Hydrocephalus

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Practice Essentials

Hydrocephalus can be defined broadly as a disturbance of cerebrospinal fluid (CSF) formation, flow, or absorption, leading to an increase in volume occupied by this fluid in the central nervous system (CNS).[1] This condition could also be termed a hydrodynamic CSF disorder. See the image below.



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Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatat....

Signs and symptoms

Clinical features of hydrocephalus are influenced by the patient's age, the cause of the hydrocephalus, the location of the obstruction, its duration, and its rapidity of onset.

Symptoms in infants include poor feeding, irritability, reduced activity, and vomiting.

Symptoms in children and adults include the following:

Children may also exhibit stunted growth and sexual maturation from third ventricle dilatation. Adults may also have nausea that is not exacerbated by head movements; incontinence (urinary first, fecal later if condition remains untreated) indicates significant destruction of the frontal lobes and advanced disease.

Symptoms of normal pressure hydrocephalus (NPH) include the following:

See Clinical Presentation for more detail.

Diagnosis

Examination in infants may reveal the following findings:

Children and adults may demonstrate the following findings on physical examination:

Children may also exhibit the Macewen sign, in which a "cracked pot" sound is noted on percussion of the head.

Patients with NPH may exhibit the following findings on examination:

Testing

No specific blood tests are recommended in the workup for hydrocephalus. However, consider genetic testing and counseling when X-linked hydrocephalus is suspected, and evaluate the CSF in posthemorrhagic and postmeningitic hydrocephalus for protein concentration and to exclude residual infection.

Obtain electroencephalography in patients with seizures.

Imaging studies

The following imaging studies may be used to evaluate patients with suspected hydrocephalus:

See Workup for more detail.

Management

Surgery

Surgical treatment is the preferred therapeutic option in patients with hydrocephalus.[4] Most patients eventually undergo shunt placements, such as the following:

Rapid-onset hydrocephalus with ICP is an emergency. The following procedures can be done, depending on each specific case:

Repeat LPs can be performed for cases of hydrocephalus after intraventricular hemorrhage (which can resolve spontaneously). If reabsorption does not resume when the CSF protein content is less than 100 mg/dL, spontaneous resorption is unlikely to occur. LPs can be performed only in cases of communicating hydrocephalus.

Alternatives to shunting include the following:

Conservative management

Medical treatment is not effective in long-term treatment of chronic hydrocephalus; it is used as a temporizing measure to delay surgical intervention. Medical therapy may be tried in premature infants with posthemorrhagic hydrocephalus (in the absence of acute hydrocephalus, repeated taps are done not only to allow for potential resolution, but also to allow the protein level to reduce low enough that it will not clog any placed shunt). Normal CSF absorption may resume spontaneously during this interim period. Medical agents include carbonic anhydrase inhibitors (eg, acetazolamide) and loop diuretics (eg, furosemide) for the treatment of hydrocephalus are controversial and should be used only as temporary measures (such as patients who already have non-programmable shunts, or when shunt placement is not able to be done at that time).

See Treatment and Medication for more detail.

Background

Hydrocephalus can be defined broadly as a disturbance of formation, flow, or absorption of cerebrospinal fluid (CSF) that leads to an increase in volume occupied by this fluid in the CNS.[1] This condition also could be termed a hydrodynamic disorder of CSF. Acute hydrocephalus occurs over days, subacute hydrocephalus occurs over weeks, and chronic hydrocephalus occurs over months or years. Conditions such as cerebral atrophy and focal destructive lesions also lead to an abnormal increase of CSF in CNS. In these situations, loss of cerebral tissue leaves a vacant space that is filled passively with CSF. Such conditions are not the result of a hydrodynamic disorder and therefore are not classified as hydrocephalus. An older misnomer used to describe these conditions was hydrocephalus ex vacuo.

Benign external hydrocephalus (benign enlargement of the subarrachnoid spaces of infancy) is a self-limiting absorption deficiency of infancy and early childhood with mildly raised intracranial pressure (ICP) and enlarged subarachnoid spaces. The ventricles usually are not enlarged significantly, and resolution within 1 year is the rule.[5]

Normal pressure hydrocephalus (NPH) describes a condition that rarely occurs in patients younger than 60 years.[6] Enlarged ventricles and normal CSF pressure at lumbar puncture (LP) in the absence of papilledema led to the term NPH. However, intermittent intracranial hypertension has been noted during monitoring of patients in whom NPH is suspected, usually at night. The classic Hakim triad of symptoms includes gait apraxia, incontinence, and dementia. Headache is not a typical symptom in NPH.

Communicating hydrocephalus occurs when full communication occurs between the ventricles and subarachnoid space. It is caused by overproduction of CSF (rarely), defective absorption of CSF (most often, includes conditions such as intracranial hemorrhage or meningitis resulting in damage to the arachnoid granulations, where CSF is reabsorbed), or venous drainage insufficiency (occasionally). See the image below.



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Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recove....

Noncommunicating hydrocephalus occurs when CSF flow is obstructed within the ventricular system or in its outlets to the arachnoid space, resulting in impairment of the CSF from the ventricular to the subarachnoid space. The most common form of noncommunicating hydrocephalus is obstructive and is caused by intraventricular or extraventricular mass-occupying lesions that disrupt the ventricular anatomy.[7] See the images below.



View Image

Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatat....



View Image

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of ....



View Image

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventric....

Congenital hydrocephalus applies to the ventriculomegaly that develops in the fetal and infancy periods, often associated with macrocephaly.[8] The most common causes of congenital hydrocephalus are obstruction of the cerebral aqueduct flow, Arnold-Chiari malformation or Dandy–Walker malformation.[9]  These patients may stabilize in later years due to compensatory mechanisms but may decompensate, especially following minor head injuries. During these decompensations, determining the extent to which any new neurological deficits may be due to the new acute event, compared with hydrocephalus that may have gone unnoticed for many years, is difficult. An extremely severe variant of congenital hydrocephalus is hydranencephaly, where the brain's cerebral hemispheres are absent to varying degrees and the remaining cranial cavity is filled with cerebrospinal fluid.

Pathophysiology

Normal CSF production is 0.20-0.35 mL/min; most CSF is produced by the choroid plexus, which is located within the ventricular system, mainly the lateral and fourth ventricles. The capacity of the lateral and third ventricles in a healthy person is 20 mL. Total volume of CSF in an adult is 120 mL.

Normal route of CSF from production to clearance is the following: From the choroid plexus, the CSF flows to the lateral ventricle, then to the interventricular foramen of Monro, the third ventricle, the cerebral aqueduct of Sylvius, the fourth ventricle, the two lateral foramina of Luschka and one medial foramen of Magendie, the subarachnoid space, the arachnoid granulations, the dural sinus, and finally into the venous drainage.

ICP rises if production of CSF exceeds absorption. This occurs if CSF is overproduced, resistance to CSF flow is increased, CSF resorption is decreased, or venous sinus pressure is increased. CSF production falls as ICP rises. Compensation may occur through transventricular absorption (subependymal flow) of CSF and also by absorption along nerve root sleeves (which may result in enlarged optic nerve sheaths). The temporal and frontal horns dilate first, often asymmetrically. This may result in elevation of the corpus callosum, stretching or perforation of the septum pellucidum, thinning of the cerebral mantle, or enlargement of the third ventricle downward into the pituitary fossa (which may cause pituitary dysfunction) as well as dorsal midbrain compression resulting in Parinaud's syndrome (aralysis of upgaze, Pseudo-Argyll Roberson pupils, convergence-retraction nystagmus, eyelide retraction, and setting sun sign).

The mechanism of NPH has not been elucidated completely. Current theories include increased resistance to flow of CSF within the ventricular system or subarachnoid villi; intermittently elevated CSF pressure, usually at night; and ventricular enlargement caused by an initial rise in CSF pressure. The enlargement is maintained despite normal pressure because of the Laplace law. Although pressure is normal, the enlarged ventricular area reflects increased force on the ventricular wall.

Frequency

United States

The incidence of congenital hydrocephalus is 3 per 1,000 live births; the incidence of acquired hydrocephalus is not known exactly due to the variety of disorders that may cause it.

International

Incidence of acquired hydrocephalus is unknown. About 100,000 shunts are implanted each year in the developed countries, but little information is available for other countries.

Mortality/Morbidity

In untreated hydrocephalus, death may occur by tonsillar herniation secondary to raised ICP with compression of the brain stem and subsequent respiratory arrest.

Shunt dependence occurs in 75% of all cases of treated hydrocephalus and in 50% of children with communicating hydrocephalus. Patients are hospitalized for scheduled shunt revisions or for treatment of shunt complications or shunt failure. Poor development of cognitive function in infants and children, or loss of cognitive function in adults, can complicate untreated hydrocephalus. It may persist after treatment. Visual loss can complicate untreated hydrocephalus and may persist after treatment.

Epidemiology

Sex

Generally, incidence is equal in males and females. The exception is Bickers-Adams syndrome (X-linked hydrocephalus with stenosis of aqueduct of Sylvius), transmitted by females and manifested in males. NPH has a slight male preponderance.

Age

Incidence of human hydrocephalus presents a bimodal age curve. One peak occurs in infancy and is related to the various forms of congenital malformations and premature birth. Another peak occurs in adulthood, mostly resulting from NPH. Adult hydrocephalus represents approximately 40% of total cases of hydrocephalus.

The outcome of pediatric hydrocephalus has been studied frequently, but much remains unresolved about long-term and social outcomes.[10]

History

Clinical features of hydrocephalus are influenced by the following:

Symptoms in infants include the following:

Symptoms in children include the following:

Symptoms in adults include the following:

Symptoms of NPH include the following:

Physical

Physical findings in infants include the following:

Physical findings in children include the following:

Physical findings in adults include the following:

The following are physical findings found in NPH:

Causes

Congenital causes in infants and children include the following:[8]

Acquired causes in infants and children include the following:

Causes of hydrocephalus in adults include:

Causes of NPH may include the following (Most cases are idiopathic and are probably related to a deficiency of arachnoid granulations.):

Laboratory Studies

No specific blood tests are recommended in the workup for hydrocephalus.

Genetic testing and counseling might be recommended when X-linked hydrocephalus is suspected.

Evaluate cerebrospinal fluid (CSF) in posthemorrhagic and postmeningitic hydrocephalus for protein concentration and to exclude residual infection.

Imaging Studies

CT can assess the size of ventricles and other structures.

MRI can evaluate for Chiari malformation or cerebellar or periaqueductal tumors. It affords better imaging of the posterior fossa than CT. MRI can differentiate normal pressure hydrocephalus (NPH) from cerebral atrophy although the distinctions may be challenging. Flow voids in the third ventricle and transependymal fluid exudates are helpful. However, numerous suitable patients have a brain pattern suggestive of atrophy and small vessel ischemic disease that may ultimately be NPH.[14] Guidelines for imaging studies in suspected NPH have been established.[15]

CT/MRI criteria for acute hydrocephalus include the following:

CT/MRI criteria for chronic hydrocephalus include the following:

Ultrasonography through the anterior fontanelle in infants is useful for evaluating subependymal and intraventricular hemorrhage and in following infants for possible development of progressive hydrocephalus.

Radionuclide cisternography can be done in NPH to evaluate the prognosis with regard to possible shunting. If a late scan (48-72 h) shows persistence of ventricular activity with a ventricular to total intracranial activity (V/T ratio) greater than 32%, the patient is more likely to benefit from shunting.[16] Because of its poor sensitivity in predicting shunt response when the V/T ration is less than 32%, this test is no longer commonly used.

Skull radiographs may depict erosion of sella turcica, or "beaten copper cranium" (called by some authors "beaten silver cranium"). The latter can also be seen in craniosynostosis. Skull radiographs, however, are seldom helpful or indicated.

MRI cine is an MRI technique to measure CSF stroke volume (SV) in the cerebral aqueduct. Cine phase-contrast MRI measurements of SV in the cerebral aqueduct does not appear to be useful in predicting response to shunting.[2]

Diffusion tensor imaging (DTI) is a novel imaging technique that detects differences in fractional anisotropy (FA) and mean diffusivity (MD) of the brain parenchyma surrounding the ventricles. Impairment of FA and MD through DTI allows the recognition of microstructural changes in periventricular white matter region that may be too subtle on conventional MRI.[3]

Other Tests

After shunt insertion, confirm correct positioning of installed hardware with a plain radiograph.

EEG can be used if seizure occurs.

Procedures

Lumbar puncture (LP) is a valuable test in evaluating NPH, but should be performed only after CT or MRI of the head. Normal LP opening pressure (OP) should be less than 180 mm H2 O (ie, 18 cm H2 O). Patients with initial OP greater than 100 mm H2 O have a higher rate of response to CSF shunting than those with OPs less than 100 mm H2 O. Improvement of symptoms after a single LP in which 40-50 mL of CSF is withdrawn appears to have some predictive value for success of CSF shunting.

Continuous CSF drainage through external lumbar drainage (ELD) is a highly accurate test for predicting the outcome after ventricular shunting in NPH, although false negative results are not uncommon.[17]

Continuous CSF pressure monitoring can help in predicting a patient's response to CSF shunting in NPH. Some patients with normal OP on LP demonstrate pressure peaks of greater than 270 mm H2 O or recurrent B waves. These patients tend to have higher rates of response to shunting than those who do not have these findings. This procedure also could differentiate NPH from atrophy.

Additionally, ICP monitoring can be helpful in patients with labile intracranial pressure, where an LP may miss the elevation, in determine when shunting may be indicated (for example, pseudotumor patients with persistent headaches despite medical treatment but normalized LP opening pressures).

Histologic Findings

Histologic findings include the following:

Medical Care

Medical treatment in hydrocephalus is used to delay surgical intervention. It may be tried in premature infants with posthemorrhagic hydrocephalus (in the absence of acute hydrocephalus). Normal CSF absorption may resume spontaneously during this interim period.

Medical treatment is not effective in long-term treatment of chronic hydrocephalus. It may induce metabolic consequences and thus should be used only as a temporizing measure.

Medications affect CSF dynamics by the following mechanisms:

Surgical Care

Surgical treatment is the preferred therapeutic option.[4]

Repeat lumbar punctures (LPs) can be performed for cases of hydrocephalus after intraventricular hemorrhage, since this condition can resolve spontaneously. If reabsorption does not resume when the protein content of cerebrospinal fluid (CSF) is less than 100 mg/dL, spontaneous resorption is unlikely to occur. LPs can be performed only in cases of communicating hydrocephalus.

Alternatives to shunting include the following:

Shunts eventually are performed in most patients. Only about 25% of patients with hydrocephalus are treated successfully without shunt placement. The principle of shunting is to establish a communication between the CSF (ventricular or lumbar) and a drainage cavity (peritoneum, right atrium, pleura). Remember that shunts are not perfect and that all alternatives to shunting should be considered first.

Rapid-onset hydrocephalus with increased intracranial pressure (ICP) is an emergency. The following can be done, depending on each specific case:

Consultations

Consultation with the following may prove helpful:

Activity

Most surgeons agree that, with the use of antisiphon devices, no special positioning is required after shunting. However, some surgeons used to leave patients in whom a standard shunt had been placed in a recumbent position for 1-2 days after surgery to minimize the risk of subdural hematoma.

In treatment of normal pressure hydrocephalus (NPH), gradual postoperative mobilization is recommended.

Medication Summary

Acetazolamide (ACZ) and furosemide (FUR) treat posthemorrhagic hydrocephalus in neonates. Both are diuretics that also appear to decrease secretion of CSF at the level of the choroid plexus. ACZ can be used alone or in conjunction with FUR. The combination enhances efficacy of ACZ in decreasing CSF secretion by the choroid plexus. If ACZ is used alone, it appears to lower risk of nephrocalcinosis significantly.

Medication as treatment for hydrocephalus is controversial. It should be used only as a temporary measure for posthemorrhagic hydrocephalus in neonates, or when shunting is not possible.

Acetazolamide (Diamox)

Clinical Context:  Noncompetitive reversible inhibitor of enzyme carbonic anhydrase, which catalyzes the reaction between water and carbon dioxide, resulting in protons and carbonate. This contributes to decreasing CSF secretion by choroid plexus.

Class Summary

These agents inhibit an enzyme found in many tissues of the body that catalyzes a reversible reaction in which carbon dioxide becomes hydrated and carbonic acid dehydrated. These changes may result in a decrease in CSF production by the choroid plexus.

Furosemide (Lasix)

Clinical Context:  Mechanisms proposed for lowering ICP include lowering cerebral sodium uptake, affecting water transport into astroglial cells by inhibiting cellular membrane cation-chloride pump, and decreasing CSF production by inhibiting carbonic anhydrase. Used as adjunctive therapy with ACZ in temporary treatment of posthemorrhagic hydrocephalus in neonates.

Class Summary

These agents increase excretion of water by interfering with the chloride-binding cotransport system, which results from inhibition of reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule.

Further Outpatient Care

Patients on acetazolamide (ACZ) or furosemide (FUR) should be followed for possible electrolyte imbalance and metabolic acidosis. Clinical signs that should prompt attention are lethargy, tachypnea, or diarrhea.

Patients with shunts should be reevaluated periodically, including assessment of distal shunt length in growing children. The first follow-up examination usually is scheduled 3 months after surgery, and CT scan or MRI of the head should be done at that time. Follow-up is performed every 6-12 months in the first 2 years of life. In children aged 2 years and older, follow-up is performed every 2 years.

Further Inpatient Care

Patients with shunt-dependent hydrocephalus should be admitted for consideration of shunt revision if shunt malfunction or infection is suspected.[18]

In children, shunt revisions are scheduled according to growth rate.

Inpatient & Outpatient Medications

Medications include acetazolamide and furosemide. These are helpful for temporizing the hydrocephalus until compensation occurs. If compensation does not occur, then shunting is indicated.

Medications should not be used in patients with functional shunts.

Medication is not effective in long-term treatment of chronic hydrocephalus, and it may induce metabolic consequences.

If seizures occur, antiepileptic drugs are recommended.

Transfer

In cases of acute hydrocephalus or shunt complications, immediately transfer the patient to a center with a neurosurgery service.

Deterrence/Prevention

See the list below:

Complications

See the list below:

Prognosis

Long-term outcome is related directly to the cause of hydrocephalus.

Up to 50% of patients with large intraventricular hemorrhage develop permanent hydrocephalus requiring shunt.

Following removal of a posterior fossa tumor in children, 20% develop permanent hydrocephalus requiring a shunt. The overall prognosis is related to type, location, and extent of surgical resection of the tumor.

Satisfactory control was reported for medical treatment in 50% of hydrocephalic patients younger than 1 year who had stable vital signs, normal renal function, and no symptoms of elevated ICP.

Criteria exist for predicting improvement with shunting in NPH, but they are controversial.

Patient Education

Knowledge of the signs and symptoms of shunt malfunction or infection and the necessity for emergent medical evaluation in these instances is mandatory in patients, family members, and caregivers.

The patient, family, and caregivers should know that periodic re-evaluation is necessary.

Pumping the shunt is contraindicated in most cases.

Patients with vascular shunts, and some patients with other types of shunts, should receive prophylactic antibiotics before dental procedures or instrumentation of the bladder.

What is hydrocephalus?What are the signs and symptoms of hydrocephalus?What are the signs and symptoms of normal pressure hydrocephalus (NPH)?Which physical findings indicate hydrocephalus in infants?Which physical findings indicate hydrocephalus in children and adults?Which physical findings indicate normal pressure hydrocephalus (NPH)?What is the role of lab testing in the diagnosis of hydrocephalus?What is the role of imaging studies in the diagnosis of hydrocephalus?What are the surgical options for treatment of hydrocephalus?What is the role of medical therapy in the treatment of hydrocephalus?How is hydrocephalus defined?What is benign external hydrocephalus?What is normal pressure hydrocephalus (NPH)?What is communicating hydrocephalus?What is noncommunicating hydrocephalus?What is congenital hydrocephalus?What is the production of cerebrospinal fluid (CSF) in a healthy human?What is the route of cerebrospinal fluid (CSF) from production to clearance in a healthy human?What is the role of intracranial pressure (ICP) in the pathophysiology of hydrocephalus?What is the pathophysiology of normal pressure hydrocephalus (NPH)?What is the incidence of hydrocephalus in the US?What is the global incidence of hydrocephalus?What causes death in untreated hydrocephalus?What is the prevalence of shunt dependence in hydrocephalus?How does the incidence of hydrocephalus vary by sex?How does the incidence of hydrocephalus vary by age?Which factors influence the presentation of hydrocephalus?What are symptoms of hydrocephalus in infants?What are symptoms of hydrocephalus in children?What are symptoms of hydrocephalus in adults?What are symptoms of normal pressure hydrocephalus (NPH)?What are physical findings of hydrocephalus in infants?What are physical findings of hydrocephalus in children?What are physical findings of hydrocephalus in adults?What are physical findings of normal pressure hydrocephalus (NPH)?What are congenital causes of hydrocephalus?What are acquired causes of hydrocephalus in infants and children?What are causes of hydrocephalus in adults?What are causes of normal pressure hydrocephalus (NPH) in adults?What are the differential diagnoses for Hydrocephalus?What is the role of lab studies in the evaluation of hydrocephalus?What is the role of CT scanning in the evaluation of hydrocephalus?What is the role of MRI in the evaluation of hydrocephalus?What are the CT/MRI criteria for diagnosis of acute hydrocephalus?What are the CT/MRI criteria for diagnosis of chronic hydrocephalus?Other than CT and MRI, which imaging studies may be helpful in the evaluation of hydrocephalus?Which imaging study is used to confirm shunt positioning in hydrocephalus?What is the role of EEG in the evaluation of hydrocephalus?Which procedures are performed in the evaluation of hydrocephalus?Which histologic findings are characteristic of hydrocephalus?What is the goal of medical care for hydrocephalus?What is the mechanism of action for medications used in the treatment of hydrocephalus?When are repeat lumbar punctures (LP) indicated in the management of hydrocephalus?What are alternatives to shunting in the management of hydrocephalus?What is the role of shunts in the treatment of hydrocephalus?What are the treatment options for rapid-onset hydrocephalus?Which specialist consultations should be sought in the management of hydrocephalus?What activity restrictions are needed following shunting for hydrocephalus?Which medications are used in the treatment of hydrocephalus?Which medications in the drug class Loop diuretics are used in the treatment of Hydrocephalus?Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Hydrocephalus?What monitoring is required following treatment of hydrocephalus?When is inpatient care indicated in the management of hydrocephalus?Which medications are used in the treatment of hydrocephalus?When is transfer to a specialized facility necessary in the treatment of hydrocephalus?How is hydrocephalus prevented?What are possible complications of hydrocephalus?What is the prognosis of hydrocephalus?What are the criteria for predicting improvement in normal pressure hydrocephalus (NPH) with shunting?What information about hydrocephalus should patients receive?

Author

Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP, Chief, Pediatric Neurology, Professor of Pediatrics, Neurology, Neurosurgery, and Psychiatry, Epileptologist, Medical Director, Tulane Center for Autism and Related Disorders, Co-Director, Developmental Neurogenetics Center, Tulane University School of Medicine

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Biomarin; Supernus<br/>Received income in an amount equal to or greater than $250 from: Biomarin; Supernus; American Board of Pediatrics.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA, Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Disclosure: Nothing to disclose.

Additional Contributors

Anthony M Murro, MD, Professor, Laboratory Director, Department of Neurology, Medical College of Georgia, Georgia Regents University

Disclosure: Nothing to disclose.

Acknowledgements

Alberto J Espay, MD, MSc Associate Professor, Director of Clinical Research, Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati College of Medicine

Alberto J Espay, MD, MSc is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Abbott Consulting fee Consulting; Chelsea therapeutics Consulting fee Consulting; Novartis Honoraria Speaking and teaching; TEVA Consulting fee Consulting; NIH Grant/research funds K23 Career Development Award; Eli Lilly Consulting fee Consulting; Great Lakes Neurotechnologies Other; Michael J Fox Foundation Grant/research funds Other; Lippincott Williams & Wilkins Royalty Book; American Academy of Neurology Honoraria Speaking and teaching

Eugenia-Daniela Hord, MD Instructor, Departments of Anesthesia and Neurology, Massachusetts General Hospital Pain Center, Harvard Medical School

Eugenia-Daniela Hord, MD is a member of the following medical societies: American Academy of Neurology and American Pain Society

Disclosure: Nothing to disclose.

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Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.

Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recovery (FLAIR) sequences. Note that apical cuts (lower row) do not show enlargement of the sulci, as is expected in generalized atrophy. Pathological evaluation of this brain demonstrated hydrocephalus with no microvascular pathology corresponding with the signal abnormality (which likely reflects transependymal exudate) and normal brain weight (indicating that the sulci enlargement was due to increased subarachnoid cerebrospinal fluid [CSF] conveying a pseudoatrophic brain pattern).

Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.

Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.

Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.

Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recovery (FLAIR) sequences. Note that apical cuts (lower row) do not show enlargement of the sulci, as is expected in generalized atrophy. Pathological evaluation of this brain demonstrated hydrocephalus with no microvascular pathology corresponding with the signal abnormality (which likely reflects transependymal exudate) and normal brain weight (indicating that the sulci enlargement was due to increased subarachnoid cerebrospinal fluid [CSF] conveying a pseudoatrophic brain pattern).