Cerebrospinal Fluid : CSF Disorders


2 Categories : intracranial hypotension OR hypertension

Spinal Fluid Leaks
Spontaneous Leak
Spontaneous intracranial hypotension (SIH) (from Pilates)
Saggy Brain Syndrome


Normal Pressure Hydrocephalus
Positional HeadachePost Dural Positional Headache

Chiari Malformation associated with either hypo or hyper
cerebellar tonsils usually sag into the foramen magnum

Cushing's Triad :   (with acute head trauma)
indicates increased intracranial pressure
brain swelling leads to brain hypoxia 
-> reflex increase systolic pressure
-> compression of medulla oblongata and CN X

becomes a positive feedback loop with increased intracranial pressure

1. hypertension (hypoxia ->inc. Systolic BP >180)
2. bradycardia  (compressed vagus nerve which controls SA Node, therefore less stimulation of SA Node by vagus.
3. dec RR  (compressed medulla oblongata -> slow erratic breathing pattern)

opposite to hypovolemic shock.

increase Respiratory Rate  reduces CO2 leads to dilated arterioles which lowers systolic pressure which reduces intracranial pressure.

urinary frequency and urgency with hydrocephalus

Empty Sella Syndrome

Empty sella syndrome is a radiological finding where spinal fluid is found within the sella, the space created for the pituitary (anchor sign).
two categories based on degree:

1.    Partial empty sella syndrome – when less than 50% of the sella is filled with spinal fluid and the pituitary gland thickness ranges from 3 to 7 mm, with 7 mm being the lower limit of normal thickness.

2.   Total empty sella syndrome – when more than 50% of the sella is filled with spinal fluid and the pituitary gland thickness is less than or equal to 2 mm.


1.  Primary empty sella syndrome – happens when there is a combination of (i) increased spinal fluid pressure and (ii) a defect in the diaphragma sellae, a membrane that sits on top of the pituitary. Primary empty sella is seen during pregnancy, obesity, and pseudotumor cerebri (a condition of increased spinal fluid pressure seen in obesity and associated with vision loss).
2.  Secondary empty sella syndrome - happens when the pituitary gland regresses after surgery to remove a pituitary tumor; radiation to treat a pituitary tumor; or a condition that damages the pituitary gland such as an old history of pituitary apoplexy that the patient was unaware of, hypophysitis, or neurosarcoidosis.

Emtpy sella syndrome patients often have impairment of one or more pituitary axes.

Empty sella is often an incidental imaging finding without associated symptoms. If there are symptoms, patients with empty sella syndrome can have headaches as symptoms of elevated spinal fluid pressure; symptoms of hypopituitarism; or visual symptoms, which can sometimes be due to downward, prolapse of the optic chiasm into the empty sella.

Treatment is often not needed since empty sella is often an incidental finding. If there is associated hypopituitarism, hormone replacement is administered as indicated. Neurosurgery may be needed if there is associated chiasm prolapse in need of neurosurgical correction; if a small mciroadenoma is identified within the empty sella (in which case the finding may reflect an apoplexy event that went undiagnosed and reabsorbed over time, leaving behind them empty sella and microadenoma); or if pseudotumor cerebri is diagnosed and a ventriculoperitoneal shunt is needed.

Fronto-Temporal Dementia

Pseudotumor cerebri   
(no tumor)  =  intracranial hypertension

can present in young and older.
mainly in females
mainly in overweight
intracranial hypertension

eyes exam for pappiledema
lumbar puncture
intracranial pressure monitoring

lose weight 
diamox : reduces fluid made in head
these two resolve 50%
surgery :
- shunting  tube from ventricles to peritoneal cavity
- optic sheath fenestration  to let fluid out
- venous stenting  intracranial veins are mildly blocked, so they are stented wider.

(can come from compressed pituitary with cranial hypertension)

caused by:
-    Tumors in or near the pituitary gland (which are usually benign, meaning not cancer)

-    Radiation treatment for a tumor, which can destroy pituitary gland tissue
-    Chemotherapy
-    Brain surgery
-    Traumatic brain injury, such as with a head injury from an accident
-    Severe bleeding in the brain or severe blood loss during childbirth
-    Tuberculosis or meningitis
-    Certain conditions present at birth
-    idiopathic

Symptoms :
-    Stomach pain, decreased appetite, nausea and vomiting, and constipation
-    Excessive thirst and urination
-    Fatigue and/or weakness
-    Anemia, meaning weakness from not having enough red blood cells
-    Headache and dizziness
-    Sensitivity to cold
-    Weight loss or weight gain
-    Stiffness in the joints
-    Hypophysitis (inflammation of the pituitary gland)
-    Histiocytosis
-    In women: loss of armpit or pubic hair, decreased sex drive, infertility, problems with breast feeding, irregular or no menstrual periods, and hot flashes
-    In men: loss of hair (on the face, or in the armpits or pubic area), decreased sex drive, infertility
-    In children, problems with growth (including height) and sexual development

How is hypopituitarism diagnosed?
- hormone levels with blood tests. 

- MRI of your pituitary gland


- hormones, sometimes for life. Your doctor also will teach you how to take extra cortisone (a hormone) when you are sick or under stress. If a tumor is causing your hypopituitarism, you might need surgery to remove it and/or possibly radiation treatment. If needed, you can take medicine for infertility.

Ehler Danos Syndrome

Joint Hypermobility Syndrome JHS

Screening tool
1.  Have you ever been able to place hands flat on floor with straight knees? 
2.  Thumb to forearm?
3.  As a child, contort your body or do the splits? 
4.  before 20yo, did you more than once dislocate shoulder or knee cap? 
5.  do you consider yourself double jointed? 

Indian Journal of Radiology and Imaging, Vol. 12, No. 2, April-June, 2002, pp. 197-200
Neuroradiology Head and Neck Imaging
External hydrocephalus in children

Although most cases are idiopathic, various authors have reported association with prematurity, trauma, subarachnoid, subdural or intraventricular hemorrhage, meningitis, vitamin A deficiency and genetic syndromes. Idiopathic EH is generally a benign, self-limited condition that presents between the ages of 3 and 12 months and resolves spontaneously by 2-3 years of age. Because of the good prognosis, surgical intervention is rarely required. Only in those patients who experience gross motor delay, rise in intracranial pressure or huge collections, ventriculoperitoneal shunting may be necessary [3]."

cranial nerve VI palsy  abducens controls lateral rectus.

Normal Pressure hydrocephalus
especially in elderly pressure is normal.
imbalance, memory, bladder control
dx 3 steps
symptoms triad gait, cognition/memory, bladder control
treatable with shunt (trial removal before shunting)

no medical treatment
surgical via shunt to abdomen

CSF leaks
intracranial hypotension
leaking into nose,
trauma to skull
brain is sagging down pulling down = severe headaches when standing

targeted blood patch over leaks only for lower spinal cord


csf filtered from blood through choroid plexi on floor of LVs and roof of 3

The choroid plexus receives its blood supply from the anterior and posterior choroidal arteries, branches of the internal carotid artery, and the posterior cerebral artery.

LVs join with 3 via interventricular foramen.

3 and 4  connected via  cerebral aqueduct, which when compressed/obstructed is most common cause of hydrocephalus.

4 is within the brainstem joins via lateral aperture with pontine cistern on ventral surface of brainstem, and medial aperture with cerebro-medullary cistern and onto either
- around cerebellum and onto superior cistern then interpeduncular cistern
- down the subdural space of spinal cord to lumbar cistern (site of lumbar puncture)

CSF then flows upwards and joins flow of 4 and superior cistern.

Ventral cisterns flow across cortical surfaces in sub arachnoid spaces draining into the superior saggital sinus which drain into the confluence of sinuses where it is joined by blood from subcortical veins in the straight sinus.  The straight and superior saggital sinus merge to form confluence of sinuses which enter venous system.

3 sits between pituitary, pineal, HT, thalamus.
ventricles contact major nuclei and cerebrum.

Melatonin produced in pineal gland, and released into CSF for broad distribution.  Highly implicated in sleep cycles.
During sleep at night, melatonin level increases 18x in CSF, and only 6x in blood.

cuboidal epithelium cells highly specialized
generate polarized electrical charge,  ionic flow, osmotic gradient, which draws water.....
so CSF has Na+, Cl-, HCO3- ions, water, bicarbonate, small amounts of amino acids, protein, and glucose,  growth factors, hormones.

No cells typically.
But small numbers of white blood cells typically monocytes exist after entering directly from blood

lateral + 3 through aqueduct to 4 in brainstem, then around the sub arachnoid spaces of outer brain and spinal cord.....then filtered out through arachnoid villi/granulations into venous sinuses (saggital sinus).
A. granulations have one way valves, so theoretically vulnerable to clogging.
Also flows into lymphatic channels i.e. along olfactory nerve through cribriform plate.
Also absorbed through cranial and peripheral nerve sheaths.

Intra Cranial CSF Pressures

Lowest normal pressure
sit or stand  -10 mmHg   parenchymal transducer in convexity. 

 -10 to 0 mmHg is normal in standing

 Supine   0 - 5 mmHg  (common accepted 7-15 mmHg)

Sit  -5 - 5     Hypo down to -20 in sit

Stand -5 - 2

Prone  can go over 25 mmHg

left sidely 
Supine and rotate head left or right (compresses venous system)
leads to increase ICP 15-30 mmHg

Intra-Cranial Hypertension can be masked by Leaks.
Then, when a blood patch is applied hypertension results. 

Cough  up to 80mmHg

Straining  (lifting weights)  may be as high.

hyponeic episodes  lead to increased ICP 70 mmHg  throughout the night.
but this person can test normal ICP during day.

100 mmHg


CSF returns to the vascular system by entering the dural venous sinuses via arachnoid granulations.[2] These are outpouchings of the arachnoid mater into the venous sinuses around the brain, with valves to ensure one-way drainage.[2] This occurs because of a pressure difference between the arachnoid mater and venous sinuses.[3] CSF has also been seen to drain into lymphatic vessels,[20] particularly those surrounding the nose via drainage along the olfactory nerve through the cribriform plate. The pathway and extent are currently not known,[1] but may involve CSF flow along some cranial nerves and be more prominent in the neonate.[3] CSF turns over at a rate of three to four times a day.[2] CSF has also been seen to be reabsorbed through the sheathes of cranial and spinal nerve sheathes, and through the ependyma.[3]


The composition and rate of CSF generation are influenced by hormones and the content and pressure of blood and CSF.[3] For example, when CSF pressure is higher, there is less of a pressure difference between the capillary blood in choroid plexuses and CSF, decreasing the rate at which fluids move into the choroid plexus and CSF generation.[3] The autonomic nervous system influences choroid plexus CSF secretion, with activation of the sympathetic nervous system increasing secretion and the parasympathetic nervous system decreasing it.[3] Changes in the pH of the blood can affect the activity of carbonic anhydrase, and some drugs (such as frusemide, acting on the Na-K-Cl cotransporter) have the potential to impact membrane channels.[3]

Normal cerebral O2 consumption   3.3ml/100g/minute
Comatose pts unlikely to regain consciousness if <1.4ml/100g/minute
CSF lactacidosis as CBF decreases

Intraventricular Fluid Pressure and Lumbar CSF pressure - lack of correlation?

CSF  125-150 mls total
500 mls made per day, turnover is 4x/day

blood 5000mls
plasma 55% = 2750 mls (18x CSF)



Spinal Fluid Leaks  - DDx discussed

Compound CSF Disorders

Covers embryonic developmental aspects, and early osteopathic theories.


Excellent detail on
Intracranial Hypertension
- empty sella syndrome w flattened pituitary (hyperprolactinemia leading to dec testosterone & hypogonadism, decreased growth hormone, hypothyroidism)

Colorado Chiari Institute
anatomy and csf disorder effect on GUT



Hypertension, Intracranial

; .
Author Information
1; 2.
1 Baptist Regional Medical Center
2 Great Plains Health
Last Update: October 27, 2018.


The human skull is a relatively fixed volume structure of approximately 1400 to 1700 mL. Physiologically its components consist of 80% brain parenchyma, 10% cerebrospinal fluid, and 10% blood. Since the skull is considered an unchangeable volume, any increase in the volume of components within the skull or an addition of a pathologic element will result in increased pressure within the skull. Pathologic structures that can cause increased ICP may include mass lesions, abscesses, and hematomas.
The physiologic volume of the brain parenchyma is a relatively constant value in adults: however, it may be adjusted by mass lesions or in the setting of cerebral edema. Cerebral edema can occur with acute hypoxic encephalopathy, large cerebral infarction, and severe traumatic brain injury. CSF and blood volume in the intracranial space will vary on a regular basis as these are the primary regulators of intracranial pressure. CSF volume is primarily regulated via choroid plexus production at a rate of approximately 20 mL per hour physiologically and through its reabsorption at a similar rate by arachnoid granulations which drain into the venous system of the skull.  The control mechanisms for maintaining appropriate CSF pressures may become damaged in neurological injuries such as stroke or trauma. Increased CSF production above the rate at which it can be reabsorbed such as in the presence of a choroid plexus papilloma leads to increased pressure.
A failure to reabsorb at a sufficient rate to match normal secretion rate is another possibility and is seen with arachnoid granulation adhesions after bacterial meningitis. Ventricular obstruction may also induce decreased reabsorption of CSF causing hydrocephalus. The primary regulator of blood volume is via cerebral blood flow. Diseases which obstruct venous outflows such as a venous sinus thrombosis, jugular vein compression, or structural changes due to neck surgery may cause blood congestion within the skull, thus increasing pressure. Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is a term for increased intracranial pressure due to unknown causes with no known structural change.
Etiology of intracranial hypertension can be divided into 2 categories:
Primary or Intracranial Causes
  • Trauma ( epidural hematoma, subdural hematoma, intracerebral hemorrhage or contusions)
  • Brain tumors
  • Stroke
  • Nontraumatic intracerebral Hemorrhage ( aneurysm rupture)
  • Idiopathic or benign intracranial hypertension
  • Hydrocephalus
  • Meningitis
Secondary or Extracranial Causes
  • Hypoventilation (hypoxia or hypercarbia)
  • Hypertension
  • Airway obstruction
  • Metabolic (drug induced)
  • Seizures
  • Hyperpyrexia
  • High altitude cerebral edema


The exact epidemiology of intracranial hypertension depends on its etiology. However, of special note is idiopathic intracranial hypertension where up to 90% of affected individuals are women of childbearing age. Individuals with chronic hypertension or obesity are also at an increased risk for developing intracranial hypertension. A frequency of occurrence has been established to be 1.0 per 100,000 in the general population, 1.6 to 3.5 per 100,000 in women, and 7.9 to 20 per 100,000 in women who are overweight.


Anytime there is an elevation in ICP, there is the risk of subsequent injury from direct brainstem compression or from a reduction in cerebral blood flow. Clinically, cerebral blood flow is evaluated via measurement of cerebral perfusion pressure where:
Cerebral perfusion pressure = Mean arterial pressure - Intracranial pressure
Cerebral perfusion pressure in simpler terms is the pressure of blood flowing to the brain and is the driving force for delivery of oxygen necessary for neuronal functioning. Normally, this is a constant value of 50 to 100 mm Hg due to autoregulation. The impact that cerebral perfusion pressure holds is in the concept that blood flow will occur from an area of higher concentration to an area of lower concentration.  When ICP becomes elevated, cerebral perfusion pressures decrease, and the net driving force of blood flow to the brain becomes decreased.  The physiologic autoregulatory response to a decrease in cerebral perfusion pressure is to increase mean arterial pressures systemically and to vasodilate cerebral blood vessels. This results in increased cerebral blood volume that further increases ICP.  Paradoxically, this further reduces cerebral perfusion pressure producing a feedback cycle that results in the total reduction of cerebral flow and perfusion. The result of this feedback loop is cerebral ischemia and brain infarction with neuronal death. In cases where intracranial hypertension is the result of hemorrhage, increased blood pressure will worsen intracranial bleeding, thus worsening intracranial hypertension.

History and Physical

Symptoms of elevated intracranial hypertension are primarily derived from neurological irritation, compression, or displacement and papilledema. Non-specific headaches are recorded in almost all cases and are likely mediated via the pain fibers of the trigeminal nerve in the dura and blood vessels of the brain. Pain is generally diffuse and worse in the mornings with exacerbation by the Valsalva maneuver. Nausea and vomiting are common presentations of elevated ICP. Patients can present with double vision most frequently with horizontal diplopia associated with CN VI palsy from compression. Transient visual abnormalities occur frequently, often described as a gradual dimming of vision in one or both of the eyes. Visual abnormalities worsen with changes in posture. Peripheral visual loss may be reported and most commonly begins in the nasal inferior quadrant with subsequent loss of the central visual field.  Alterations in visual acuity with blurring or distortion may occur.  Variable degrees of loss of color distinction may occur. In more severe or chronic cases, a sudden visual loss can occur due to intraocular hemorrhage. Tinnitus with a pulsing rhythm exacerbated by supine or bending positions and Valsalva maneuver can occur. Radicular pain, numbness, or paresthesias are possible and most commonly associated with localized compression or possible herniation of the brain. Neurological findings are indications of severe disease. The anatomical locations where herniation is most likely to occur include the subfalcine, central transtentorial, uncal transtentorial, cerebellar tonsillar/foramen magnum, and transcalvarial lobes. These types of changes may lead to decreased consciousness or responsiveness. Focal neurological constellations depend on which region of the brain has herniated. Often this results in a stupor state or more severely with coma due to the local effect of mass lesions or pressure on the reticular formations of the midbrain. It may further lead to respiratory compromise.
Physical exam findings can vary widely depending on etiology. A change in mental status or comatose patient should prompt urgent evaluation. A complete neurological assessment is essential whenever intracranial hypertension is suspected. Cranial nerve assessment is particularly important for identifying lesions. Cranial nerve VI palsy is most common. Blunting of the pupillary reflex with fixed dilation of one pupil is also highly associated with herniation syndromes. Spontaneous periorbital bruising may be present as well. 
A classic triad of bradycardia, respiratory depression, and hypertension is known as Cushing's triad and is highly indicative of intracranial hypertension.

Fundoscopic examination looking for retinal hemorrhages or papilledema is essential. Alterations in respiratory drive and effort may occur leading to failure of respiration and oxygenation.
Infants can have widening of cranial sutures and bulging fontanelle.


Complete blood count (CBC) and complete metabolic panel (CMP) are usually checked in all patients with suspected intracranial hypertension to evaluate for infection, anemia, and electrolyte abnormalities. Initial evaluation should include a head CT scan. CT scan findings of cerebral edema such as compressed basal cisterns and midline shift are predictive of elevated ICP. However, the absence of these findings does not rule out intracranial hypertension. A head MRI is more accurate than head CT in evaluating elevated ICP and to looking for potential etiology. Bedside ultrasonography also can be used to measure the diameter of the optic nerve sheath to determine intracranial hypertension. However, this study is limited by operator skill and not frequently used. A lumbar puncture may sometimes be needed for diagnosis. However, it should be delayed until neuroimaging, especially in those with suspicion of impending herniation. When LP is performed, in addition to measuring opening pressures, CSF should also be tested for infection and other potential etiology. Invasive measurement of ICP is definitive for diagnosis and improves the physician’s ability to maintain adequate cerebral perfusion pressure (CPP). There are 4 main anatomical sites used for clinical measurement of intracranial pressure: intraventricular, intraparenchymal, subarachnoid, and epidural. Ventriculostomy catheter is preferred device for ICP monitoring and can be used even for therapeutic CSF drainage to lower ICP. When ventricles cannot be cannulated, intraparenchymal devices using microsensor and fibreoptic transducer may be used. Subdural and epidural monitors are not as accurate as ventriculostomy and parenchymal monitors.

Treatment / Management

Treatment of chronic intracranial hypertension is mainly focused on treating and reversing the etiology.
A sudden increase in ICP is a neurosurgical emergency, requiring close monitoring in an intensive care unit (ICU) setting. For acute intracranial hypertension, a patient should first be stabilized with healthcare professionals aiming for hemodynamic stability, and preventing and treating factors that may aggravate or precipitate intracranial hypertension. These patients should have close monitoring of heart rate, blood pressure, body temperature, ventilation and oxygenation, blood glucose, input and output, and ECG. Patients with suspected intracranial hypertension, especially with severe traumatic brain injury, should also have ICP monitoring.
It is vital to prevent and treat factors that may aggravate or precipitate intracranial hypertension. These interventions are used to buy time until the underlying etiology is identified and corrected.
  • Keep the head elevated to 30 degrees and neutrally positioned to minimize venous outflow resistance and improve cerebral spinal fluid displacement from the intracranial to the spinal compartment.
  • Hypoxia and hypercapnia can increase ICP. Controlling ICP through optimal respiratory management is crucial. It is essential to control ventilation to maintain a normal PaCO2 and maintain adequate oxygenation without increasing the PEEP.
  • Agitation and pain can increase blood pressure and ICP. Adequate sedation and analgesia is an important adjunctive treatment. Since most sedating medications can have effects on blood pressure, medications with minimal hypotensive effect should be preferred. Hypovolemia can precipitate the hypotensive side effects and should be treated before administering sedative agents. Shorter-acting agents have the advantage of allowing brief interruption of sedation to evaluate neurological status.
  • Fever can increase brain metabolic rate and is a potent vasodilator, which in turn, increase the cerebral blood flow and increased ICP. Fever should be controlled with antipyretics and cooling blankets and infectious causes must be ruled out.
  • Elevated blood pressure is commonly seen in patients with intracranial hypertension especially when due to traumatic brain injury. In patients with untreated intracranial mass lesions, cerebral perfusion is maintained by the higher blood pressure, and systemic hypertension should not be treated. The absence of an intracranial mass lesion presents a more individualized, controversial decision when treating systemic hypertension. When antihypertensive are used, the preferred treatment includes beta-blockers like labetalol and esmolol or calcium channel blockers because they reduced blood pressure without affecting ICP. Agents with short half-lives should be preferred. Avoid vasodilators like sodium nitroprusside, nitroglycerin, and nifedipine.
  • Seizures can contribute and complicate elevated ICP and should be prevented by prophylactic medications, especially in severe traumatic brain injuries.
For patients with sustained intracranial hypertension, additional measures are needed to control the ICP.
  • Emergent surgical management should be considered when there is sudden intracranial hypertension, or it is refractory to medical management.
  • Nondepolarizing muscle relaxants along with sedatives may be used to treat intracranial hypertension caused by posturing, coughing or agitation. When a neuromuscular blockade is used, EEG should be monitored to rule out convulsive states.
  • Hyperosmolar therapy is used for severe, acute intracranial hypertension.
Mannitol is commonly used as a hyperosmolar agent and is usually given as a bolus of 0.25 to 1 g/kg body weight. Serum osmolality should be kept less than 320 mOsm to avoid side effects of therapy like renal failure, hypokalemia, and hypo-osmolarity.
Hypertonic saline can also create an osmotic shift from the interstitial space of brain parenchyma into the intravascular compartment in the presence of an intact blood-brain barrier. Hypertonic saline has an advantage over mannitol for hypovolemic and hypotensive patients. Adverse effects of hypertonic saline administration include hematological and electrolyte abnormalities. Hyponatremia should be excluded before administering hypertonic saline to reduce the risk of central pontine myelinolysis.
  • Hyperventilation can be used for rapid reduction in ICP if there are clinical signs of herniation or with severe intracranial hypertension. Hyperventilation decreases PaCO2 which causes vasoconstriction of cerebral arteries, resulting in reduced cerebral blood flow and reduced intracranial pressure.
  • Barbiturate coma should be considered for patients with refractory intracranial hypertension.
  • Routine induction of hypothermia is not indicated; however, moderate hypothermia may be an effective adjunctive treatment for increased ICP refractory to other medical management.
  • Steroids are commonly used for primary and metastatic brain tumors to decrease vasogenic cerebral edema. For other neurosurgical disorders like traumatic brain injury or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit, and sometimes may even be detrimental.
Surgical Interventions
  • Resection of intracranial mass lesions producing elevated ICP should be done as soon as possible.
  • CSF drainage lowers ICP immediately by reducing intracranial volume. This modality can be an important adjunct treatment for lowering ICP. However, it has limited utility when the brain is diffusely swollen and the ventricles are collapsed.
  • Decompressive craniectomy is used to treat severe uncontrolled intracranial hypertension. It involves surgical removal of part of the calvaria to create a window in the skull, allowing for herniation of swollen brain through the bone window to relieve pressure.

Differential Diagnosis

  • Acute nerve injury
  • Benign intracranial hypertension (Pseudotumor cerebri)
  • Cerebrovascular ischemia/hemorrhage
  • Hydrocephalus
  • Intracranial epidural abscess
  • Intracranial hemorrhage
  • Leptomeningeal carcinoma
  • Low-grade astrocytoma
  • Lyme disease
  • Meningioma
  • Meningitis
  • Migraine headache
  • Papilledema
  • Subarachnoid hemorrhage
  • Venous sinus thrombosis


Prognosis is highly variable depending on etiology and varies from benign to lethal. Children usually can tolerate higher intracranial pressure (ICP) for a longer period.


To access free multiple choice questions on this topic, click here.


Gupta S, Maan V, Agarwal P. Diagnostic criteria in pediatric intracranial hypertension. J AAPOS. 2018 Aug;22(4):333. [PubMed]
Griffith B, Capobres T, Patel SC, Marin H, Katramados A, Poisson LM. CSF Pressure Change in Relation to Opening Pressure and CSF Volume Removed. AJNR Am J Neuroradiol. 2018 Jun;39(6):1185-1190. [PubMed]
Burkett JG, Ailani J. An Up to Date Review of Pseudotumor Cerebri Syndrome. Curr Neurol Neurosci Rep. 2018 May 02;18(6):33. [PubMed]
Mazzeo AT, Gupta D. Monitoring the injured brain. J Neurosurg Sci. 2018 Oct;62(5):549-562. [PubMed]
Binder DK, Dillon WP, Fishman RA, Schmidt MH. Intrathecal saline infusion in the treatment of obtundation associated with spontaneous intracranial hypotension: technical case report. Neurosurgery. 2002 Sep;51(3):830-6; discussion 836-7. [PubMed]
Fishman RA. The cerebrospinal fluid production rate is reduced in dementia of the Alzheimer's type. Neurology. 2002 Jun 25;58(12):1866; author reply 1866. [PubMed]
Fishman RA, Dillon WP. Intracranial hypotension. J. Neurosurg. 1997 Jan;86(1):165. [PubMed]
Fishman RA. The pathophysiology of pseudotumor cerebri. An unsolved puzzle. Arch. Neurol. 1984 Mar;41(3):257-8. [PubMed]
Fishman RA. Brain edema. N. Engl. J. Med. 1975 Oct 02;293(14):706-11. [PubMed]
Friedman DI, Jacobson DM. Idiopathic intracranial hypertension. J Neuroophthalmol. 2004 Jun;24(2):138-45. [PubMed]
Dotan G, Cohen E, Klein A, Kesler A. Reduced Suprathreshold Odor Identification in Patients with Pseudotumor Cerebri: A Non-Randomized Prospective Study. Isr. Med. Assoc. J. 2018 Jan;20(1):34-37. [PubMed]
Lassen NA, Agnoli A. The upper limit of autoregulation of cerebral blood flow--on the pathogenesis of hypertensive encepholopathy. Scand. J. Clin. Lab. Invest. 1972 Oct;30(2):113-6. [PubMed]
Enevoldsen EM, Jensen FT. Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury. J. Neurosurg. 1978 May;48(5):689-703. [PubMed]