Intracranial pressure

In general, symptoms and signs that suggest a rise in ICP include headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache that may wake the person up. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours leading to hypercapnia and vasodilation. Cerebral edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing, or bending, and progressively worsens over time. There may also be personality or behavioral changes. In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern. In children, a low heart rate is especially suggestive of high ICP. Intracranial hypertension syndrome is characterized by an elevated ICP, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluid chemical and hematological constituents. Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Biot's respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged. Papilledema (swelling of the optic disc) can be a reliable sign of elevated ICP. Unlike other conditions that may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected. ==Causes of abnormal intracranial pressure==

Increased ICP Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased: • Mass effect such as brain tumor, infarction with edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain. • Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts. • Increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins. • Obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold–Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption). • Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor. • Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger women) • Craniosynostosis One of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure. ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. It is a cause of reflex bradycardia. Drug-induced intracranial hypertension Drug-induced intracranial hypertension (DIIH) or medication-induced intracranial hypertension is a condition of higher than normal intracranial pressure with the main cause being a drug. This condition is similar to idiopathic intracranial hypertension, however the etiology in this instance is a drug. The most frequent symptoms are headaches, pulsatile tinnitus, diplopia, and impairment of visual acuity. The only observable signs of the condition may be papilledema and bilateral sixth cranial nerve (abducens) palsies. The International Classification of Headache Disorders (ICHD) Third Edition diagnostic criteria for spontaneous intracranial hypotension includes any headache attributed to low CSF pressure (low CSF opening pressure) or CSF leakage (evidence of CSF leakage on imaging). Further, the headache must have a temporal relation to the low CSF pressure or leakage and the headache cannot be better explained by another ICHD diagnosis. The final criteria is that in the rare cases of spontaneous intracranial hypotension with no headache present, the neurologic symptoms that are present must be attributable to low CSF or explained by the diagnosis of spontaneous intracranial hypotension. ==Pathophysiology==

Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP − ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The body's response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP. Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus. Monro–Kellie hypothesis The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis. The Monro–Kellie hypothesis states that the cranial compartment is inelastic and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie. ==Diagnosis==

The most definitive way of measuring the intracranial pressure is with transducers placed within the brain. A catheter can be surgically inserted into one of the brain's lateral ventricles and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICPs. This type of drain is known as an external ventricular drain (EVD). ==Treatment==

The treatment for ICP depends on the cause. In addition to management of the underlying causes, major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma. For long-term or chronic forms of raised ICP, especially idiopathic intracranial hypertension (IIH), a specific type of diuretic medication (acetazolamide) is used. In cases of confirmed brain neoplasm, dexamethasone is given to decrease ICP. Although the exact mechanism is unknown, current research shows that dexamethasone is capable of decreasing peritumoral water content and local tissue pressure to decrease ICP. Ventilation In people who have high ICP due to an acute injury, it is particularly important to ensure adequate airway, breathing, and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise. Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilating blood vessels and exacerbating the problem. Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels were returned to normal too quickly. It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes. Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure. Analgesia and sedation are used to reduce agitation and metabolic needs of the brain, but these medications may cause low blood pressure and other side effects. in which a part of the skull is removed and the dura mater is expanded to allow the brain to swell without crushing it or causing herniation. The section of bone removed, known as a bone flap, can be stored in the patient's abdomen and resited back to complete the skull once the acute cause of raised ICP's has resolved. Alternatively a synthetic material may be used to replace the removed bone section (see cranioplasty) == See also ==