Normal and Pathological Findings see Tables262 263 and 264

The general appearance of CSF is clear and colorless, because it is more than 99 percent water. Color of CSF is observed only in pathological circumstances. Whereas the term xanthochromia means yellow color, it has been used for the presence of other colors as well. Because of this practice, the actual color of the CSF should be stated and a gradation of its magnitude (from 1+ to 4+) should be noted. A yellowish tinge can be found with any cause of a markedly increased protein (greater than 200 mg percent). A yellow or pink color is found when hemoglobin has been released into the CSF from prior bleeding and sufficient time has passed for its breakdown to bilirubin and other pigments. Oxyhemoglobin is red but becomes pink or yellow when diluted. The concentration of oxyhemoglobin is maximal within the first 36 hours and disappears by 14 days. Bilirubin is yellow and is first detected in the CSF 10 hours after subarachnoid bleeding. Its concentration is maximal at 2 days and may persist for up to a month. 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.

Fluid that is obviously blood tinged or bloody indicates a traumatic tap or the presence of a subarachnoid hemorrhage. In traumatic taps, the CSF usually clears as sequential amounts are collected and is unlikely to have a pink-or yellow-tinged supernatant. The CSF may occasionally clot if the ratio of blood to CSF is high. Bloody CSF from subarachnoid hemorrhage does not clear with sequentially collected tubes and may demonstrate xanthochromia if the bleeding occurred over 2 to 4 hours before the LP. If the CSF is acquired over 12 hours after the onset of subarachnoid hemorrhage, virtually all patients' CSF will demonstrate xanthochromia. y

Whenever the viscosity of CSF is increased, the most likely explanation is a marked increase of protein content. If sufficient fibrin is present, the free flow of CSF can be impaired and spontaneous clotting of the CSF can occur (Froin's syndrome). Turbidity detected in CSF when a collection tube is twirled in the beam of a bright light is indicative of the presence of at least 200 or more leukocytes per mm3 . Turbidity may also be caused by the presence of microscopic fat globules that have traveled to the brain as emboli. The presence of erythrocytes will impart turbidity up to a concentration of 400 cells per mm 3 , above which there will be pink coloration from their hemoglobin content.

Six common CSF studies include the cell count and differential, Gram's stain and culture, blood glucose, and protein concentrations and direct observation for color and character.

CELL COUNTS

CSF cell counts (red blood count and white blood count) with differentials should be performed on every specimen. Typically, the CSF contains no RBC/mm 3 and 0 to 1 WBC/mm3 . Cook and Brooksy reported that the normal CSF WBC in 11 patients was 0.826 + 0.733 cells/mm3 with differentials of approximately 66 percent lymphocytes, 33 percent monocytes, and 1 percent polymorphonuclear cells (PMNs). Fishman has also noted that the normal CSF should contain no more than five lymphocytes or mononuclear cells/mm3 , and counts greater than 6 cells/mm3 are abnormal. A traumatic LP causes elevations of RBCs and WBCs, but these elevations are differentiated from subarachnoid hemorrhage because the former elevations are high in the first tube but clear in the later tubes. To determine whether an elevated CSF WBC is due to blood from a traumatic tap or other causes, an expected ratio can be used. If the elevated WBC is due to blood in the CSF, one WBC/mm3 for every 700 RBC/mm3 is found. If the WBC exceeds this ratio, its origin must be accounted for from other etiologies such as infection or inflammation.

GLUCOSE

As notedin Table...26-2 , the CSF glucose concentration is normally 60 percent of the plasma glucose concentration, and under nonpathological conditions this ratio changes

TABLE 26-4 -- S

ELECTED DISORDERS AND ASSOCIATED CSF STUDIES

Domain

Disorder

Useful CSF Studies

Expected Results

Comments

CEREBRAL DYSFUNCTION

Infectious

Meningitis (purulent)

pr, gl, cell cts, gs, ex, op

CSF PMNs, + gs and cx, + bacterial ag's, op

+ cryptococcal ag & india ink in cryptococcal meningitis

LA

Mononuclear cells possible in partially rx'd bacterial meningitis

Meningitis (aseptic)

CSF WBC (10 to 1000 mononuc cells/mm3 )

PMNs possible in early aseptic meningitis

Encephalitis

pr, gl, cell cts, gs, cx

mildly pr (50 to 100 mg/dl), nl gl, CSF WBC 50 to 100/mm3 (monunuc)

RBC/xanthochromia, + CSF PCR

Herpes simplex encephalitis

HIV encephalopathy

pr, gl, cell cts

mildly pr, nl gl, nl or few WBC

Neurosyphilis (acute)

WBC (5 to 500 mononuc/mm3 ), + VDRL

CSF parameters may be normal.

Neuroborreliosis

100 mononuc/mm3 ), + OCB, + Lyme ab's

CSF normalizes in stage III

Tuberculous meningitis

pr, gl, cell cts, op, acid-fast stain, cx

WBC (25 to l00 mononuc/mm3 ), op

May be spinal block; stain and culture require large amts. of CSF

Abscess

Not recommended

May be dangerous to perform LP in the face of abscess; risk of herniation or ventricular rupture

Creutzfeldt-Jakob

pr, gl, cell cts

Normal

14-3-3 protein in CSF (not readily available)

Progressive multifocal leukoencephalopathy

JC virus PCR

+ JC virus PCR

CSF o/w normal

Cysticercosis

pr, gl, cell cts, op

pr,

CSF eosinophils constitute 20 to 75 percent

Cerebrovascular

Dementia Degenerative

Neoplastic

Metabolic

Demyelinating

Autoimmune

Other diorders

Cysticercosis

Stroke

Subarachnoid hemorrhage

Venous thrombosis

Anoxic brain

Alzheimer's disease Huntington's disease

Wilson's disease Meningeal carcinomatosis

Craniopharyngioma

Hepatic encepalopathy

Uremic encephalopathy

Myxedema coma

Mitochondrial encepalopathies

Multiple sclerosis

Acute disseminated encephalomyelitis

Sarcoid

Behcet's disease

Angiitis

Normal pressure hydrocephalus

Pseudotumor cerebri

Migraine

Generalized seizure pr, gl, cell cts, op pr, cell cts pr, gl, cell cts, color cell cts, op pr, gl, cell cts pr, gl, cell cts pr, gl, cell cts pg gl, cell cts, cyt, op cell cts pr, color pr, cells cts, urea pr pyruvate, lactate pr, gl, cell cts, OCB, MBP, IgG index pr, gl, cell cts, OCB

Diagnostic high volume LP, op pr, cell cts, op

See comments pr, cell cts pr, gl,

WBC (mixed w/eosinophilia), op mildly pr and WBC

RBC,

WBC, xanth

RBC, op normal parameters normal normal pr (24 to 1200 m/dl), gl,

WBC (mononuc)

pr possible xanth mildly pr & WBC, urea pr (100 to 300 mg/dl) pyruvate, lactate pr, mildly

WBC, nl gl, + OCB, + MBP, IgG index mildy pr & WBC, nl gl, + OCB

pr (50 to 200 mg/dl), mildly gl (30 to 0 mg/dl), WBC (10 to 100 mononuc/mm3 )

WBC (mixed response) 10 to 200 cell/mm2

WBC (mononuc) op

Gait & mental status improvement after LP, nl op pr, nl cell cts, op (250 to 600 mm H2 O)

pr, mild WBC

CSF eosinophils constitute 20 to 75 percent

Not routinely performed; LDH, AST and CK-BB in cortical CVA

pr can be normal or significantly , gl can be normal or slightly

WBC may be if 2° to septic thrombosis

Not routinely performed; CK-BB, NSE, MBP may be useful

Abnormal CSF helps r/o AD

Abnormal CSF helps r/o Huntington's disease

Abnormal CSF helps r/o Wilson's disease

Large volumes of CSF and multiple LPs increase cytology yield

A cause of chronic chemical meningitis

Not routinely performed. op may be ; CSF glutamine

Not routinely performed

MELAS

Abnormal CSF in 90 percent of cases; Pr and cell cts nl in 2/3

OCBs may disappear after resolution ACE

in 50 percent, but not specific

CSF results quite varied

Abnormal CSF in S0 to 90 percent

High volume LP (40 to 50 cc of CSF)

CSF removal may be therapeutic in some cases

Little available data. May have pr and cell cts in severe complicated migraine

Postictal

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