Lumbar Puncture and CSF Examination

Cerebrospinal fluid (CSF) was first examined in the 19th century using primitive techniques
(eg, sharpened bird quills). CSF analysis reached a peak in the 1950s and early 1960s, when almost no
workup of a significant central nervous system (CNS) problem was performed without a lumbar
puncture (LP).

With the advent of sophisticated imaging techniques, particularly computerized tomography

(CT) and magnetic resonance imaging (MRI), LP is no longer an important test in the diagnosis of
most intracranial mass lesions. This is especially true with the potential risk of brain herniation if
intracranial pressure (ICP) is increased markedly. LP remains a critical procedure in the diagnosis of
CNS infections and inflammatory diseases.

Diagnostic and therapeutic uses

The past 2 decades have seen an increase in the sophistication of CSF analysis allowing
immunologic confirmation of certain infections (eg, Lyme disease) and fractionation of CSF proteins
(eg, myelin basic protein). CSF analysis remains important in the diagnosis of infections (eg,
bacterial, mycobacterial, fungal, viral, protozoan) and certain inflammatory diseases (eg, multiple
sclerosis, Guillain-Barre syndrome, vasculitis).
CSF analysis also is an important diagnostic tool in subarachnoid hemorrhage and
leptomeningeal carcinomatosis. Indeed, the extent to which CSF reflects the chemistry of surrounding
tissue, and the significant differences in composition from plasma, are reviewed elegantly by
Hochwald in his chapter in Clinical Neurology.
LP itself can be therapeutic, particularly in benign intracranial hypertension (ie,
pseudotumor cerebri), in which serial LPs may be used for treatment. It is used as an access method,
most commonly for spinal anesthesia, but also for introduction of radioopaque contrast media (eg,
myelography), corticosteroids, antibiotics, and chemotherapeutic agents. However, this article
concentrates on the primary diagnostic uses of LP and the examination of CSF.

LUMBAR PUNCTURE TECHNIQUE

LP is performed in the interspaces between the lumbar vertebrae, usually at the L4-L5 level. In
unusual circumstances, a tap can be done at higher levels. Even at these higher levels the probability of
injuring the spinal cord is small. Nevertheless, this should be reserved for situations in which access to
the usual sites has been obliterated (eg, by extensive orthopedic fusion) and a specific need exists for
the information obtained from the procedure.
The spinal cord typically ends at the L1 level in adults (slightly lower in children). If
consideration is being given to an LP above the L4-L5 level, it should be performed with subspecialist
assistance and with great caution. Fluoroscopic guidance may be helpful in these and other difficult
situations. A "clean" specimen obtained fluoroscopically is more helpful than a "traumatic" (ie, blood
contaminated) specimen obtained at the bedside.
CSF also can be obtained from the cisterna magna by a tap below the external occipital
protuberance. However, this technique should rarely, if ever, be required and again should be
performed with subspecialist assistance.

Preparation
The spinal needle used today is disposable. The clinician should inspect the spinal needle for
any defects. A 20-gauge needle for adults, or a 22-gauge needle for children, is used typically. Various
designs have been marketed, with the aims of increasing ease of use and reducing incidence of post-LP
dural leak that could result in spinal headache.
After carefully explaining the procedure to the patient and/or responsible caregiver, including
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the risks and benefits of the procedure, the most important determinant in successfully obtaining a CSF
specimen is patient positioning. This may require the assistance of a nurse and/or other paramedical
personnel. Sedative medication may be required in children or in the confused or combative patient.
The bed/gurney should be flat, and the patient should be lying on his/her side (horizontal lateral
decubitus position). The patient’s body needs to be perfectly perpendicular to the bed/gurney. The
patient should assume the fetal position (ie, head/neck, arms, legs flexed as much as possible). The
apex of the pelvic bone should be identified and a direct line should be visualized to the spine. The
location so identified should be well below the tip of the conus. Two spinous processes in this area (ie,
L4 and L5 levels) should be identified by palpation.

Procedure
Local anesthetic should be infiltrated and then the area should be prepared carefully and
draped. The spinal needle then is positioned between the 2 spinous processes already identified and
introduced into the skin with the bevel of the needle facing up. The needle should be advanced slowly
at a slightly upward angle (ie, toward the patient’s head).
Accurate placement of the needle is rewarded by a slight "give" and flow of fluid, which
normally is clear and colorless. Some resistance may be noted, usually in patients who have some
thickening of the dura (eg, elderly patient), but if a feeling of hitting bone is noted, this is probably
what is occurring. As with any procedure, experience improves the success rate. One of the primary
goals is to prevent the introduction of blood into the CSF sample.
A measurement of opening pressure should be attempted, unless the patient is so uncooperative
as to invalidate the reading. CSF pressure should be measured with the subject in the horizontal lateral
decubitus position (as described previously) and relaxed as much as possible. Normal range is 80-180
mm H20, with small, visible excursions related to respiration and pulse. In cases of extremely high
pressure (eg, 400 mm H20) the smallest sample possible (for the required testing) should be removed,
followed by consideration of CSF pressure-lowering treatment, with continuous monitoring of the
pressure until it decreases significantly.
Although radiographic screening identifies patients with intracranial mass lesions (with
possible associated increased ICP), ICP increases may be due to cerebral edema secondary to causes
such as infection, tumor cell infiltration, and benign intracranial hypertension. Detection of increased
CSF pressure (ie, >220 mm H20) permits treatment (eg, mannitol, corticosteroids, hyperventilation)
even before the etiology is identified. Commercially available LP sets contain a manometer and
stopcock for this purpose.
Following determination of CSF pressure, CSF samples should be obtained. Only a few
milliliters are needed for basic studies (eg, protein, glucose). Specialized tests that require
concentration of the CSF (eg, cell count, specific antibody studies) require more CSF.
In the event of a very low pressure, the question of spinal block may need to be addressed. In
1916, Queckenstedt described a technique for compression of the jugular veins (by an assistant) with
concomitant rise in CSF pressure if the subarachnoid space is open. Although this technique is
potentially useful, more frequently spinal block is confirmed and its cause determined by standard
myelography.

Important points
If the opening pressure is high, the specimens still should be collected, because any change in
intracranial dynamics caused by the LP has occurred already. Premature needle removal without
collecting CSF will not change this situation. If the fluid appears to be bloody, several specimens
should be collected. If the blood clears in successive tubes then the blood, at least in part, was
traumatic in origin. Unfortunately, this sign is neither specific nor sensitive, as in some traumatic taps
the amount of blood increases in subsequent tubes.
In cases in which the clarity of the CSF is in doubt (eg, a hazy appearance can be produced by
either RBCs or WBCs), a tube of CSF should be compared with a tube of water against a fluorescent
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light bulb or X-ray view box.

When sufficient fluid is obtained, the needle is withdrawn and a dry sterile dressing applied to
the puncture site. Prolonged compression of the site, or keeping the patient supine for an extended
period, has not been proven to reduce the incidence of spinal headache. Spinal headache is
characterized by pulsatile head pain, with or without nausea, relieved by lying down and aggravated by
standing and Valsalva maneuvers. It is self-limited but may last up to a week (or rarely longer).
The placement of an epidural blood patch using the patient’s own venous blood often corrects
this problem. However, the need for a blood patch is uncommon. The use of intravenous caffeine
benzoate (500 mg infusion over 1 h) also has been found to treat post-LP headaches effectively in
double-blind, controlled trials.

CSF ANALYSIS
Separate specimens should be sent for microscopic study and for centrifugation. The latter must
be done promptly, as RBCs hemolyze within a few hours. Normal CSF may contain as many as 5
lymphocytes per cubic millimeter.
A larger-than-usual number of WBCs suggests infection or, more rarely, leukemic infiltration.
While bacterial infections traditionally are associated with a preponderance of polymorphonuclear
leukocytes (PMNs), many cases of viral meningitis/encephalitis also have a high percentage of PMNs
in the acute phase of the illness (when in fact, most LPs are done). In addition, inflammation from any
source (eg, CNS vasculitis) can raise the WBC count.
A traumatic tap will, of course, introduce both WBCs and RBCs into the CSF. An
approximation of 1 WBC per 1000 RBCs can be made, although a repeat tap is preferable. While no
normal value for RBCs in the CSF is known, an occasional RBC may be incident to the tap.

Xanthochromia
The best way to distinguish RBCs related to intracranial bleeding is examination of the
centrifuged supernatant CSF for xanthochromia (yellow color). Although xanthochromia can be
confirmed visually, it is identified and quantified more accurately in the laboratory.
While xanthochromia can be produced by spillover from a very high serum bilirubin level (ie,
>15 mg/dL), patients with severe hyperbilirubinema usually have been identified prior to the LP (eg,
jaundice, known liver disease). With this exception, the presence of xanthochromia in a freshly spun
specimen is evidence of preexistent blood in the subarachnoid space. However, note that an extremely
high CSF protein level, as seen in LPs below a complete spinal block, also renders the fluid
xanthochromic, though without RBCs.
Xanthochromia can persist up to several weeks following a subarachnoid hemorrhage (SAH).
Thus it has greater diagnostic sensitivity than a CT scan of the head without contrast, especially if the
SAH has occurred more than 3-4 days prior to presentation. Patients with aneurysmal leaks (ie, sentinel
hemorrhages) may present days after headache onset, increasing the likelihood of a false-negative head
CT scan.
In some cases, the CSF may be another color that strongly suggests a diagnosis. For example,
pseudomonal meningitis may be associated with bright green CSF.

Other tests
Assuming the CSF has been collected under sterile conditions, microbiologic studies can be
performed. Stains, cultures, and immunoglobulin titers can be obtained. The latter are of special
importance in diseases in which peripheral manifestations fade while CNS symptoms persist (eg,
syphilis, Lyme disease).
Assessment of CSF protein level, while nonspecific, can be a clue to otherwise unsuspected
neurologic disease. The high protein levels in demyelinating polyneuropathies, or postinfectious states,
can be informative. A traumatic tap can introduce protein into the CSF. An approximation of 1 mg of
protein per 750 RBCs may be used, although a repeat tap is preferable.
CSF glucose level normally approximates 60% of the peripheral blood glucose level at the time
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of the tap. A simultaneous measurement of blood glucose (especially if the CSF glucose level is likely
to be low) is recommended. Low CSF glucose level usually is associated with bacterial infection
(probably due to enzymatic inhibition rather that actual bacterial consumption of the glucose). It also is
seen in tumor infiltration, and may be one of the hallmarks of meningeal carcinomatosis, even with
negative cytologic findings. High CSF glucose level has no specific diagnostic significance and is most
often spillover from elevated blood glucose level.
Leptomeningeal malignancies: Multiple LP examinations may be required in this situation. At
least 3 negative cytologic evaluations (ie, 3 separate samplings) are required to rule out leptomeningeal
malignancy (eg, leptomeningeal carcinomatosis).

Indications for CSF examination and LP

A. CSF examination is key to the diagnosis and management of various CNS infections,
including acute and chronic meningitis and encephalitis. In many patients with fever of
unknown origin, even in the absence of meningeal signs, early LP is commonly of value,
especially because meningeal signs may be minimal or absent in very young or elderly
patients. Meningeal infection especially should be sought in patients with fever and
impaired sensorium or an immunocompromised state (e.g., patients with AIDS). If a patient
has unexplained acute confusion, stupor, or coma, even if afebrile, CSF examination is
necessary for evaluation for meningoencephalitis. In most clinical settings, CT of the brain
or other neuroimaging should be performed before LP to rule out a possible intracranial
mass (e.g., hemorrhage or abscess), which would make LP a potentially lethal procedure.
However, if the patient is extremely ill and acute meningitis, such as meningococcal
meningitis, is suspected, LP should be performed without delay to avoid losing
valuable time in beginning appropriate therapy.
B. In patients with suspected subarachnoid hemorrhage, urgent CT is indicated
to evaluate for the presence of blood. However, in approximately 10% of patients with
subarachnoid hemorrhage, CT does not show blood, and a spinal tap is indicated. If the
diagnostic LP shows subarachnoid blood or xanthochromia, cerebral angiography is
needed to determine the source of the hemorrhage.
C. In patients with unexplained dementia, CSF examination may be necessary to
evaluate for CNS vasculitis, infection, or granulomatous disease. The CSF should always be
examined if the patient has dementia and a positive result of a fluorescent treponemal
antibody absorption test. Patients with radiographic hydro-cephalus also may need a
CSF study to exclude chronic meningitis as a cause of symptomatic hydrocephalus. In
patients with suspected Creutzfeldt-Jakob disease, a positive result of radioimmunoassay of
the CSF for "prion protein" (14-3-3 protein) is a sensitive and relatively specific marker for
prion disease, although false-positive results have been described with encephalitis and with
recent stroke.
D. CSF examination usually is not warranted for and can be dangerous for most
patients with stroke. However, CSF analysis can assist in the etiologic diagnosis of
unexplained stroke in young or middle-aged patients who lack atherosclerotic risk factors.
Causes such as CNS vasculitis, meningovascular syphilis, and AIDS may be diagnosed.
E. CSF studies can aid in the diagnosis of MS, although there is no specific CSF
marker for this disease. Elevated CSF immunoglobulin G (IgG) levels with normal serum IgG
levels and the presence of oligoclonal bands in the CSF are characteristic but not specific for MS.
An elevated CSF gamma globulin level can occur in neu- rosyphilis, viral meningoencephalitis,
and subacute sclerosing panencephalitis.
F. CSF analysis often is necessary, after appropriate neuroimaging, in the evalua-
tion of patients admitted with an initial tonic-clonic seizure or status epilepticus to exclude
active CNS infection or hemorrhage.
G. LP is necessary to confirm the clinical suspicion of carcinomatous or leukemic
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meningitis. Numerous LPs sometimes are needed. The typical CSF pattern is pleocytosis
with elevated protein, low glucose, and a positive cytologic results for a malignant tumor.
H. CSF studies can aid in the diagnosis of certain inflammatory or demyelinat-ing
forms of neuropathy, such as Guillain—Barre syndrome or chronic idio-pathic demyelinating
polyradiculoneuropathy. The CSF protein level often is elevated without an abnormal
cellular response.
I. Although LP is generally contraindicated in the evaluation of patients with
papilledema, LP is indicated to document increased intracranial pressure in a patient with
suspected idiopathic intracranial hypertension (pseudotu-mor cerebri) after results of
neuroimaging studies have proved normal. The spinal fluid is under increased pressure but is
otherwise normal in this entity, except for occasional decreases in CSF protein level. LP is
needed to document low CSF pressure in rare low-pressure syndromes in a patient with
headaches that occur on standing and are relieved by lying down.
J. LP can be used to deliver intrathecal antibiotics and chemotherapy in the
management of certain CNS infections and meningeal malignant tumors. LP also is needed
in certain diagnostic procedures, such as myelography and cisternography.

Contraindications to LP
A. LP is contraindicated in evaluation of any patient with increased intracranial
pressure, except idiopathic intracranial hypertension, because of the real danger of cerebral
herniation and death.
B. LP is contraindicated if there is suppuration in the skin or deeper tissues
overlying the spinal canal because of the danger of inducing purulent meningitis.
C. LP is dangerous in the presence of anticoagulation therapy or a bleeding
diathesis. Heparin administration should not be reinstituted for a minimum of 2 hours after
LP is performed. In general, LP is hazardous if the platelet count is less than 50,000/mL, or
especially if it is less than 20,000/mL. In such cases, platelet transfusions should be initiated
if possible before LP.
D. LP should not be performed when a spinal mass is suspected unless the proce-
dure is part of a myelogram with neurosurgical assistance readily available. A dramatic
deterioration in spinal cord or cauda equina function can occur after LP.

Complications of LP
A. Brain herniation and death can occur if an LP is performed on a patient with
increased intracranial pressure from a cerebral mass lesion. LP is contraindicated in the
evaluation of any patient believed to have an intracranial mass.
B. Headache of low-pressure type occurs in as many as 10% of patients after LP
(spinal headache). This type of headache occurs only on standing and is relieved by lying
down. It usually is self-limiting, but it can require an epidural auto logous blood patch for
relief. Post-LP headache is most common among young women with lower body mass. Use of
a higher-gauge (smaller diameter) needle, needle insertion parallel to dural fibers (bevel up
with patient on side), and replacing the stylet before needle removal may help prevent post-
LP headache. The occurrence of post-LP headache is unrelated to CSF opening pressure, cells,
and protein; patient position during LP; duration of recumbency after LP; amount of
CSF removed; or hydration after LP.
C. Diplopia, which usually results from unilateral or bilateral cranial nerve
VI palsy, occurs rarely and usually is self-limiting.
D. Aseptic meningitis occurs rarely and is characterized by posterior neck
pain, headache, and neck stiffness. This process usually is self-limiting.
E. Spinal epidural, subdural, and subarachnoid hematoma can occur,
especially in patients taking anticoagulants or with bleeding diatheses. Such hematomas
usually are self-limiting and can cause local pain and meningeal irritation.
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However, in rare instances, epidural hematoma causes flaccid and potentially irreversible
paraplegia that necessitates emergency surgical evacuation.

General comments on evaluation of LP results

A. Normal CSF pressure is 70 to 180 mm of water in the lateral recumbent
position. Pressure should be greater than 200 mm of water to be considered elevated. In an
obese patient with possible idiopathic intracranial hypertension, the pressure should be
greater than 250 mm of water to establish this diagnosis.
B. Normal CSF glucose level is approximately two-thirds the serum glucose
level, which must be measured at the time of the LP. Hypoglycorrhachia (low CSF glucose)
with few white blood cells suggests fungal infection. Many white cells suggest bacterial
infection. Abnormal (malignant) cells suggest a malignant meningeal tumor.
C. The CSF protein level may be increased (>100 mg/dL) in many CNS
infectious and malignant processes. Causes of elevation of CSF protein level with normal
findings at neuroimaging include myxedema, inflammatory demyelinating
polyneuropathy, diabetic polyneuropathy, neurofibroma within the CSF pathways,
resolving subarachnoid hemorrhage, gliomatosis cerebri, CNS vasculitis, and any process
that causes spinal compression or obstruction of CSF flow.
D. Normally, the CSF can contain up to five lymphocytes or mononuclear cells
per milliliter. Pleocytosis causes CSF clouding when there are at least 200 cells/mL. White
blood cell count increases with subarachnoid infection, hemorrhage, chemical meningitis, or
meningeal neoplasms. Pleocytosis also can occur for approxi mately 24 hours after a
generalized seizure.
E. If initial spinal fluid appears bloody, one must attempt to determine whether
the source of the blood is a traumatic tap or subarachnoid hemorrhage. If the initial tube of
fluid is bloody and subsequent tubes are progressively clear, it is most likely that the tap
was traumatic. One should then immediately centrifuge the fluid to see whether the
supernatant is clear, which suggests a traumatic tap. If the supernatant fluid is
xanthochromic (yellow-tinged), it is likely that the blood has been present in the CSF for a
few hours. Xanthochromia occurs several hours
after subarachnoid hemorrhage, reaches its greatest intensity at the end of
1 week, and clears in approximately 2 to 4 weeks. Xanthochromia also can be observed in
jaundice and hypercarotenemia.
F. Polymerase chain reaction testing of the CSF has been found to have great
utility in the diagnosis of several CNS infections. These include
1. Herpes simplex virus I (herpes simplex encephalitis)
2. Herpes simplex II (herpes simplex encephalitis in neonates, recurrent
meningitis)
3. JC virus (progressive multifocal leukoencephalopathy)
4. Cytomegalovirus (CMV ependymitis and polyradiculopathy associated with
AIDS)
5. Borrelia burgdorferi (Lyme disease)
6. Tropheryma whippleii (Whipple's disease of the CNS)
7. Toxoplasmosis (CNS toxoplasmosis in AIDS)
8. Mycobacterium tuberculosis (tubercular meningitis)
9. Other viruses causing encephalitis, including enteroviruses, varicella-zoster
virus, Epstein-Barr virus, and herpesvirus type 6

CONCLUSIONS
Virtually any CSF analysis should include cell counts, examination for xanthochromia, and
protein and glucose studies. Beyond this, culture, serologic tests for syphilis, Lyme titer,
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electrophoretic pattern, myelin basic protein (for multiple sclerosis), cryptococcal antigen, angiotensin-
converting enzyme level (ie, in suspected sarcoidosis), bacterial stains, and cytologic studies should be
ordered on an individual basis. Because a CSF specimen is comparatively difficult to obtain, a bit more
tolerance for more tests usually is allowed. In summary, LP and CSF examination, while their
indications have been reduced, remain indispensable tools in the armamentarium of neurologic
diagnosis.

INTRACRANIAL PRESSURE
Whenever the circulation of CSF becomes impeded, intracranial pressure rises, producing
headaches, dizziness, or nausea and vomiting. Headaches are probably caused by irritation of dural
nerve endings responding to pressure and tension. Nausea and vomiting are probably caused by
irritation of the vagus nerve. Fast-developing intracranial pressure may produce the objective signs
of beginning or fully developed hemorrhagic papilledema. Longer-lasting papilledema leads to
secondary atrophy of the optic nerve head, characterized by marked paleness of the papilla. This
atrophy is often associated with deterioration of vision. If the third ventricle is part of a
hypertensive internal hydrocephalus, its distended suprachiasmatic recess may press on the center
of the chiasm, causing it to deform in the shape of an inverted horseshoe. The pressure may result in
atrophy of crossing fibers and therefore in bitemporal hemianopic field defects. This may occur
even if the tumor responsible for the internal hydrocephalus is far away in the cerebellum.
Once the fontanelles are closed the skull is a rigid box which can only accommodate a
limited volume. At an early age some separation of the sutures may occur.
The normal structures within the skull have more or less stable volume. There are some
variations in volume depending on the person’s activities ,cardiovascular as well as pulmonary
status. These variations are temporary and the intracranial pressure goes back quickly to its normal
level.
The skull is not a completely closed sphere, there are several openings mainly in the base of
the skull. It is believed that intracranial pressure is a reflection of the atmospheric pressure which is
conducted through the large neck vessels.
NORMAL INTRACRANIAL PRESSURE
The normal pressure for is 15 mm/Hg or 150 mm - 200 mm of water. Accurate measurement
of pressure in new born and infants is difficult to obtain but it is believed that in the first few
months of life the intracranial pressure is lower . Values up to 8 mm/Hg has been considered to be
normal in the first few months of life.
The intracranial pressure is closely related to brain perfusion. The cerebral blood flow is
dependent on the intracranial pressure. In a simplified statement cerebral perfusion pressure is the
difference between the systemic blood pressure and the intracranial pressure. For this reason the
intracranial pressure needs to be maintained at a steady state. This is accomplished by dynamic
equilibrium of intracranial components.
As the skull is a rigid box any extra volume added to the intracranial cavity needs to be at
the expense of normal intracranial components in order to maintain the intracranial pressure at a
normal level.
The relationship between the intracranial volume and the intracranial pressure is in
following. In the early stages adjustment is made to maintain an ICP within normal range. This is
called autoregulation. If the process continues the increase in volume will be associated with
gradual rise in ICP. This continues up to an ICP of about 50mm hg when the pattern changes and
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the intracranial cavity loses its compliance and behaves as a solid box. There will be steep rise and
incremental rise of the intracranial pressure.
DYNAMICS OF RAISED INTRACRANIAL PRESSURE
Raised intracranial pressure could be the result of the following:
1 Increase of the volume of the normal content of the intracranial cavity, as increase in the
volume of CSF as in hydrocephalus, increase in the volume of the brain tissue itself as in brain
oedema or increased cerebral blood volume.
2 Extra volume added to the intracranial cavity as in tumours or haematomas.
Where an extra volume is added to the intracranial cavity this has to be at the expense of the
normal contents. To start with the cerebrospinal fluid is squeezed out, one finds that the ventricles
become compressed and displaced. There will be paucity of subarachnoid spaces and the basal
cisterns become less discernible. Once a state is reached where no more CSF could be expulsed, a
change in the cerebral blood flow occurs. Cerebral blood perfusion is related to intracranial
pressure. With the rise of intracranial pressure there is diminished cerebral blood flow and more
space is provided for the extra volume. However a state would be reached where any further
decrease in cerebral blood flow would lead to cerebral ischaemia. In this situation the brain itself
starts to herniate through the hiatus of the tentorium and foramen magnum. At this stage the
patient’s condition is precarious and needs urgent action to reduce the intracranial pressure.
Increase blood volume can occur as a result of a blockage to venous drainage from the
cranial cavity or due to vasodilatation. It is very important to appreciate that cerebral blood vessels
are very sensitive to changes in blood gases especially carbon dioxide. High PCO2 results in
vasodilatation and increase in cerebral blood volume.
The average brain weight varies from 1000 to 1500 grams.
CLINICAL PRESENTATION
Raised intracranial pressure can produce specific as well as non specific signs and
symptoms. Cushing triad of headache, papilloedema and vomiting is considered the classical
presentation of raised intracranial pressure.
Headache:
Headache is caused by distortion of intracranial blood vessels as well as stretching of the
intracranial dura. Typically the headache is worse in the morning. The morning headache is related
to poor venous drainage during sleep and probably a rise of PCO2 due to diminished respiratory
efforts, these factors lead to rise in intracranial pressure.
Papilloedema :
Ophthalmoscopy would reveal various degrees of disc swelling depending on the severity of
the raised intracranial pressure. The optic nerve is part of the brain and is surrounded by meningeal
covering. With severe disc swelling haemorrhages could develop. Sustained raised intracranial
pressure for long periods of time could lead to loss of vision. During this period intermittent loss of
vision (Amaurosis fugax) is a grave sign and would necessitate an urgent action to reduce the
pressure otherwise visual loss would be permanent. With prolonged periods of raised intracranial
pressure visual loss might continue in spite of relief of intracranial pressure.
The mechanism of disc swelling is not fully understood but it is believed that it is due to
several factors which include the interference with the axoplasmic transport in the retina, vascular
 9

congestion and may be transmission of raised cerebral spinal fluid pressure along the optic nerve
leading to compression of the central retinal vein and oedema of the optic disc.
VOMITING
This is particularly common in children especially with lesions involving the floor of the
fourth ventricle and direct irritation of the vagus nucleus. In raised intracranial pressure vomiting is
more common in the morning.
Other signs and symptoms are seen with the raised intracranial pressure. The patient can
present with signs related to the lesion causing the raised intracranial pressure i.e. tumours or
haematoma. Other signs seen are changes in the level of consciousness pulse and blood pressure.
There is usually bradycardia and rise in blood pressure. Respiratory changes can occur in the form
of periodic breathing or apnea.
Non- localizing signs can occur. These are indirect involvement of cranial nerves or long
tracts as a result of brain shift. Stretching of the sixth cranial nerve can result in diplopia. This nerve
is particularly vulnerable because of its long course within the cranial cavity and its small calliper.
Compression of the third cranial nerve can result in papillary dilatation and loss of ocular
movements. This usually starts on the ipsilateral side but at a later stage the other side could be
involved. Compression of the cerebral peduncle due to brain herniation can result in hemiplegia.
Assessment of the state of consciousness is done according to the Paediatric Coma Scale.
Measurement of Intracranial Pressure:
Intracranial pressure is not a constant value but is variable. It can rises sharply with
coughing and sneezing, up to 50 or 60 mm/Hg to settle down to normal values in a short time. It
also varies according to the activity the person is involved with. For these reasons single
measurement of intracranial pressure is not a true representation. Intracranial pressure needs to be
measured over 24 to 48 hours to get a true representation. During this period close observation
should be done to monitor patient activity at the time of change in intracranial pressure.
Measurement of intracranial pressure using closed fluid system has been replaced by more
accurate means.
In the closed fluid system ventricular catheter is introduced into the ventricle which will be
attached to a transducer.
The most accurate method of measuring the intracranial pressure is by the use of electrodes
with a sensor attached to its tip. There are several versions of these catheters manufactured by
different companies.

MANAGEMENT OF RAISED INTRACRANIAL PRESSURE

The first step is to find the cause of the raised intracranial pressure and remove it if possible.
If there is excessive cerebrospinal fluid as in hydrocephalus then shunt procedure or external
drainage should be instituted. If there is a resectable tumour then this should be removed. In cases
where there are no surgically treatable cause efforts should be directed at reducing intracranial
pressure by one of the following means:
1 Osmotic Diuretic: This acts by dehydrating the brain. This is achieved by removing
extracellular fluid by creating an osmotic gradient across the capillary wall. The most commonly
used agent is Mannitol. This is a carbohydrate which is not metabolised in the blood and remains
 10

entirely in the extracellular space. The dose is.25- 1 gram per kilogram body weight over 10 - 15
minutes. 20% of the solution is used. The effect of Mannitol lasts about 4 to 6 hours.
Mannitol has some side effects, its action is reduced with repeated doses and can cause
systemic acidosis and renal failure due to increase plasma osmolarity. After Mannitol is stopped
there is rebound of intracranial pressure.
Other diuretics used is Furosemide which is a renal diuretic.
Diuretics could be used as a temporary measure while the patient is prepared for definitive
surgical treatment.
STEROIDS
These are mainly used to reduce brain swelling around brain tumours. They are very
effective in these conditions.
CSF DRAINAGE
This is an effective and rapid way of reducing intracranial pressure in cases where ventricles
are visible and can be cannulated. However in severe brain oedema with collapsed ventricles it is
difficult to get into the ventricle. The ventricular catheter could be used to monitor intracranial
pressure at the same time.
HYPERVENTILATION
As mentioned before cerebral blood vessels are sensitive to changes in blood gases. The aim
of hyperventilation is to reduce the PCO2 to a level around 30 mm/Hg. Low PCO2 will cause
vasoconstriction and reduced intracranial blood volume. Levels below 30 mm hg should be avoided
as it can cause cerebral ischaemia.
BARBITURATE
Barbiturate is used to induce deep coma, where there is a reduction in metabolic rate,
oxygen consumption and CO2 production. This method is used only when all other means of
treatment failed.

Meningeal syndrom
Pathophysiology
When the protecting barriers of the brain, including the skull, meninges, and blood-brain
barrier, are broached by a pathogen, meningitis can result. Predisposing factors include preexisting
diabetes mellitus, immunosuppression, otitis media, pneumonia, sinusitis, and alcohol abuse.
Meningeal inflammation and irritation elicit a protective reflex to prevent stretching of the inflamed
and hypersensitive nerve roots, which is detectable clinically as neck stiffness or meningeal signs.
Meningeal irritation due to inflammation also may cause headache and cranial nerve palsies. When
cerebral edema and elevated intracranial pressure occur, alterations in mental status, headache,
vomiting, seizures, and cranial nerve palsies may ensue.
Most acute viral meningitides produce symptoms with variations depending on the particular
virus. Some individuals may experience a biphasic type of illness with nonspecific constitutional
symptoms followed by meningitis.
In some cases meningeal syndrome appears without infection and there is aseptic meningitis.
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Headache, fever, stiff neck, photophobia, drowsiness, myalgias, malaise, chills, sore throat,
abdominal pain, nausea, and vomiting usually characterize acute meningial syndrom. Focal signs,
seizures, and profound lethargy are rarely a part of this syndrome.
Meningeal signs
Neck stiffness in meningitis is tested by gentle forward flexion of the neck with the patient
lying in the supine position. Meningeal irritation also can be tested by the jolt accentuation of
headache. This is tested by asking the patient to turn his or her head horizontally at a frequency of
2-3 rotations per second. Worsening of a baseline headache represents a positive sign.
Severe meningeal irritation may result in the patient assuming the tripod position (termed
Amoss sign or Hoyne sign) with the knees and hips flexed, the back arched lordotically, the neck
extended, and the arms brought back to support the thorax.
When passive neck flexion in a supine patient results in flexion of the knees and hips, a
positive Brudzinski sign is entertained. Yet another sign, the contralateral reflex, is present if
passive flexion of one hip and knee causes flexion of the contralateral leg.
Kernig sign is elicited with the patient lying supine and the hip flexed at 90°. A positive sign
is present when extension of the knee from this position elicits resistance or pain in the lower back
or posterior thigh.