosis is not difficult. However, in acute or chronic increased intracranial pressure increased intracranial pressure early, many ignore the disk edema, the patient may have only a headache and (or) vomiting. Easily misdiagnosed as functional diseases, resulting in serious consequences. Therefore, should be treated with every headache and (or) vomiting in patients with increased intracranial pressure may be wary of.[Aftertreat]
how to prevent intracranial hypertension syndrome?
1. cause of treatment is for the cause of increased intracranial pressure caused by reasonable treatment. For intracranial space-occupying intracranial hematoma or surgical treatment should be taken; have hydrocephalus shunt cerebrospinal fluid was feasible; for intracranial infection or parasite given antibiotics or anti-parasite treatment. At the same time to keep the airway open, improve cerebral hypoxia and brain metabolism, oxygen and correcting water, electrolyte and acid-base balance disorders, to break the vicious cycle caused by cerebral edema.
2. to reduce intracranial pressure and anti-cerebral edema commonly used drugs: 20% mannitol 250ml rapid intravenous infusion, every 4 to 6 hours; furosemide 20 40mg, daily intravenous injection of 2 to 4 times, and often used interchangeably with mannitol; Gan fructose (glycerol and fructose) injection 250 ~ 500ml, intravenous infusion every 2 to 3 times; dexamethasone 5 ~ 10mg, intravenous or intramuscular injection, 2 to 3 times / d, or intravenous infusion of hydrocortisone 100mg, 1-2 times / d; 20% of human serum albumin concentration of 10 ~ 20g dried plasma and other macromolecules or colloid infusion; Recent drug aescin with steroid hormone-like role for increased intracranial pressure is not serious, each 20 ~ 40mg, 2 ~ 3 times / d. Such as increased intracranial pressure is not serious, but also oral administration of 50% glycerol saline, hydrochlorothiazide (hydrochlorothiazide urea thiophene) and triamterene and so on.
if medical treatment fails or worsening symptoms of increased intracranial pressure, ventricular puncture and drainage feasible, or administration of the temporal muscle under decompression, hemicraniectomy patients and so on.
3. control of fluid intake to prevent the rapid infusion of fluid intake per day is generally limited to 2000ml or so, patients should be based on the dehydration reaction of the drug, how much urine output, central venous pressure and electrolyte changes and other factors into account and the amount of fluid into the infusion rate.
4. monitoring the patient's condition closely observe the patient's chief complaint, the state of consciousness, pupil size and changes in vital signs, conditions may be continuous intracranial pressure monitoring.
5. others such as hibernation temperature treatment, by reducing the metabolic activity of brain tissue, reduce oxygen consumption, to prevent the occurrence and development of brain edema, intracranial pressure play a reduced the role. But it's not obvious, now less.
(b) the prognosis
dehydration by effective treatment or surgical treatment, control of intracranial hypertension syndrome was not difficult, but the cause of the effects of treatment varies due to illness. The cause is not removed, then there will be repeated intracranial hypertension syndrome.
No related information
1. cerebrospinal fluid pressure is generally higher than 200mmH2O, CSF routine laboratory tests were normal. For patients with increased intracranial pressure, lumbar puncture to promote the risk of hernia, the clinical suspicion of increased intracranial pressure, and other tests positive nor discoverer, in the absence of posterior fossa signs or neck stiffness, can be carefully considered should be given to dehydration after lumbar puncture manometry is properly sealed.
1. of chronic intracranial hypertension syndrome, skull x-ray can be found in the sella, saddle back, and especially before and after clinoid bone destruction or absorption; skull sparse diffuse thinning; increased brain pressure trace back and deepened.
2. For those who have objective signs of increased intracranial pressure or neurological examination with positive findings or clinically highly suspected in patients with increased intracranial pressure, early CT or should mri examination.[Diff]
1. traumatic brain injury (craniocerebral injury) for any reason, caused the head injury caused by cerebral contusion, intracranial hematoma, cerebral edema and increased intracranial pressure can make . Acute severe brain injury can occur early increased intracranial pressure. Minority of patients can occur later, such as chronic subdural hematoma. Traumatic brain injury patients often quickly into a coma, vomiting. Intracerebral hematoma appear to follow different parts of hemiplegia, aphasia, seizure, etc. brain CT can directly determine the size of intracranial hematoma, location and type, and can not be found in diagnostic cerebral angiography of the intraventricular hemorrhage.
2. cerebrovascular disease (cerebrovascular disease) mainly hemorrhagic cerebrovascular disease, hypertensive intracerebral hemorrhage is most common. Generally more acute onset of increased intracranial pressure manifested as 1 to 3 days developed to its peak. Patients often have different levels of consciousness. Headache, dizziness, vomiting, paralysis, aphasia, incontinence, etc. Often have a significant incidence of high blood pressure. Most patients with meningeal irritation-positive. cerebrospinal fluid pressure, and often has bloody. CT can clearly bleeding brain size and the bleeding site.
3. hypertensive encephalopathy (hypertensive encephalopathy) hypertensive encephalopathy is a sudden dramatic increase in blood pressure caused by acute brain dysfunction comprehensiveness. Common in radical-type hypertension, acute and chronic nephritis or eclampsia, or even due to pheochromocytoma or taking monoamine oxidase inhibitors with tyramine while taking food, lead poisoning, such as Cushing's syndrome. Often rapid-onset, blood pressure suddenly increased significantly to 33.3/20kPa (250/150mmHg) or more, systolic blood pressure more than diastolic blood pressure increased significantly. Often also severe headache, nausea, vomiting, neck stiffness and other symptoms of increased intracranial pressure. Neuropsychiatric symptoms, including visual impairment, hemiplegia, aphasia, epileptic seizures, or limb muscle rigidity, disturbance of consciousness. fundus showed a high blood pressure can fundus, retinal artery spasm, and even retinal hemorrhage, exudation, and optic disc edema. CT examination showed cerebral edema, ventricular narrowing.
4. intracranial tumor (intracranial tumour) can be divided into primary intracranial tumors and malignant tumors from the other parts of the body transferred to the formation of intracranial metastases. intracranial pressure caused by brain tumors is a common feature of the typical chronic increased intracranial pressure. Although in the course of the disease symptoms can be slight ups and downs, but the overall trend is gradually increased. A small number of patients with chronic increased intracranial pressure suddenly became acute. according to the site of tumor growth may be associated with different symptoms, such as visual field changes, pyramidal tract damage, seizures, aphasia, sensory disturbances, psychiatric symptoms, cerebellar pontine angle syndrome. head CT can be clearly the location and nature of tumor growth.
5. brain abscess (brain abscess) is often of primary foci, such as otogenic, nose or traumatic origin. blood-borne early acute inflammation may have systemic symptoms such as fever, chills, meningeal irritation, increased white blood cells, erythrocyte sedimentation rate block, lumbar puncture and cerebrospinal fluid white blood cell count and so on. However, after mature abscess, the symptoms and signs disappeared, only the performance of chronic increased intracranial pressure, with or without focal neurological signs. brain abscess is generally a shorter duration, more severe mental retardation. CT scans often show reduced density of round or oval shadow edge image after intravenous contrast agent markedly enhanced the ring was thin and smooth wall the shadow of increased density, in addition to low-density abscess of brain edema around the more significant.
6. infection of the brain disease (brain infectious disease) is a bacterial infection of the brain, viruses, parasites, rickettsia, spirochetes caused by the brain and meninges inflammatory diseases. Acute or subacute intracranial hypertension, a few manifestations of chronic increased intracranial pressure, onset often have symptoms of infection such as fever, general malaise, increased blood and so on. Some patients have disturbance of consciousness, mental confusion, myoclonus and seizures, severe development of deep coma within a few days. Important feature of focal symptoms often appear, such as hemiplegia, aphasia, with the skewed eyes, partial seizures, involuntary movements. The other can still have stiff neck, meningeal irritation and so on. CSF inflammatory changes often, such as cerebrospinal fluid leukocytosis, increased protein, or sugar or chloride reduction, complement fixation test was positive and so on. head CT shows inflammatory change.
7. hydrocephalus (hydrocephalus) due to various reasons cerebrospinal fluid within the ventricular system increased, while a corresponding reduction in the brain parenchyma, ventricular dilatation and associated with increased intracranial pressure, said as hydrocephalus, also known as progressive or high-pressure hydrocephalus. ventricular angiography shows marked widening of ventricles. CT examination can be found in the tumor, accurate observation of the size of ventricles and shows periventricular edema.
8. benign intracranial hypertension (benign intracranial hypertension), also known as "false brain tumor", Department of Only patients with symptoms and signs of increased intracranial pressure, but no accounting position of the lesions present. May cause arachnoiditis, otogenic hydrocephalus, sinus thrombosis, endocrine disease, but regular checks clear. clinical manifestations of chronic increased intracranial pressure, in general, no focal signs.
9. other systemic diseases caused by increased intracranial pressure in the clinical situation is also quite common. Such as infection, toxic encephalopathy, uremia, water, electrolyte and acid-base balance disorders, diabetic coma, hepatic coma, food poisoning. These diseases can be developed to the extent the performance of increased intracranial pressure appear. Combination of medical history and medical check-up and more to make a clear diagnosis.
when increased intracranial pressure to the brain or skull fracture displacement of the pore embedded in the dura mater, the herniation is. Common with temporal lobe uncus hernia (hernia canopy, canopy hiatal hernia, tentorial hernia) and foramen magnum herniation (the extension of cerebellar herniation) two. Identified in table 1.
mania alternating with drowsiness-related diseases
more other symptoms
"frozen" phenomenon "three fears" (water, sound, light 21 - hydroxylase deficiency igm antibodies sm accumulation increased belching physical scars, daytime sleepiness, nighttime insomnia, leukopenia, leukocytosis, signs of leukemic cell infiltration in sepsis to maintain sleep disorder galactosemia lost hold of a passive position overeating addiction rage stolen or hypochondriacal paranoia delusions
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