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OUTLINE
Anatomy Cerebrospinal fluid circulation Physiology Function CSF analysis Hydrocephalus pseudotumor cerebri Low CSF pressure syndrome
ANATOMY
Lateral ventricle
Anterior or frontal horn Body Atrium Posterior or occipital horn Inferior or temporal horn
Interventricular foramen (foramen of Monro) Third ventricle(separating right and left diencephalon) Cerebral aqueduct of Sylvius Fourth ventricle (between pons and cerebellum extending as far caudal as medulla) Foramen of Luschka Foramen of Magendie Subarachnoid space (between pia and arachnoid) Choroid plexus Arachnoid granulation
CSF CIRCULATION
Choriod plexus (lateral, third, and fourth ventricle) Lateral ventricle Subarachnoid cistern Foramen of Monro Third ventricle Cerebral aqueduct of Sylvius Fourth ventricle Foramen of Luschka Foramen of Magendie Subarachnoid space (between pia and arachnoid) Arachnoid granulation
the average intracranial volume is 1,700 mL the volume of the brain is from 1,200 to 1,400 mL, CSF volume ranges from 70 to 160 mL (mean: 104),
the spinal subarachnoid space contains 10 to 20 mL of CSF the CSF occupies somewhat less than 10 percent of the intracranial and intraspinal spaces
CSF pressure less than 150 mmH20. lateral recumbent position with the legs extended, the normal CSF pressure is 60 to 200 mmH20 obese patients may have CSF pressures up to 250 mmH20 Pressures >250 mmH20 are considered to be elevated
from : uptodate 17.1
serves to remove the waste products of cerebral metabolism : CO2, lactate, hydrogen ions helps to preserve a stable chemical environment for neurons and their myelinated fibers
BLOOD-BRAIN BARRIER
separate the brain and the CSF from the blood prevent entry by simple diffusion of fluids, electrolytes, and other substances from blood into the CSF or brain 5000-fold greater surface area than the blood-CSF barrier controls the content of brain interstitial fluid anatomic basis for the blood-brain barrier
series of high-resistance, tight junctions between endothelial cells of capillaries in the CNS as well as astrocytes with processes Lipid-soluble small molecules with a molecular mass less than 400 to 600 Da are transported readily through the blood-brain barrier
Pia mater A continuous layer of astrocytes overlies the basement membrane of cells and CSF
2. Area Postrema
at the wall of the 4th ventricle in the junction with the spinal canal the vomiting center : emetic substances (apomorphine and digitalis glycosides neurophysin, oxytocin, and vasopressin
luteinizing hormone releasing factor (LHRH) and somatostatin, which inhibits the release of somatotropin (growth hormone)
4. Sub-commissural Organ
beneath the posterior commissure at the junction of the third ventricle and the cerebral aqueduct the function is unknown
5. Pineal Gland
pinealocytes produces the hormone melatonin under the influence of light deprivation
6. Subfornical Organ
COMPOSITION OF CSF
Color :
Clear and colorless Turbid appearance:
RBC > 400 cell/ml WBC > 200 cell/ml RBC 6,000 cell/ml oxyhemoglobin (pink) early and later to bilirubin (yellow) known as xanthochromia. Appear 2-4 hours after RBCs have entered the subarachnoid space, (90 % in 12 hrs.) persists for 2-4 weeks protein 150 mg/dL systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL) traumatic LP with more than 100,000 red blood cells/ml
COMPOSITION OF CSF
Traumatic tap
Predicted CSF WBC count/microL = CSF RBC count x (peripheral blood WBCcount peripheral blood RBC count)
If : A CSF WBC count > 10 times the predicted value had a 48 % positive predictive value for bacterial meningitis A CSF WBC count < 10 times the predicted value had a 99% negative predictive value for meningitis.
COMPOSITION OF CSF
WBC :
acellular, although up to 5 WBCs and 5 RBCs are considered normal in adults More than 3 polymorphonuclear leukocytes (PMNs)/ml are abnormal in adults PMN predominated in
Early (within 12-24 hrs onset) 2/3 of viral meningitis cases Bacterial meningitis Viral meningitis (Rare) early phase of bacterial meningitis
Lymphoctye predominated in
Eosinophilia
parasitic infestations Mycobacterium tuberculosis Mycoplasma pneumoniae Rickettsia rickettsii some fungi non-infectious conditions (lymphomas, leukemias of various types , subarachnoid hemorrhage, and obstructive hydrocephalus)
COMPOSITION OF CSF
Protein :
Normal range 23-38 mg/dl Mild elevation in DM False elevation :
Subarachnoid hemorrhage or traumatic tap Correction : protein 1mg/dl : RBC 1,000 cell/dl
Elevation in :
Infection Non infection CSF flow obstruction
elevations may persist for weeks or months following recovery from meningitis and have little utility in assessing cure or the response to therapy
COMPOSITION OF CSF
Glucose
Capillaries to CSF : Facilitated transport and simple diffusion CSF to capillaries : transport across capillaries and arachnoid villi cells lining the ventricular cavities and subarachnoid spaces several hours for the serum glucose to equilibrate with the CSF glucose CSF-to-serum glucose ratio is approximately 0.6 glucose concentration : ventricular CSF > CSF in the lumbar : 6 - 18 mg/dL
COMPOSITION OF CSF
Non infections :
Malignant processes infiltrating the meninges Subarachnoid hemorrhage CNS sarcoidosis
Viral CNS infection (except : mumps, enteroviruses, lymphocyticchoriomeningitis (LCM), herpes simplex, and herpes zoster viruses) Hyperglycemia (CSF glucose levels rarely exceed 300 mg/dL even in patients with severe hyperglycemia)
COMPOSITION OF CSF
Lactate Higher sensitivity and specificity > the ratio of CSF-toblood glucose Cytology
useful for the diagnosis of malignancy involving the CNS at least 10 to 15 mL of fluid
FUNCTION OF CSF
Transports hormones and removes metabolic waste products Cushions and floats brain
INTRACRANIAL PRESSURE
B. With ventricular obstruction C. With obstruction at or near the points of outlet of the CSF D. With obstruction of the venous outflow
brain tumor massive infarction with edema extensive traumatic contusion parenchymal, subdural, or extradural hematoma Abscess ischemicanoxic states acute hepatic failure hypertensive encephalopathy Hypercarbia Reye hepatocerebral syndrome
obstruction is within the ventricles or in the subarachnoid space at the base of the brain
CLINICAL
MANIFESTATION OF RAISED
ICP
Manifestation
Headache Nausea and vomiting Drowsiness Ocular palsies Papilledema After several days or longer
papilledema may result in periodic visual obscurations If papilledema is protracted, optic atrophy and blindness may follow
Normal mental alertness with ICP < 25 to 40 mm Hg loss of consciousness : ICP exceeds 40 to 50 mmHg decreased cerebral blood flow
ventricular pathway or aqueduct of Sylvius (most common) The medullary foramina of exit (Luschka and Magendie) the basal or convexity subarachnoid spaces
Myelinated fibers and axons are injured and astrocytic gliosis and loss of oligodendrocytes in affected areas
ACUTE HYDROCEPHALUS
Decreased CSF absorbtion rapidly expand the volume of CSF produce the most dramatic forms of acute hydrocephalus generalized dilatation of the ventricular system and basal cisterns (possibly because of increased CSF volume)
Types
1.intraventricular matrix hemorrhages in premature infants 2. fetal and neonatal infections 3. type II Chiari malformation 4. aqueductal atresia and stenosis 5. the Dandy-Walker syndrome
Clinical manifestation
the head usually enlarges rapidly and soon surpasses the ninetyseventh percentile The anterior and posterior fontanels are tense even when the patient is in the upright position. The infant is fretful, feeds poorly, and may vomit frequently
Late manifestation
the upper eyelids are retracted the eyes tend to turn down there is paralysis of upward gaze the sclerae above the irises are visible
Definition :
A stage is reached where the CSF pressure reaches a high normal level of 150 to 200 mm H2O while the patient still manifests the cerebral effects of the hydrocephalic state
compression of the choroid plexuses and absorption increases in proportion to CSF pressure Formation of CSF = CSF absorption
Clinical triad
a slowly progressive gait disorder (earliest feature) (unsteadiness and impairment of balance) impairment of mental function
broadly speaking, "frontal" in character embody mainly apathy dullness in thinking and actions slight inattention.
Etiology
Sequelae of subarachnoid hemorrhage from ruptured aneurysm or head trauma resolved acute meningitis or a chronic meningitis (tubercular, syphilitic, or other) Paget disease of the base of the skull mucopolysaccharidosis of the meninges Achondroplasia Unknown
Diagnosis
difficult to differentiate from the periventricular white matter change that is ubiquitous in the elderly Difficult to selected the patients for ventriculoatrial or ventriculoperitoneal shunt CT or MRI finding :
lateral ventricular span at the level of the anterior horns was in excess of 50 mm (~ 18 mm on the usual CT film) disproportionate enlargement of the ventricular system in comparison to the degree of cortical atrophy (CT or MRI) degree of transependymal egress of water surrounding the ventricles (MRI)
Lumbar puncture
Most cases CSF pressure > 155mmH2O Drainage of large amounts of CSF (20 to 30 mL or more) by lumbar puncture Clinical improvement in stance and gait for a few days (high predictive value for success of shunting)
Treatment
ventricular shunt tubing with one-way valves (ventriculoatrial shunt) or (ventriculoperitoneal shunt) a complete or nearly complete restoration of mental function and gait after several weeks or months (after shunting)
Overdrainage
causes headaches (chronic or orthostatic headache) small subdural collections of fluid (CSF and proteinaceous fluid derived from blood products)
Complication of shunting
Subdural hygroma or hematoma Valve and catheter infection Ventriculitis Occasionally bacteremia
headaches that are diffuse, worse at night, and often wake them from sleep in the early hours of the morning. Sudden movements, such as coughing, aggravate headache Headaches may be present for several months before a diagnosis is made Transient loss of vision (transient obscuration) enlarged blind spot papilledema false localizing sign of CN VI palsy
diagnosis
Clinical criteria ( headache, papilledema, visual loss) ruling out other causes of increased intracranial pressure All patients require a CT or MRI scan to look for hydrocephalus and mass lesions lumbar puncture is needed
the CSF include normal or low protein, normal glucose, no cells, elevated CSF pressure
Goals of treatment :
Treatment
No RCT Natural history of untreated IIH is unknown Avoided tetracycline derivatives
Pathophysiology
Traction on pain-sensitive intracranial and meningeal structures, particularly sensory nerves and bridging vein Secondary vasodilation of the cerebral vessels to compensate for the low CSF pressure Because jugular venous compression (vanodilation)
Epidemiology
The estimated annual incidence is 5 per 100,000 The peak incidence is around age 40, but children and elderly are also affected Women are affected more frequently than men, with a female to male ratio of 2:1
Clinical manifestation
Headache :
sudden or gradual onset Intense, throbbing, and dull pain Mild to severe form Diffuse or focal location Relieved with recumbency (within minutes) Not relieved with analgesics Exacerbating factors : upright posture, head movement, coughing, straining, sneezing, jugular venous compression, and high altitude
Clinical manifestation
Associated symptoms
50 % of cases
Other symptoms
Change in hearing (eg, hyperacusis, echoing, or tinnitus) Anorexia Vertigo Dizziness Diaphoresis Blurred vision Diplopia Transient visual obscurations Photophobia Unsteadiness or staggering gait Hiccups Dysgeusia
Examination
Normal finding Opening pressure : 0- 70 mmH2O clear and colorless Moderate lymphocytic pleocytosis (up to 50 cells/mm3) (a reactive phenomenon secondary to hydrostatic pressure changes) the presence of red blood cells Elevated protein (commonly up to 100 mg/dL) (disruption of normal hydrostatic and oncotic pressure across the venous sinus and arachnoid villi) cytology and microbiology is always normal CSF glucose is normal (never low)
CSF analysis
LOW CSF
PRESSURE SYNDROME
Imaging (MRI finding) > 20% of cases : normal finding Prominent abnormal features on brain MRI include the following:
Diffuse meningeal enhancement (DME) (secondary to vascular dilatation) Subdural hematomas or hygromas, presumably from rupture of the bridging veins as the CSF volume decreases "Sagging" of the brain, with cerebellar tonsillar herniation and descent of the brain stem mimicking a Chiari I malformation Engorgement of cerebral venous sinuses Pituitary enlargement flattening of the optic chiasm, and increased anteroposterior diameter of the brainstem Decrease in the size of cisterns and ventricles
SEEPS (for Subdural fluid collections, Enhancement of the pachymeninges, Engorgement of the venous structures, Pituitary enlargement, and Sagging of the brain)
Imaging ( CT finding)
Usually normal Subdural fluid collections increased tentorial enhancement Slit- shaped ventricles Tight basal cisterns scant CSF over the cortex
Diagnosis criteria A. Diffuse and/or dull headache that worsens within 15 minutes after sitting or standing, with at least one of the following (and fulfilling criterion D):
- Tinnitus - Photophobia
C. No history of dural puncture or other cause of CSF fistula D. Headache resolves within 72 hours after epidural blood patching
Treatment
No RCT Epidural blood patch (history of CSF leakage post lumbar puncture)
Non-specific treatment
Bed rest Oral or intravenous hydration High oral caffeine intake (200 to 300 mg of caffeine, given two to three times daily) High oral salt intake
Epidural fibrin glue Continuous epidural infusion (saline or dextran) Surgical repair
Prognosis
Spontaneously improvement : within 2 weeks Rare cases :within years
THE END