Idiopathic intracranial hypertension

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Idiopathic intracranial hypertension
Other namesBenign intracranial hypertension (BIH), [1] pseudotumor cerebri (PTC) [2]
MRI brain.jpg
For the diagnosis, brain scans (such as MRI) should be done to rule out other potential causes.
Specialty Neurology
Symptoms Headache, vision problems, ringing in the ears with the heartbeat [1] [2]
Complications Vision loss [2]
Usual onset20–50 years old [2]
Risk factors Hypervitaminosis A, obesity, tetracyclines [1] [2]
Diagnostic method Based on symptoms, lumbar puncture, brain imaging [1] [2]
Differential diagnosis Brain tumor, arachnoiditis, meningitis [3]
TreatmentHealthy diet, salt restriction, exercise, surgery [2]
Medication Acetazolamide [2]
Prognosis Variable [2]
Frequency2 per 100,000 per year [4]

Idiopathic intracranial hypertension (IIH), previously known as pseudotumor cerebri and benign intracranial hypertension, is a condition characterized by increased intracranial pressure (pressure around the brain) without a detectable cause. [2] The main symptoms are headache, vision problems, ringing in the ears, and shoulder pain. [1] [2] Complications may include vision loss. [2]

Contents

This condition is idiopathic, meaning there is no known cause. Risk factors include being overweight or a recent increase in weight. [1] Tetracycline may also trigger the condition. [2] The diagnosis is based on symptoms and a high opening pressure found during a lumbar puncture with no specific cause found on a brain scan. [1] [2]

Treatment includes a healthy diet, salt restriction, and exercise. [2] The medication acetazolamide may also be used along with the above measures. [2] A small percentage of people may require surgery to relieve the pressure. [2]

About 2 per 100,000 people are newly affected per year. [4] The condition most commonly affects women aged 20–50. [2] Women are affected about 20 times more often than men. [2] The condition was first described in 1897. [1]

Signs and symptoms

The most common symptom of IIH is severe headache, which occurs in almost all (92–94%) cases. It is characteristically worse in the morning, generalized in character and throbbing in nature. It may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. The pain may also be experienced in the neck and shoulders. [5] Many have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse. [5] [6] Various other symptoms, such as numbness of the extremities, generalized weakness, pain and/or numbness in one or both sides of the face, loss of smell, and loss of coordination, are reported more rarely; none are specific for IIH. [5] In children, numerous nonspecific signs and symptoms may be present. [7]

The increased pressure leads to compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck. Most commonly, the abducens nerve (sixth nerve) is involved. This nerve supplies the muscle that pulls the eye outward. Those with sixth nerve palsy therefore experience horizontal double vision which is worse when looking towards the affected side. More rarely, the oculomotor nerve and trochlear nerve (third and fourth nerve palsy, respectively) are affected; both play a role in eye movements. [7] [8] The facial nerve (seventh cranial nerve) is affected occasionally – the result is total or partial weakness of the muscles of facial expression on one or both sides of the face. [5]

The increased pressure leads to papilledema, which is swelling of the optic disc, the spot where the optic nerve enters the eyeball. This occurs in practically all cases of IIH, but not everyone experiences symptoms from this. Those who do experience symptoms typically report "transient visual obscurations", episodes of difficulty seeing that occur in both eyes but not necessarily at the same time. Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision. [5] [9]

Physical examination of the nervous system is typically normal apart from the presence of papilledema, which is seen on examination of the eye with a small device called an ophthalmoscope or in more detail with a fundus camera. If there are cranial nerve abnormalities, these may be noticed on eye examination in the form of a squint (third, fourth, or sixth nerve palsy) or as facial nerve palsy. If the papilledema has been longstanding, visual fields may be constricted and visual acuity may be decreased. Visual field testing by automated (Humphrey) perimetry is recommended as other methods of testing may be less accurate. Longstanding papilledema leads to optic atrophy, in which the disc looks pale and visual loss tends to be advanced. [5] [9]

Causes

"Idiopathic" means of unknown cause. Therefore, IIH can only be diagnosed if there is no alternative explanation for the symptoms. Intracranial pressure may be increased due to medications such as high-dose vitamin A derivatives (e.g., isotretinoin for acne), [10] long-term tetracycline antibiotics (for a variety of skin conditions). [11] Hormonal contraceptives, particularly the oral contraceptive pill (OCP), are not associated with IIH. [12]

There are numerous other diseases, mostly rare conditions, that may lead to intracranial hypertension. If there is an underlying cause, the condition is termed "secondary intracranial hypertension". [5] Common causes of secondary intracranial hypertension include obstructive sleep apnea (a sleep-related breathing disorder), systemic lupus erythematosus (SLE), chronic kidney disease, and Behçet's disease. [9]

On July 1, 2022, the FDA issued an update that gonadotropin-releasing hormone agonists, drugs that are approved for treating precocious puberty, may be a risk factor for developing pseudotumor cerebri. [13]

Mechanism

The cause of IIH is not known. The Monro–Kellie rule states that the intracranial pressure is determined by the amount of brain tissue, cerebrospinal fluid (CSF) and blood inside the bony cranial vault. Three theories therefore exist as to why the pressure might be raised in IIH: an excess of CSF production, increased volume of blood or brain tissue, or obstruction of the veins that drain blood from the brain. [5]

The first theory, that of increased production of cerebrospinal fluid, was proposed in early descriptions of the disease. However, there is no experimental data that supports a role for this process in IIH. [5]

The second theory posits that either increased blood flow to the brain or increase in the brain tissue itself may result in the raised pressure. Little evidence has accumulated to support the suggestion that increased blood flow plays a role, but recently Bateman et al. in phase contrast MRA studies have quantified cerebral blood flow (CBF) in vivo and suggests that CBF is abnormally elevated in many people with IIH. Both biopsy samples and various types of brain scans have shown an increased water content of the brain tissue. It remains unclear why this might be the case. [5]

The third theory suggests that restricted venous drainage from the brain may be impaired resulting in congestion. Many people with IIH have narrowing of the transverse sinuses. [14] It is not clear whether this narrowing is the pathogenesis of the disease or a secondary phenomenon. It has been proposed that a positive biofeedback loop may exist, where raised ICP (intracranial pressure) causes venous narrowing in the transverse sinuses, resulting in venous hypertension (raised venous pressure), decreased CSF resorption via arachnoid granulation and further rise in ICP. [15]

Diagnosis

Ultrasound of the optic nerve showing IIH UOTW 5 - Ultrasound of the Week 2 (cropped).jpg
Ultrasound of the optic nerve showing IIH

The diagnosis may be suspected on the basis of the history and examination. To confirm the diagnosis, as well as excluding alternative causes, several investigations are required; more investigations may be performed if the history is not typical or the person is more likely to have an alternative problem: children, men, the elderly, or women who are not overweight. [8]

Investigations

Neuroimaging, usually with computed tomography (CT/CAT) or magnetic resonance imaging (MRI), is used to exclude any mass lesions. In IIH these scans typically appear to be normal, although small or slit-like ventricles, dilatation and buckling [17] of the optic nerve sheaths and "empty sella sign" (flattening of the pituitary gland due to increased pressure) and enlargement of Meckel's caves may be seen.

An MR venogram is also performed in most cases to exclude the possibility of venous sinus stenosis/obstruction or cerebral venous sinus thrombosis. [5] [7] [8] A contrast-enhanced MRV (ATECO) scan has a high detection rate for abnormal transverse sinus stenoses. [14] These stenoses can be more adequately identified and assessed with catheter cerebral venography and manometry. [15] Buckling of the bilateral optic nerves with increased perineural fluid is also often noted on MRI imaging.

Lumbar puncture is performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude alternative diagnoses. If the opening pressure is increased, CSF may be removed for transient relief (see below). [8] The CSF is examined for abnormal cells, infections, antibody levels, the glucose level, and protein levels. By definition, all of these are within their normal limits in IIH. [8] Occasionally, the CSF pressure measurement may be normal despite very suggestive symptoms. This may be attributable to the fact that CSF pressure may fluctuate over the course of the normal day. If the suspicion of problems remains high, it may be necessary to perform more long-term monitoring of the ICP by a pressure catheter. [8]

Classification

The original criteria for IIH were described by Dandy in 1937. [18]

Dandy criteria [18]
1 Signs & symptoms of increased ICP – CSF pressure >25 cmH2O
2 No localizing signs with the exception of abducens nerve palsy
3 Normal CSF composition
4 Normal to small (slit) ventricles on imaging with no intracranial mass

They were modified by Smith in 1985 to become the "modified Dandy criteria". Smith included the use of more advanced imaging: Dandy had required ventriculography, but Smith replaced this with computed tomography. [19] In a 2001 paper, Digre and Corbett amended Dandy's criteria further. They added the requirement that the person is awake and alert, as coma precludes adequate neurological assessment, and require exclusion of venous sinus thrombosis as an underlying cause. Furthermore, they added the requirement that no other cause for the raised ICP is found. [5] [9] [20]

Modified Dandy criteria [20]
1 Symptoms of raised intracranial pressure (headache, nausea, vomiting, transient visual obscurations, or papilledema)
2 No localizing signs with the exception of abducens (sixth) nerve palsy
3 The patient is awake and alert
4 Normal CT/MRI findings without evidence of thrombosis
5 LP opening pressure of >25 cmH2O and normal biochemical and cytological composition of CSF
6 No other explanation for the raised intracranial pressure

In a 2002 review, Friedman and Jacobson propose an alternative set of criteria, derived from Smith's. These require the absence of symptoms that could not be explained by a diagnosis of IIH, but do not require the actual presence of any symptoms (such as headache) attributable to IIH. These criteria also require that the lumbar puncture is performed with the person lying sideways, as a lumbar puncture performed in the upright sitting position can lead to artificially high pressure measurements. Friedman and Jacobson also do not insist on MR venography for every person; rather, this is only required in atypical cases (see "diagnosis" above). [8]

Treatment

The primary goal in treatment of IIH is the prevention of visual loss and blindness, as well as symptom control. [9] IIH is treated mainly through the reduction of CSF pressure and IIH may resolve after initial treatment, may go into spontaneous remission (although it can still relapse at a later stage), or may continue chronically. [5] [8] There are three main treatment approaches: weight loss, different medications and surgical interventions. Remission is seen for most patients that achieve a weight loss of around 6–10%. Bariatric surgery can be an option for those patients that don't achieve weight loss with lifestyle changes and diet. [21]

Lumbar puncture

A lumbar puncture in progress. A large area on the back has been washed with an iodine-based disinfectant leaving brown colouration. In this image the person is seated upright, which can make the procedure easier to perform but makes any measurement of the opening pressure unreliable. Wikipedian getting a lumbar puncture (2006).jpg
A lumbar puncture in progress. A large area on the back has been washed with an iodine-based disinfectant leaving brown colouration. In this image the person is seated upright, which can make the procedure easier to perform but makes any measurement of the opening pressure unreliable.

The first step in symptom control is drainage of cerebrospinal fluid by lumbar puncture. If necessary, this may be performed at the same time as a diagnostic LP (such as done in search of a CSF infection). In some cases, this is sufficient to control the symptoms, and no further treatment is needed. [7] [9]

The procedure can be repeated if necessary, but this is generally taken as a clue that additional treatments may be required to control the symptoms and preserve vision. Repeated lumbar punctures are regarded as unpleasant by people, and they present a danger of introducing spinal infections if done too often. [5] [7] Repeated lumbar punctures are sometimes needed to control the ICP urgently if the person's vision deteriorates rapidly. [9]

Medication

The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels of newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not tolerated, but this drug sometimes has little effect on the ICP. [5] [9]

Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief. [9]

The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged. [5]

Venous sinus stenting

Venous sinus stenoses leading to venous hypertension appear to play a significant part in relation to raised ICP, and stenting of a transverse sinus may resolve venous hypertension, leading to improved CSF resorption, decreased ICP, cure of papilledema and other symptoms of IIH. [15]

A self-expanding metal stent is permanently deployed within the dominant transverse sinus across the stenosis under general anaesthesia. In general, people are discharged the next day. People require double antiplatelet therapy for a period of up to 3 months after the procedure and aspirin therapy for up to 1 year.

In a systematic analysis of 19 studies with 207 cases, there was an 87% improvement in overall symptom rate and 90% cure rate for treatment of papilledema. Major complications only occurred in 3/207 people (1.4%). [22] In the largest single series of transverse sinus stenting there was an 11% rate of recurrence after one stent, requiring further stenting. [15]

Due to the permanence of the stent and small but definite risk of complications, most experts will recommend that person with IIH must have papilledema and have failed medical therapy or are intolerant to medication before stenting is undertaken.

Surgery

Two main surgical procedures are used for the treatment of IIH: optic nerve sheath decompression and fenestration and cerebral shunting. Surgery would normally only be offered if medical therapy is either unsuccessful or not tolerated. [7] [9] The choice between these two procedures depends on the predominant problem in IIH. Neither procedure is perfect: both may cause significant complications, and both may eventually fail in controlling the symptoms. There are no randomized controlled trials to guide the decision as to which procedure is best. [9]

Optic nerve sheath fenestration is an operation that involves the making of an incision in the connective tissue lining of the optic nerve in its portion behind the eye. It is not entirely clear how it protects the eye from the raised pressure, but it may be the result of either diversion of the CSF into the orbit or the creation of an area of scar tissue that lowers the pressure. [9] The effects on the intracranial pressure itself are more modest. Moreover, the procedure may lead to significant complications, including blindness in 1–2%. [5] The procedure is therefore recommended mainly in those who have limited headache symptoms but significant papilledema or threatened vision, and those who have undergone unsuccessful treatment with a shunt or have a contraindication for shunt surgery. [9]

Shunt surgery, usually performed by neurosurgeons, involves the creation of a conduit by which CSF can be drained into another body cavity. The initial procedure is usually a lumboperitoneal (LP) shunt, which connects the subarachnoid space in the lumbar spine with the peritoneal cavity. [23] A pressure valve is usually included in the circuit to avoid excessive drainage when the person is erect. LP shunting provides long-term relief in about half the cases; others require revision of the shunt, often on more than one occasion, usually due to shunt obstruction. If the lumboperitoneal shunt needs repeated revisions, a ventriculoatrial or ventriculoperitoneal shunt may be considered. These shunts are inserted in one of the lateral ventricles of the brain, usually by stereotactic surgery, and then connected either to the right atrium of the heart or the peritoneal cavity. [5] [9] Given the reduced need for revisions in ventricular shunts, it is possible that this procedure will become[ when? ] the first-line type of shunt treatment. [5]

It has been shown that in obese people, bariatric surgery (and especially gastric bypass surgery) can lead to resolution of the condition in over 95%. [5]

Prognosis

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease. [9]

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of one's vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%. [5] [9]

Epidemiology

The number of new cases per year of IIH is strongly determined by sex and body weight. The figures in females are in women between 20 and 45 years old. IIH incidence.png
The number of new cases per year of IIH is strongly determined by sex and body weight. The figures in females are in women between 20 and 45 years old.

On average, IIH occurs in about one per 100,000 people, and can occur in children and adults. The median age at diagnosis is 30. IIH occurs predominantly in women, especially in the ages 20 to 45, who are four to eight times more likely than men to be affected. Overweight and obesity strongly predispose a person to IIH: women who are more than ten percent over their ideal body weight are thirteen times more likely to develop IIH, and this figure goes up to nineteen times in women who are more than twenty percent over their ideal body weight. In men this relationship also exists, but the increase is only five-fold in those over 20 percent above their ideal body weight. [5]

Despite several reports of IIH in families, there is no known genetic cause for IIH. People from all ethnicities may develop IIH. [5] In children, there is no difference in incidence between males and females. [7]

From national hospital admission databases it appears that the need for neurosurgical intervention for IIH has increased markedly over the period between 1988 and 2002. This has been attributed at least in part to the rising prevalence of obesity, [24] although some of this increase may be explained by the increased popularity of shunting over optic nerve sheath fenestration. [9]

History

The first report of IIH was by the German physician Heinrich Quincke, who described it in 1893 under the name serous meningitis. [25] The term "pseudotumor cerebri" was introduced in 1904 by his compatriot Max Nonne. [26] Numerous other cases appeared in the literature subsequently; in many cases, the raised intracranial pressure may actually have resulted from underlying conditions. [27] For instance, the otitic hydrocephalus reported by London neurologist Sir Charles Symonds may have resulted from venous sinus thrombosis caused by middle ear infection. [27] [28] Diagnostic criteria for IIH were developed in 1937 by the Baltimore neurosurgeon Walter Dandy; Dandy also introduced subtemporal decompressive surgery in the treatment of the condition. [18] [27]

The terms "benign" and "pseudotumor" derive from the fact that increased intracranial pressure may be associated with brain tumors. Those people in whom no tumour was found were therefore diagnosed with "pseudotumor cerebri" (a disease mimicking a brain tumor). The disease was renamed benign intracranial hypertension in 1955 to distinguish it from intracranial hypertension due to life-threatening diseases (such as cancer); [29] however, this was also felt to be misleading because any disease that can blind someone should not be thought of as benign, and the name was therefore revised in 1989 to "idiopathic (of no identifiable cause) intracranial hypertension". [30] [31]

Shunt surgery was introduced in 1949; initially, ventriculoperitoneal shunts were used. In 1971, good results were reported with lumboperitoneal shunting. Negative reports on shunting in the 1980s led to a brief period (1988–1993) during which optic nerve fenestration (which had initially been described in an unrelated condition in 1871) was more popular. Since then, shunting is recommended predominantly, with occasional exceptions. [5] [9]

Related Research Articles

<span class="mw-page-title-main">Cerebrospinal fluid</span> Clear, colorless bodily fluid found in the brain and spinal cord

Cerebrospinal fluid (CSF) is a clear, colorless body fluid found within the tissue that surrounds the brain and spinal cord of all vertebrates.

<span class="mw-page-title-main">Papilledema</span> Eye disorder

Papilledema or papilloedema is optic disc swelling that is caused by increased intracranial pressure due to any cause. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare.

<span class="mw-page-title-main">Hydrocephalus</span> Abnormal increase in cerebrospinal fluid in the ventricles of the brain

Hydrocephalus is a condition in which an accumulation of cerebrospinal fluid (CSF) occurs within the brain. This typically causes increased pressure inside the skull. Older people may have headaches, double vision, poor balance, urinary incontinence, personality changes, or mental impairment. In babies, it may be seen as a rapid increase in head size. Other symptoms may include vomiting, sleepiness, seizures, and downward pointing of the eyes.

<span class="mw-page-title-main">Lumbar puncture</span> Procedure to collect cerebrospinal fluid

Lumbar puncture (LP), also known as a spinal tap, is a medical procedure in which a needle is inserted into the spinal canal, most commonly to collect cerebrospinal fluid (CSF) for diagnostic testing. The main reason for a lumbar puncture is to help diagnose diseases of the central nervous system, including the brain and spine. Examples of these conditions include meningitis and subarachnoid hemorrhage. It may also be used therapeutically in some conditions. Increased intracranial pressure is a contraindication, due to risk of brain matter being compressed and pushed toward the spine. Sometimes, lumbar puncture cannot be performed safely. It is regarded as a safe procedure, but post-dural-puncture headache is a common side effect if a small atraumatic needle is not used.

<span class="mw-page-title-main">Cerebral edema</span> Excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain

Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, death.

<span class="mw-page-title-main">Intracranial pressure</span> Pressure exerted by fluids inside the skull and on the brain

Intracranial pressure (ICP) is the pressure exerted by fluids such as cerebrospinal fluid (CSF) inside the skull and on the brain tissue. ICP is measured in millimeters of mercury (mmHg) and at rest, is normally 7–15 mmHg for a supine adult. The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF.

<span class="mw-page-title-main">Intracranial hemorrhage</span> Hemorrhage, or bleeding, within the skull

Intracranial hemorrhage (ICH), also known as intracranial bleed, is bleeding within the skull. Subtypes are intracerebral bleeds, subarachnoid bleeds, epidural bleeds, and subdural bleeds.

Normal-pressure hydrocephalus (NPH), also called malresorptive hydrocephalus, is a form of communicating hydrocephalus in which excess cerebrospinal fluid (CSF) occurs in the ventricles, and with normal or slightly elevated cerebrospinal fluid pressure. As the fluid builds up, it causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications. The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problems/gait deviations. The disease was first described by Salomón Hakim and Adams in 1965.

Cushing reflex is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. It is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation. It can also be seen after the intravenous administration of epinephrine and similar drugs. It was first described in detail by American neurosurgeon Harvey Cushing in 1901.

<span class="mw-page-title-main">Brain herniation</span> Potentially deadly side effect of very high pressure within the skull

Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum. Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.

<span class="mw-page-title-main">Sixth nerve palsy</span> Medical condition

Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI, which is responsible for causing contraction of the lateral rectus muscle to abduct the eye. The inability of an eye to turn outward, results in a convergent strabismus or esotropia of which the primary symptom is diplopia in which the two images appear side-by-side. Thus, the diplopia is horizontal and worse in the distance. Diplopia is also increased on looking to the affected side and is partly caused by overaction of the medial rectus on the unaffected side as it tries to provide the extra innervation to the affected lateral rectus. These two muscles are synergists or "yoke muscles" as both attempt to move the eye over to the left or right. The condition is commonly unilateral but can also occur bilaterally.

<span class="mw-page-title-main">Cerebral venous sinus thrombosis</span> Presence of a blood clot in the dural venous sinuses or cerebral veins

Cerebral venous sinus thrombosis (CVST), cerebral venous and sinus thrombosis or cerebral venous thrombosis (CVT), is the presence of a blood clot in the dural venous sinuses, the cerebral veins, or both. Symptoms may include severe headache, visual symptoms, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures, which occur in around 40% of patients.

<span class="mw-page-title-main">External ventricular drain</span> Medical device

An external ventricular drain (EVD), also known as a ventriculostomy or extraventricular drain, is a device used in neurosurgery to treat hydrocephalus and relieve elevated intracranial pressure when the normal flow of cerebrospinal fluid (CSF) inside the brain is obstructed. An EVD is a flexible plastic catheter placed by a neurosurgeon or neurointensivist and managed by intensive care unit (ICU) physicians and nurses. The purpose of external ventricular drainage is to divert fluid from the ventricles of the brain and allow for monitoring of intracranial pressure. An EVD must be placed in a center with full neurosurgical capabilities, because immediate neurosurgical intervention can be needed if a complication of EVD placement, such as bleeding, is encountered.

<span class="mw-page-title-main">Foster Kennedy syndrome</span> Medical condition

Foster Kennedy syndrome is a constellation of findings associated with tumors of the frontal lobe.

<span class="mw-page-title-main">Cerebrospinal fluid leak</span> Medical condition

A cerebrospinal fluid leak is a medical condition where the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord leaks out of one or more holes or tears in the dura mater. A CSF leak is classed as either nonspontaneous (primary), having a known cause, or spontaneous (secondary) where the cause is not readily evident. Causes of a primary CSF leak are those of trauma including from an accident or intentional injury, or arising from a medical intervention known as iatrogenic. A basilar skull fracture as a cause can give the sign of CSF leakage from the ear nose or mouth. A lumbar puncture can give the symptom of a post-dural-puncture headache.

A lumbar–peritoneal shunt is a technique to channelise the cerebrospinal fluid (CSF) from the lumbar thecal sac into the peritoneal cavity.

The monitoring of intracranial pressure (ICP) is used in the treatment of a number of neurological conditions ranging from severe traumatic brain injury to stroke and brain bleeds. This process is called intracranial pressure monitoring. Monitoring is important as persistent increases in ICP is associated with worse prognosis in brain injuries due to decreased oxygen delivery to the injured area and risk of brain herniation.

Increased intracranial pressure (ICP) is one of the major causes of secondary brain ischemia that accompanies a variety of pathological conditions, most notably traumatic brain injury (TBI), strokes, and intracranial hemorrhages. It can cause complications such as vision impairment due to intracranial pressure (VIIP), permanent neurological problems, reversible neurological problems, seizures, stroke, and death. However, aside from a few Level I trauma centers, ICP monitoring is rarely a part of the clinical management of patients with these conditions. The infrequency of ICP can be attributed to the invasive nature of the standard monitoring methods. Additional risks presented to patients can include high costs associated with an ICP sensor's implantation procedure, and the limited access to trained personnel, e.g. a neurosurgeon. Alternative, non-invasive measurement of intracranial pressure, non-invasive methods for estimating ICP have, as a result, been sought.

<span class="mw-page-title-main">Visual impairment due to intracranial pressure</span>

Spaceflight-associated neuro-ocular syndrome (SANS), previously called spaceflight-induced visual impairment, is hypothesized to be a result of increased intracranial pressure (ICP), although, experiments directly measuring ICP in parabolic flight have shown ICP to be in normal physiological ranges during acute weightless exposure. The study of visual changes and ICP in astronauts on long-duration flights is a relatively recent topic of interest to space medicine professionals. Although reported signs and symptoms have not appeared to be severe enough to cause blindness in the near term, long term consequences of chronically elevated intracranial pressure are unknown.

John Douglas Pickard is a British professor emeritus of neurosurgery in the Department of Clinical Neurosciences of University of Cambridge. He is the honorary director of the National Institute for Health Research (NIHR) Healthcare Technology Cooperative (HTC) for brain injury. His research focuses on advancing the care of patients with acute brain injury, hydrocephalus and prolonged disorders of consciousness through functional brain imaging, studies of pathophysiology and new treatments; as well as focusing on health, economic and ethical aspects.

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  10. ↑ Gasparian, Suzie; Geng, Xianzhang; Hawy, Eman (2021-09-01). "Intracranial hypertension associated with topical tretinoin use". American Journal of Ophthalmology Case Reports. 23: 101130. doi:10.1016/j.ajoc.2021.101130. ISSN   2451-9936. PMC   8207225 . PMID   34169180.
  11. ↑ Holst, Anders Vedel; Danielsen, Patricia Louise; Romner, Bertil (2011-01-31). "A severe case of tetracycline-induced intracranial hypertension". Dermatology Reports. 3 (1): e1. doi:10.4081/dr.2011.e1. ISSN   2036-7406. PMC   4211491 . PMID   25386253.
  12. ↑ Lee, Brendon W. H.; Lau, Fiona S.; Francis, Ian C. (2019-07-01). "In Pseudotumor Cerebri, Hormonal Contraception is Not Associated, and the Diagnosis Remains Idiopathic Intracranial Hypertension". American Journal of Ophthalmology. 203: 116. doi:10.1016/j.ajo.2019.02.019. ISSN   0002-9394. PMID   31014540. S2CID   129943755.
  13. ↑ url=https://www.fda.gov/media/159663/download]]
  14. 1 2 Farb, RI; Vanek, I; Scott, JN; Mikulis, DJ; Willinsky, RA; Tomlinson, G; terBrugge, KG (May 13, 2003). "Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis". Neurology. 60 (9): 1418–24. doi:10.1212/01.wnl.0000066683.34093.e2. PMID   12743224. S2CID   34459740.
  15. 1 2 3 4 Ahmed, RM; Wilkinson, M; Parker, GD; Thurtell, MJ; Macdonald, J; McCluskey, PJ; Allan, R; Dunne, V; Hanlon, M; Owler, BK; Halmagyi, GM (Sep 2011). "Transverse sinus stenting for idiopathic intracranial hypertension: a review of 52 patients and of model predictions". AJNR. American Journal of Neuroradiology. 32 (8): 1408–14. doi: 10.3174/ajnr.a2575 . PMC   7964366 . PMID   21799038.
  16. ↑ "UOTW #5 - Ultrasound of the Week". Ultrasound of the Week. 17 June 2014. Retrieved 27 May 2017.
  17. ↑ Tan YJ, Choo C (2020). "Idiopathic Intracranial Hypertension – Characteristic MRI Features". Headache. 60 (9): 267–8. doi:10.1111/head.13931. PMID   32757392. S2CID   221014881.
  18. 1 2 3 Dandy WE (October 1937). "Intracranial pressure without brain tumor - diagnosis and treatment". Annals of Surgery. 106 (4): 492–513. doi:10.1097/00000658-193710000-00002. PMC   1390605 . PMID   17857053.
  19. ↑ Smith JL (1985). "Whence pseudotumor cerebri?". Journal of Clinical Neuroophthalmology. 5 (1): 55–6. PMID   3156890.
  20. 1 2 Digre KB, Corbett JJ (2001). "Idiopathic intracranial hypertension (pseudotumor cerebri): A reappraisal". Neurologist. 7: 2–67. doi:10.1097/00127893-200107010-00002.
  21. ↑ Thurtell, Matthew J. (October 2019). "Idiopathic Intracranial Hypertension". CONTINUUM: Lifelong Learning in Neurology. 25 (5): 1289–1309. doi:10.1212/CON.0000000000000770. ISSN   1538-6899. PMID   31584538. S2CID   203659948.
  22. ↑ Teleb, MS; Cziep, ME; Lazzaro, MA; Gheith, A; Asif, K; Remler, B; Zaidat, OO (2013). "Idiopathic Intracranial Hypertension. A Systematic Analysis of Transverse Sinus Stenting". Interventional Neurology. 2 (3): 132–143. doi:10.1159/000357503. PMC   4080637 . PMID   24999351.
  23. ↑ Yadav, YadR; Parihar, Vijay; Sinha, Mallika (1 January 2010). "Lumbar peritoneal shunt". Neurology India. 58 (2): 179–84. doi: 10.4103/0028-3886.63778 . PMID   20508332.
  24. ↑ Curry WT, Butler WE, Barker FG (2005). "Rapidly rising incidence of cerebrospinal fluid shunting procedures for idiopathic intracranial hypertension in the United States, 1988-2002". Neurosurgery. 57 (1): 97–108, discussion 97–108. doi:10.1227/01.NEU.0000163094.23923.E5. PMID   15987545. S2CID   38715388.
  25. ↑ Quincke HI (1893). "Meningitis serosa". Sammlung Klinischer Vorträge. 67: 655.
  26. ↑ Nonne M (1904). "Ueber Falle vom Symptomkomplex "Tumor Cerebri" mit Ausgang in Heilung (Pseudotumor Cerebri)". Deutsche Zeitschrift für Nervenheilkunde (in German). 27 (3–4): 169–216. doi:10.1007/BF01667111. S2CID   31708166.
  27. 1 2 3 Johnston I (2001). "The historical development of the pseudotumor concept". Neurosurgical Focus. 11 (2): 1–9. doi: 10.3171/foc.2001.11.2.3 . PMID   16602675.
  28. ↑ Symonds CP (1931). "Otitic hydrocephalus". Brain. 54: 55–71. doi:10.1093/brain/54.1.55. Also printed in Symonds CP (January 1932). "Otitic hydrocephalus". Br Med J. 1 (3705): 53–4. doi:10.1136/bmj.1.3705.53. PMC   2519971 . PMID   20776602.
  29. ↑ Foley J (1955). "Benign forms of intracranial hypertension; toxic and otitic hydrocephalus". Brain. 78 (1): 1–41. doi:10.1093/brain/78.1.1. PMID   14378448.
  30. ↑ Corbett JJ, Thompson HS (October 1989). "The rational management of idiopathic intracranial hypertension". Archives of Neurology. 46 (10): 1049–51. doi:10.1001/archneur.1989.00520460025008. PMID   2679506.
  31. ↑ Bandyopadhyay S (2001). "Pseudotumor cerebri". Archives of Neurology. 58 (10): 1699–701. doi:10.1001/archneur.58.10.1699. PMID   11594936.

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