Cerebrospinal Fluid CSF

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Cerebrospinal Fluid CSF Powered By Docstoc
					 Production , circulation and absorption
  of CSF
 Function of CSF
 Composition of CSF
   The cerebrospinal fluid is formed mainly
    in the choroid plexuses of the lateral,
    third, and fourth ventricles; some
    originates from the ependymal cells
    lining the ventricles and from the brain
    substance through the perivascular
   The circulation begins with its secretion from the
    choroid plexuses in the ventricles
   The fluid passes from the lateral ventricles into t third
    ventricle through the interventricular foramina
   It then passes into the fourth ventricle through the
    narrow cerebral aqueduct. The circulation is aided
    by the arterial pulsations of the choroid plexuses and
    by the cilia on the ependymal cells lining the
   From the fourth ventricle, the fluid passes slowly
    through the median aperture and the lateral
    foramina of the lateral recesses of the fourth ventricle
    and enters the subarachnoid space
 The fluid then moves through the
  cerebellomedullary cistern and pontine
  cisterns and flows superiorly through the
  tentorial notch of the tentorium cerebelli to
  reach the inferior surface of the cerebrum
 Some of the cerebrospinal fluid moves
  inferiorly in the sub arachnoid space
  around the spinal cord
 The cerebrospinal fluid not only bathes the
  ependymal and pial surfaces of the brain
  and spinal cord but also penetrates the
  nervous tissue along the blood vessels
   The main sites for the absorption of the
    cerebrospinal flu: are the arachnoid villi that
    project into the dural venous s nuses, especially
    the superior sagittal sinus
   arachnoid villi tend to be grouped together to
    form e " vations known as arachnoid
   Structural. each arachnoid villus is a
    diverticulum of the subarachno: space that
    pierces the dura mater. The arachnoid divertict
    lum is capped by a thin cellular layer, which, in
    turn, is co ered by the endothelium of the
    venous sinus
   The normal pressure of CSF is 10 mmHg

Regulation of CSF by the arachnoidal villi
 It work as one way valve to allow CSF to
  flow to the blood venous sinus .while it not
  allow the blood to flow backward in the
  opposite direction
 The villi allow CSF begin to flow into the
  blood when CSF pressure is 1.5 mmHg or
  more greater than the pressure in the blood
  venous sinus .
   Increase of CSF pressure often caused by large tumor
    that elevate the CSF pressure by decreasing
    reabsorption of CSF back into the blood .

   CSF pressure also rises when hemorrhage or infection
   In this case large number of red and white blood cells
    appear in CSF and They can cause blockage of small
    absorption channels throw the arachnoidal villi .
   Some congenital condition may cause high pressure
    of CSF caused by few number of arachnoidal villi or
    abnormal proprieties of the villi
   accumulation of cerebrospinal fluid (CSF) in
    the ventricles, or cavities, of the brain .

two types :
 communicating hydrocephalous :

 fluid flows from the ventricular system into
  the subarachnoid space.
 In communicating type blockage is in the
  subarchnoid space by blockage of
  arachnoidal villi themselves .
   Non communicating :
   Fluid cant pass to the subarachnoid
   In this type is blockage of the aqueduct
    of sylvius .

Obstruction of villi blockage  ↑ CSF
 pressure hydrocephalous  may lead
 to edema .
 Cushion and protect the CNS from
 Provides mechanical buoyancy and
  support for the brain
 Serves as reservoir and assistant in the
  regulation of the content of the skull
 Nourishes the CNS
 Remove metabolic wastes from CNS
 Serves as pathway for pineal secretion to
  reach the pituitary gland.
 it protects against acute changes in
  arterial and venous blood pressure;
 it is involved in intra-cerebral transport,
  ex. hypothalamic releasing factors
In addition to the major ions, CSF contains oxygen,
sugars (e.g., glucose, fructose, polyols), lactate,
proteins (e.g., albumin, globulins), amino acids,
urea, ammonia, creatinine, lipids, hormones (e.g.,
insulin), and vitamins.
                   Substance           Plasma                     CSF

Sodium (mEq/L)                 140.0            144.0

Potassium (mm/L)               4.6              2.9

Magnesium (mEq/L)              1.6              2.2

Calcium (mg/dL)                8.9              4.6

Chloride (mEq/L)               99.0             113.0

Bicarbonate (mm/L)             26.8             23.3

Inorganic phosphate (mg/dL)    4.7              3.4

Protein (g/dL)                 6.8              0.028 (28mg/dL)

Glucose (mg/dL)                110.0            50 to 80

Osmolality                     0.3              0.29

pH                             7.4              7.3

PCO2 (mmHg)                    41.1             50.5
- the CSF glucose concentration is normally 60% of the
plasma glucose concentration, and under nonpathological
conditions, this ratio changes falling . proportionately in
response to a rising or
plasma glucose
-This linear ratio of CSF to plasma glucose concentration
decreases as the plasma glucose exceeds 500mg/dL.
-- The reason for this decrease is unclear, but it may reflect
the saturation of the carrier-mediated transport of glucose
at high plasma concentrations.
-- Although an elevated CSF glucose level
(hyperglycorrachia) results from an elevated plasma
glucose level, a decreased CSF glucose concentration
(hypoglycorrachia) may be due to a variety of causes
including hypoglycemia.
-The CSF glucose value often returns to normal before other
CSF determinations (such as protein or lactate).
-The CSF glucose level may take several weeks to return to
normal despite the normalization of the protein
concentration and cell count.

- A CSF hypoglycorrhachia is seen in a number of CNS
infections. The pathogenesis of CSF hypoglycorrhachia is
multifactorial and may include an increased rate of
macrovesicular glucose transport across arachnoid villi,
increased glycolysis by leukocytes and bacteria, increased
metabolic rate of the brain and spinal cord, and/or
inhibition of glucose entry into the subarachnoid space
caused by alterations in the membrane carrier system
responsible for glucose transfer from blood to CSF.[
- Theactual CSF glucose concentration may be falsely low in the
presence of hypoglycemia or may be incorrectly interpreted as normal
when the patient is hyperglycemic (e.g., in diabetic patients). Therefore,
the CSF glucose should always be compared with a simultaneous serum
glucose that is drawn prior to lumbar puncture; the normal CSF:serum
glucose ratio is approximately 0.6, and ratios less than 0.5 should be
considered abnormal.
-The majority of CSF protein is derived from the serum, and the
CSF/serum albumin ratio is approximately 1:200. This ratio implies that
the entry rate of protein from the serum to the CSF is approximately 200
times less than its exit rate.

-The CSF protein concentration varies at different levels of the neuroaxis
and generally increases from the cephalad to caudal levels. Elevation in
lumbar CSF protein is a nonspecific but sensitive indicator of CNS
- The presence of 1000 RBCs in the CSF results in the increase of protein
by 1mg/dL.
-A spinal-subarachnoid block can cause Froin's syndrome and is usually
the result of a spinal cord tumor and can cause very significant
elevations in CSF protein (greater than 1000mg/dL).
-Protein concentrations of 100mg/dL or greater have sensitivity and
specificity for bacterial meningitis of 82% and 98%, respectively, as
compared with aseptic meningitis, and if the concentration is 200mg/dL,
the sensitivity is 86% and the specificity is 100%.

- A lower than normal CSF protein level may occur in young children (6
months to 2 years of age), in patients with pseudotumor cerebri, and in
patients with unintended loss of CSF from frequent LPs, a lumbar drain,
or a lumbar dural CSF leak.
- Certain proteins arise within the intrathecal compartment.
Among these are immunoglobulins produced by CNS
lymphocytes, transthyretin (produced by choroid plexus),
and various structural proteins found in brain tissue (including
glial fibrillary acidic, and myelin basic proteins). The last
group of proteins and transthyretin are found only in trace
amounts, whereas immunoglobulins compose a substantial.

- The CSF protein concentration is also elevated in a number
of CNS infections, presumably due to disruption of the
blood-brain barrier, manifested morphologically by
separation of intercellular tight junctions and increased
numbers of pinocytotic vesicles in microvascular endothelial
- The general appearance of CSF is clear and colorless,
because it is more than 99% water. Color of CSF is observed
only in pathological circumstances.

- A yellowish tinge can be found with any cause of a
markedly increased
protein (greater than 200mg per 100mL).

xanthochromic (yellow) - If there is no liver failure (jaundice
can cause CSF to be yellow), xanthochromic CSF suggests
that a subarachnoid hemorrhage has recently occurred
[within days). The yellow color is due to bilirubin generated in
the CNS by the breakdown of hemoglobin released from
- Other causes for coloration of CSF include an elevated
systemic bilirubin from liver disease; a brownish or gray
coloration in the presence of CNS melanoma; and a
greenish tinge related to leukemic
meningeal infiltration.

- turbid - This indicates the presence of white cells and is
suggestive of a CNS infection.
CSF lactate
Because the concentration of CSF lactate is dependent on CNS
glycolysis,the measurement of this agent may be helpful in the diagnosis
of bacterial meningitis. This concentration of lactate increases
proportionally to the number of inflammatory cells in the CSF. A lactate
concentration of 4.2mmol/L accurately predicted 24 out of 25 cases of
bacterial meningitis.

Increased lactate may also result from a cerebral hemorrhage,
malignant hypertension, hepatic encephalopathy, diabetes mellitus, and
hypoglycemic coma.
CSF glutamine :
The measurement of CSF glutamine can be a
helpful test in diagnosing patients with confusion
in the setting of hepatic encephalopathy.

This process helps protect the CNS from the effects
of ammonia. Normally, the CSF concentration of
ammonia is less than one half of arterial levels, but
may increase dramatically in patients with hepatic
Various biogenic amines:
Various biogenic amines (and their metabolites) may be
measured within the CSF, including dopamine (homovanillic
acid [HVA]), serotonin (5-hydroxyindoleacetic acid [5-HIAA]),
and norepinephrine (3-methoxy-4-hydroxyphenylglycol
[MHPG]). Significant ventricular to lumbar gradients exist for
HVA and 5-HIAA, although MHPG levels are nearly equivalent.
Decreased lumbar CSF levels of HVA and 5-HIAA have been
reported in patients with parkinsonism and Alzheimer's
disease. Whereas decreased HVA levels have also been
documented in the ventricular CSF of patients with dystonia.
enzymes in the CSF :
An elevated lactate dehydrogenase (LDH)
may occur in bacterial meningitis.

whereas adenosine deaminase (ADA)
elevations can occur in tuberculous

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