Medicine II

NEUROLOGY o Pons - 4 nucleus

Midterm Coverage – Dr. Rabo  CN V
AMS 204  CNVI
 CN VII
Coverage of Midterm Examination:  CN VIII
I. Headaches o Medulla – 4 nucleus
II. Increased ICP  CN IX
III. Brain Tumor  CN X
IV. CNS Infection  CN XI
V. Seizures  CN XII

Note: EOM problem (medial rectus palsy) problem in the midbrain;

Lateral rectus palsy  non-localizing sign; shallow right nasolabial
HEADACHES
fold (CN VII)  problem in the pons
Case: A 22 y/o female patient comes to you with history of
Headache is a common symptom presented in clinics. Headaches
headaches
- Is this a neurologic problem? occur because there are pain and non-pain sensitive structures in
the brain. The brain is non-pain sensitive. Generally, the brain
o It is based on the location, severity, duration, and
accompanying signs and symptoms such as: parenchyma is insensitive.
 Headache + n/v = NOT a neurologic problem - Secondary to other causes
- Neurologic and not neurologic
 Headache + n/v + focal neurologic deficit
(motor and sensory) = neurologic problem - should encompass all aches and pains located in the head, but
in practice its application is restricted to discomfort in the region
 (+) problems in neurologic exam
of the cranial vault.
 Headache + n/v + altered sensorium =
neurologic problem
Pain sensitive structures
 Headache + n/v + seizure episodes
1. skin, subcutaneous tissue, muscles, extracranial arteries,
 Headache + n/v + diplopia secondary to lateral
and periosteum of the skull;
rectus palsy = neurologic problem
2. delicate structures of the eye, ear, nasal cavities, and
 Diplopia – doubling of vision
paranasal sinuses;
o A patient with diplopia due to
3. intracranial venous sinuses and their large tributaries,
lateral rectus palsy appears with
especially pericavernous structures;
internal squint. This is a false
4. parts of the dura at the base of the brain and the arteries
localizing sign which means
within the dura, particularly the proximal parts of the
that there is an increased
anterior and middle cerebral arteries and the intracranial
intracranial pressure but it cannot
segment of the internal carotid artery;
be localized specifically to which
5. the middle meningeal and superficial temporal arteries;
part of the brain. The nucleus of
and
the lateral rectus (CN VI) is
6. the optic, oculomotor, trigeminal, glossopharyngeal,
located in the pons
vagus, and first three cervical nerves. Interestingly, pain is
o Diplopia due to medial rectus
practically the only sensation produced by stimulation of
palsy (CN III) is a focal
these structures;
neurologic deficit. This is a
localizing sign. (can be
Face and scalp are more richly supplied with pain receptors than
lateralized, localized, and
many other parts of the body, perhaps to protect the precious
levelized)
contents of the skull. Also, the nasal and oral passages, the eye, and
Note: Bilateral and lateral rectus palsy is a non-localizing sign
the ear—all delicate and highly sensitive structures—reside here and
unlike if you have a medial rectus palsy which is a localizing sign.
must be protected; when afflicted by disease, each is capable of
Cranial nerve VI involvement is not a localizing sign because CN VI
inducing pain in its own way. Finally, for the intelligent person, there
that is responsible for the function of the lateral rectus has a very
is greater concern about what happens to the head than to other
long course (umiikot sa buong brainstem that is why anywhere na
parts of the body, since the former houses the brain, and headache
maipit will cause lateral rectus palsy) so it cannot be localized. Medial
frequently raises the specter of brain tumor or other cerebral disease.
rectus palsy (CN III – short course)
Non pain sensitive
12 CN and corresponding brainstem area:
1. Pia, arachnoid, and dura over the convexity of brain
- Three brain stem segments + 12 CNs
- Dura over the base of the brain are sensitive unlike the dura
o Midbrain - 4 nucleus
over the convexity of the brain which is non-sensitive
 CN III
2. Parenchyma of brain
 CN IV
3. Ependyma and choroid plexus.
Note: CN I and CN II are supratentorial

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MECHANISM OF HEADACHE
- There are receptors which are located in the blood vessels
(pain-sensitive) therefore the displacement, stretching of the
blood vessels and the nerves causes the pain.
Deformation, displacement, and traction of the vessels and
dural structures at the base of the brain
(intracranial mass lesions)
THRE E MOST COMMON CAUSES OF HEADACHES:
1. Migraine
2. Tension headaches
3. Cluster headaches
Note: These are primary headaches. There are also secondary
headaches which are secondary to tumors, benign intracranial
hypertension, and pseudotumor cerebri. (Secondary cause of
headaches – primary brain tumor and metastasis (most common);
primary brain tumors: gliomas and meningiomas)
PRIMARY HEADACHES
1. MIGRAINE
- Classic description of migraine: Unilateral/one-sided,
pulsating or throbbing
- More common in women
- Usually in the younger age group
 Recurrent migraines is possible in the elderly
 Migraine starts when you are young, disappear in
between, and return when you are old and it never
starts at an old age.
 It diminishes through the years
- This condition can be inherited
Highly prevalent and largely familial disorder characterized by
periodic, commonly unilateral, often pulsatile headaches that begin in
childhood, adolescence, or early adult life and recur with diminishing
frequency during advancing years.
Two Types of Migraine:
3..a. With Aura
3..b. Without Aura
Note: It is important to ask if there is aura or not because it will
matter with the treatment of the patient.
- With aura (classic or neurologic)
 Aura is a neurologic symptom complex occurring 1-
2 hours before the onset of the headache. Aura is
experienced prior to the headache phase:
 Visual (most common) – flashes of light
 Smell
 Heard
 Felt – paresthesias, tingling sensation
 Can easily be treated
 When the aura starts, the pain relievers can
already be given even without the
appearance of the headache. When you
drink the pain medications when the aura
starts it will not continue to the headache
phase (or lessen it)
 It is hard to stop the migraine when it is
already in the painful headache phase
because the medication will have no effect
and will only be vomited by the patient.
Ushered in by a disturbance of nervous function, most often visual,
followed in a few minutes to hours by hemicranial (or, in about one-
third of cases, bilateral) headache, nausea, and sometimes vomiting,
all of which last for hours or as long as a day or more.
- Without aura (common)
 More common migraine
 aura is characterized by an unheralded onset over
minutes or longer of increasing hemicranial
headache or, less often, by generalized headache
with or without nausea and vomiting, which then
follows the same temporal pattern as the migraine
with aura.
 The ratio of classic to common migraine is 1:5
 Either type may be preceded by vague premonitory
changes in mood and appetite.
 Sensitivity to light, noise, and often smells attends
both types, and intensification with movement of the
head is common. If the pain is severe, the patient
prefers to lie down in a quiet, darkened room and
tries to sleep. The hemicranial and the throbbing
(pulsating) aspects of migraine are its most
characteristic features in comparison to other
headache types.
 Each patient displays a proclivity for the pain to
affect one side or the other of the cranium, but not
exclusively so that some bouts are on the other
side.
Pathophysiology
- Migraine is a vascular condition which means that it
involves the blood vessels
- During the aura phase, there is vasoconstriction
 Vasoconstriction  decrease blood supply 
stroke-like symptoms (blindness, weakness
(hemiparesis))
- During the headache phase  vasodilation
 Vasodilation  hyperperfusion  causes traction
of the blood vessels  pain
- Migraine is a risk factor for stroke
Aura is due to cortical depression  vasoconstriction 
hypoperfusion.
Difficult to control when it reached the thalamic pathway
Best to stop when BV dilates and substances released.
TRIGGERS
- Menstrual cycle – premenstruation and perimenstruation
- Tends to decrease or cease during the 2nd and 3rd trimester
of pregnancy
- Use of OCP associated with an increase frequency and
severity of migraine
- Foods such as tyramine – as provocative factor in migraine
- Excess caffeine intake or withdrawal of caffeine
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 - Induced by exposure to glare or other strong sensory stimuli,
sudden jarring of head (frontalis migraine)
Menstrual migraine had been considered to be solelyrelated to the
withdrawal of estradiol. It is now acknowledged that the influence of
sex hormones on headache is more complex.
- Migraine tends to cease during the second and third
trimesters of pregnancy in 75 to 80 percent of women, and in
others they continue at a reduced frequency; less often, attacks
of migraine or the associated neurologic symptoms first appear
during pregnancy, usually in the first trimester
- Although migraine commonly diminishes in severity and
frequency with age, it may actually worsen in some
postmenopausal women, and estrogen therapy may either
increase or, paradoxically, diminish the incidence of headaches.
- The use of birth control pills is associated with an
increased frequency and severity of migraine and in rare
instances has resulted in a permanent neurologic deficit.
- Some of these foods are rich in tyramine, which has been
incriminated as a provocative factor in migraine. Alcohol,
particularly red wine or port, regularly provokes an attack in
some persons;
- headaches are fairly consistently induced by exposure to
glare or other strong sensory stimuli, sudden jarring of the head
(“footballer’s migraine”), or by rapid changes in barometric
pressure.
- A very common trigger is excess caffeine intake or
withdrawal of caffeine.
CLASSIC MIGRAINE
Prodromal
o Preceded by a period of variable prodromal phenomenon
lasting a few hours to 2 days.
o Mos patients complain of sensitivity to smell and moise,
irritability, restlessness…
Aura
o 15 % of patients
o Neuro symptoms, most common is visual
o Slowly over several to 20 mins, last less than 1 hour.
o Visual aura- flashes of white or silver, or rarely,
multicolored light followed by enlarging blind spot with a
shimmering edge (scintillation scotoma), or formation of dazzling
zigzag lines.
o Other focal neuro defect
 Numbness and tingling of lips, face and hands.
 Slight confusion of thinking
 Weakness of arm or leg
 Mild aphasia or aphasia
 Dizziness and uncertainty of gait and drowsiness.
Headache phase
o Most patients complain of pulsating, throbbing or
continuous pain on one side of head.
o Others have pain on the entire head, part behind the eyes,
in the nuchal regions and temples.
Resolution
- Migraine with aura frequently has its onset soon after
awakening, but it may occur at any time of day.
- During the preceding day or so, there may have been mild
changes in mood (sometimes a surge of energy or a
feeling of well-being), hunger or anorexia, drowsiness, or
frequent yawning.
- Then, abruptly, there is a disturbance of vision consisting
usually of unformed flashes of white, or silver, or, rarely, of
multicolored lights (photopsia).
- This may be followed by an enlarging blind spot with a
shimmering edge ( scintillating scotoma), or formations
of dazzling zigzag lines (arranged like the battlements of a
castle, hence the term fortification spectra or
teichopsia).
- Other patients complain instead of blurred or shimmering
or cloudy vision, as though they were looking through thick
or smoked glass or the wavy distortions produced by heat
rising from asphalt.
- These luminous hallucinations move slowly across the
visual field for several minutes and may leave an island of
visual loss in their wake (scotoma); the latter is usually
bilateral and often homonymous (involving corresponding
parts of the field of vision of each eye), pointing to their
origin in the visual cortex. Patients may attribute these
visual symptoms to one eye rather than to parts of both
fields. Ophthalmologic abnormalities of retinal and optic
nerve vessels have been described in some cases but are
not typical.
- The visual or neurologic symptoms usually last for less
than 30 min, sometimes longer.
- As they recede, a unilateral dull pain develops of slowly
increasing intensity that progresses to a throbbing
headache (usually but not always on the side of the
cerebral disturbance).
- At the peak of the pain, within minutes to an hour, the
patient may be forced to lie down and to shun light
(photophobia) and noise (phonophobia). Light is irritating
and may be painful to the globes, or it is perceived as
overly bright (dazzle) and strong odors are disagreeable.
- Nausea and, less often, vomiting may occur.
- The headache lasts for hours and sometimes for a day or
even longer and is always the most unpleasant feature of
the illness.
 The temporal scalp vessels may be tender (allodynia) and
the headache is worsened by strain or jarring of the body
or head. Pressure on the scalp vessels or carotid artery
may momentarily reduce the pain and releasing pressure
accentuates it.
Migraine with aura
- At least 5 attacks
- Lasting 4-72 hrs.
- >2 of:
 unilateral
 Pulsating
 Moderate to severe intensity
- Typical aura with migraine headache
- Typical aura with non migraine headache
- Typical aura without headache
- Familial hemiplegic migraine
- Basilar type migraine
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TREATMENT
- Non-pharmacologic – treat acute attacks, prophylaxis
- Pharmacologic – control of acute attacks and prevention
CONTROL OF ACUTE ATTACKS
- Acute treatment: Pain relievers (no specific drug)
 Paracetamol, COX-2 inhibitors, Ibuprofen, etc
- Pain  Abortive treatment  pain disappears
Initiate treatment during the neuro (visual) prodrome or at the very
onset of migraine. To prevent progression (abort the pain): Analgesic
(acetaminophen, aspirin, NSAID), Ergot alkaloids (ergotamine,
dihydroestrogen), Serotonin receptor agonist (triptans), and
Tramadol – N/V
MIGRAINE PROPHYLAXIS
- Maintenance treatment
 Some patients have recurrent migraines
- Give prophylactic treatment to lessen the frequency of
attacks and the intensity or severity of pain (role)
- The patient still needs to take abortive treatment during
acute headache attacks
- Prophylactic treatment: Beta blockers, anticonvulsant
(valproic acid, topiramate), and antidepressant (if the
migraine is secondary to a psychosomatic cause)
Daily administration of drug therapy for various periods is usually 2-
12 mins. Goal is to reduce frequency and severity of attacks, to
improve and reduce disability, and to minimize or eliminate the need
for abortive day therapy. Patients that may be candidates: patients
with 2 or more attacks per week, last >48 hrs.
Case: 23 y/o female who considers getting pregnant with migraine
that happens every other week for 3 days
Solution: Give anticonvulsant topiramate as prophylactic treatment
instead of valproic acid which is metabolized in the liver because it is
teratogenic, causes hepatitis and weight gain. Topiramate which is
metabolized in the kidneys is less teratogenic but causes renal
calculi and weight loss.
Complicated Migraine
- Migraine variant that when the migraine attacks there will be
hemiparesis which normalized after the attack.
- This is secondary to the “vascular theory”
 Ischemia due to the constriction of the blood
vessels
- Difficult to diagnose
2. TENSION TYPE
- Most common among the headaches encountered in the
clinics.
- Does not respond to a lot of medications because it is
secondary to stress.
- Classic description: bilateral, occipitonuchal, temporal, or
frontal (most common)
 Frontotemporal constricting type of headache
- Duration: it occurs all throughout the day lasting for days
to weeks to months without affecting daily activities
- Patient can still do activities of daily living
- It is the only type of headache that exhibit the peculiarity of
being present throughout the day
- It is constricting, dull, hard to explain
Pain is dull, aching but questions uncover the other sensations, such
as fullness, tightness. Does not progress but never disappear. This is
the most common variety of headache, is usually bilateral, with
occipitonuchal, temporal, or frontal predominance, or diffuse
extension over the top of the cranium. The pain is usually described
as dull and aching, but questioning often uncovers other sensations,
such as fullness, tightness, or pressure (as though the head were
surrounded by a band or clamped in a vise) or a feeling that the head
is swollen and may burst. On these sensations, waves of aching pain
are superimposed.
DIFFERRENCE WITH MIGRAINE
- More common in women (same)
- Tension headaches happen in the adolescent years while
migraine usually happens in the middle age group
- Without persistent throbbing, nausea, photophobia,
phonophobia and clear lateralization of migraine
- Do not interfere with activities
PATHOPHYSIOLOGY
- Muscle contractions
TREATMENT
- Muscle relaxant
 The pain may be secondary to muscle contraction
so muscle relaxants are given
 The most effective treatment for these patients are
benzodiazepines (diazepam, clorazepam,
altrazolam, etc) because these are muscle
relaxants and anxiolytics (prone to abuse)
- Analgesics ( aspirin, acetaminophen, NSAID)
- Drugs that can reverse anxiety and depression
- Massages are also effective
CLUSTER HEADACHE
- This is also called as nocturnal cephalalgia, migrainous
neuralgia, histaminic cephalalgia
- It occurs in clusters
- The most typical symptom of cluster headache is
vasomotor phenomenon (redness of the eyes with severe
headache which occurs deep and around the eyes)
- This headache pattern occurs predominantly in adult men
(age range: 20 to 50 years; male-to-female ratio
approximately 5:1)
- Characterized by a consistent unilateral orbital localization.
Consistent unilateral or bilateral localization
- The pain is felt deep in and around the eye, is very intense
and nonthrobbing as a rule, and often radiates into the
forehead, temple, and cheek—less often to the ear, occiput,
and neck.
- Very intense and throbbing and is usually unilateral
- Occurs regularly at the same time
- Its other characteristic feature is a nightly recurrence,
between 1 and 2 h after the onset of sleep, or several times
during the night; less often, it occurs during the day,
unattended by aura or vomiting.
- The headache has been called the “alarm clock headache”
because it recurs with remarkable regularity each night for
periods extending over 6 to 12 weeks, followed thereafter by
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 complete freedom for many months or even years. However,
in approximately 10 percent of patients, the headache
becomes chronic, persisting over days, months, or even
years.
- There are several associated vasomotor phenomena by
which cluster headache can be identified: a blocked nostril,
rhinorrhea, injected conjunctivum, lacrimation, miosis, and a
flush and edema of the cheek, all lasting on average for 45
min (range: 15 to 180 min).
- Some of our patients, when alerted to the sign, also report a
slight ptosis on the side of the orbital pain; in a few, the
ptosis has become permanent after repeated attacks.
- The homolateral temporal artery may become prominent
and tender during an attack, and the skin over the scalp and
face may be hyperalgesic.
- Cluster headache patients want to move about to relieve the
headache unlike in migraine who opted to rest to relieve the
condition.
Pathogenesis
- Paroxysmal dischages
TREATMENT
- Abortive + prophylactic treatment
 Since it is difficult, higher doses of the abortifacient
drugs are given
 For prophylactic, steroids can be given to prevent
the severe cluster headache attack
- Hard to treat
- Higher doses of carbamazepine (anti-convulsant) can be
given
- 100% oxygen for 10 – 15 mins to abort attacks
- Verapamil
- Ergotamine
- Triptan
Lumbar puncture (LP) or spontaneous low CSF pressure
headache
- Secondary to Lumbar Puncture procedure producing headache
upon standing up (common complication) due to the use of large
bore needles because it does not easily clot. The patient is
recommended to lie flat on bed for at least 6 hours.
NOT DISCUSSED
(+ those italicized above)
Dilatation of intracranial or extracranial artery
- The headaches that follow seizures, infusion of histamine,
and ingestion of alcohol are
- probably all caused by cerebral vasodilatation.
- Nitroglycerin, nitrites in cured meats (“hot-dog headache”),
and monosodium glutamate in Chinese food may cause
headache by the same mechanism.
- It seems probable that the throbbing or steady headache
that accompanies febrile illnesses has a vascular origin as well;
it is likely that the increased pulsation of meningeal vessels
activates painsensitive structures within their walls or around the
base of the brain. Febrile headache may be generalized or
predominate in the frontal or occipital regions and is relieved on
one side by carotid or superficial temporal artery compression
and on both sides by jugular vein compression
- A similar mechanism may be operative in the severe,
bilateral, throbbing headaches associated with extremely rapid
rises in blood pressure (in contrast to the absolute level), as
occurs with pheochromocytoma, malignant hypertension, sexual
activity, and in patients being treated with monoamine oxidase
inhibitors. Mild to moderate degrees of hypertension, however,
do not cause headaches despite a popular notion to the
contrary. So-called cough and exertional headaches may also
have their basis in the distention of intracranial vessels.
Infection or blockage of paranasal sinuses
- is accompanied by pain over the affected maxillary or
frontal sinuses.
- Usually it is associated with tenderness of the skin and
cranium in the same distribution.
- Pain from the ethmoid and sphenoid sinuses is localized
deep in the midline behind the root of the nose or occasionally
at the vertex (especially with disease of the sphenoid sinus).
The mechanism in these cases involves changes in pressure
and irritation of pain-sensitive sinus walls.
Headache of ocular origin
- located as a rule in the orbit, forehead, or temple, is of the
steady, aching type and tends to follow prolonged use of the
eyes in close work.
- The main faults are hypermetropia and astigmatism (rarely
myopia), which result in sustained contraction of extraocular as
well as frontal, temporal, and even occipitalmuscles. Correction
of the refractive error abolishes the headache.
- Traction on the extraocular muscles or the iris during eye
surgery will evoke pain. Patients who develop diplopia from
neurologic causes or are forced to use one eye because the
other has been occluded by a patch often complain of frontal
headache.
- Another mechanism is involved in iridocyclitis and in
acute angle closure glaucoma ,in which raised intraocular
pressure causes steady, aching pain in the region of the eye,
radiating to the forehead.
*headaches from supratentorial structures
-referred to the anterior two thirds of the head
-i.e., to the territory of the sensory supply of the first and
second divisions of thetrigeminal nerve
*headaches from infratentorial structures
-referred to the vertex and back of the head and neck by
the upper cervical roots
Headaches that accompany disease of ligaments,muscles, and
apophysial joints in the upper part of the cervical spine
- are referred to the occiput and nape of the neck on the
same side and sometimes to the temple and forehead.
- These headaches have been reproduced by the injection of
hypertonic saline solution into the affected ligaments, muscles,
and facet joints. Such pains are especially frequent in late life
because of the prevalence of degenerative changes in the
cervical spine and tend also to occur after whiplash injuries or
other forms of sudden flexion, extension, or torsion of the head
on the neck.
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The headache of meningeal irritation (infection or hemorrhage) HEADACHE SYNDROME
- is acute in onset, usually severe, generalized, deepseated,
constant, and associated with stiffness of the neck,particularly PRIMARY
on forward bending. - Without significant neurological pathology
- It has been ascribed toincreased intracranial pressure; - Headache itself is a disease
indeed, the withdrawal of - Treat the headache
- CSF may afford some relief. SECONDARY
- dilatation and inflammation of meningeal vessels and the - Intracranial pathology
chemical irritation of pain receptors in the large vessels and - Headache is only a symptom of an underlying disease
meninges by endogenous chemical agents, particularly - Treat the underlying disease
serotonin and plasma kinins, are probably more important
factors in the production of pain and spasm of the neck DIAGNOSIS
extensors. - Accurate history and neuro exam
- Example: haemorrhage or infection - Further investigation is determined by presence of Red Flag
sign.
Lumbar puncture (LP) or spontaneous low CSF pressure
headache DESCRIPTION
- is characterized by a steady occipitonuchal and frontal pain - Quality
coming on within a few minutes after arising from a recumbent - Intensity of pain
position and is relieved within a minute or two by lying down. - Location and radiation
- Its cause is a persistent leakage of CSF into the lumbar - Mode of onset, variation of pain, time and duration
tissues through the needle track or a tear of the meninges that - Relationship of headache to certain biologic events and
may be spontaneous or induced by spinal trauma. also to certain precipitating or aggravating or relieving factor.
- Usually this type of headache is increased by compression Acute onset – red flag sign
of the jugular veins but is unaffected by digital obliteration of the Warning signs
carotid artery. - Presence of systemic symptoms
- It is likely that, in the upright position, a low intraspinal and - Presence of secondary factors
negative intracranial pressure permits caudal displacement of - Presence of neuro signs and symptoms
the brain, with traction on dural attachments and dural sinuses. - Sudden onset
- Older age of onset
Headaches that are aggravated by lying down or lying on one - Increase frequency and severity compare to prior
side headache
- occur with acute and chronic subdural hematoma and with
some brain tumors, particularly those in the posterior fossa. PRIMARY HEADACHE
- The headache of subdural hematoma, when itoccurs, is dull - Most common type
and unilateral, perceived over most of the affected side of - Have no organic cause
the head. - Usually recurrent
- The global and nuchal headaches of idiopathic intracranial - Normal neuro exam
hypertension (pseudotumorcerebri) are also generally worse - Key to correct diagnosis is history
in the supine position. - Migraine, tension, cluster, and other primary headache
- In all these states of raised intracranial pressure, headaches
are typically worse in the early morning hours after a long
period of recumbency.

Exertional headaches
- are usually benign but they are sometimes related to
pheochromocytoma, arteriovenous malformation, or other
intracranial lesions, in addition to the aforementioned
subarachnoid hemorrhage from ruptured aneurysm.
- The same applies to headaches induced by stooping, most
of which are benign or, at worst, are accounted for by sinus
infection but there are exceptions and subdural hematoma is
a known cause.

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 INCREASED INTRACRANIAL PRESSURE
Increased ICP
- Increase in the pressure within the intracranial cavity
- One of its consequences is brain herniation
- ICP increases because the skull is fixed. Even in the
presence of a enlarging brain tumor the skull will never
expand resulting to an increase in the pressure in the
cranium.
Intracranial Compartments
- Composed of:
o Brain Tissue
 Approximately 87%, of which 77% is
water
o CSF
 Approximately 9%
o Blood Vessels
 Approximately 4%
o Meninges
 occupy a negligible volume
Note: Brain tissue, CSF, and the blood vessels are the three most
important components. Adding more to this composition will lead to
increased ICP because there will be no more space to accommodate
it. There are still some spaces provided by the sulci which contain
some fluid (water) that can be displaced somewhat. This is the
reason why there is an initial phase where it can adjust but will
eventually lose this adjustment capability if the patient does not
recover.
Monroe Kellie Doctrine
- States that the sum of the intracranial volumes of blood,
brain and CSF is constant at all times
- The skull is considered as an enclosed and inelastic
container
- Therefore, an increase in the volume of any one of these
three components must be at the expense of the other two
- Intracranial blood (especially in the venous compartment)
and CSF are the two components whose volume can adapt
most easily to accommodate an increase in the volume
intracranial contents
o Displacement of the CSF from the cranial cavity
into the spinal canal
o Reduction of intracranial blood volume contained
in the veins and dural sinuses
- As the brain, blood or CSF volumes continue to increase,
the accommodative mechanisms starts to fail and ICP
rises exponentially (intracranial compliance)
- Once these compensatory mechanisms are exhausted,
further increase in volume result in large rises in ICP
Note: If the brain needs to expand because of a tumor, the two other
compartments should be sacrificed (less blood and CSF) to
accommodate it. The brain parenchyma cannot adjust, only the CSF
and blood can adjust. In order to adjust either the blood or the CSF,
there should be an increase in the drainage (Ex: Give a diuretic to
decrease the CSF).
Volume Pressure Relationship
Note: In the first 1 and 2 units of volume (ml), it can still adapt or
adjust. There is an increase in volume but there is no increase in
intracranial pressure (mmHg). Once the adaptive mechanism has
been exhausted, there is a stiff rise in the intracranial pressure and
volume. This is where herniation occurs. This is why herniation does
not happen after a week or two, herniation suddenly happens
because it relies on ICP. In cases of herniation, patient dies in a
matter of hours, at most a day or two if without intervention.
Intracranial Pressure
- Pressure Component
o Cerebral Perfusion Pressure (CPP)
o Mean Arterial Pressure (MAP)
o Intracranial Pressre (ICP)
- Intracranial pressure is computed using this formula
CPP = MAP-ICP
Note:
- MAP is computed using this equation:
MAP = [(2 x diastolic) + systolic] / 3
- ICP is computed using an ICP monitor
- CPP
o If there is an increased ICP, the BP of the patient
is increased to maintain cerebral perfusion.
Case: There is a patient with sudden massive infarct with shifting of
the midline structure (massive edema, massive stroke) with a BP of
180/100. Lowering it down will have consequences such as a
decrease in the cerebral perfusion pressure so there is a need to
analyze the situation. Maybe, the increase in ICP is secondary to the
autoregulatory mechanism of the brain to maintain the cerebral
perfusion that is why you don’t even need to lessen the blood
pressure. What you need to lessen is the ICP then the BP goes down
as well to maintain the CPP. There are also instances that a patient
comes to you with headache which disappears after two days but the
BP keeps on going up. Beta blockers or Calcium channel blockers
are given but are not effective because the patient has a bleed or an
intracranial hemorrhage (ex: in the temporal area = asymptomatic
with forgetfullness). It actually is a compensatory mechanism of the
brain.
Note: Keeping the MAP too low compromises the CPP. What you
should do is to lower the ICP and the MAP which will subsequently
lower down to maintain CPP. Analyze first before aggressively
lowering down the BP of a patient because it might just be a
compensatory mechanism.
Cerebral Perfusion Pressure
7|JKCP V illar am a
 Additional Notes:
I. Localized pathology that deform the adjacent brain tissue
- Cerebral or extra cerebral mass such as brain tumor
- Massive infarction with edema
- Extensive traumatic contusion
- Parenchymal, subdural, or extradural hematoma
- Abscess

II. Generalized brain swelling

- Ischemic-anoxic states
- Acute hepatic failure
- Hypertensive encephalopathy
- Hypercarbia

Note: There is always an autoregulatory mechanism. MAP is usually III. Increase in Venous Pressure
up to 130. If it exceeds 150, there will be no more MAP so there will - Cerebral venous sinus thrombosis
be no more autoregulatory mechanism. It is already destructive to the - Heart Failure
brain. It is important to maintain MAP up to 130. - Depressed fractures overlying major venous sinuses

Causes of Increased ICP IV. Idiopathic

1) Localized pathology that deform the adjacent brain tissue - Benign Intracranial Hypertension
a. Stroke
b. Tumor V. Obstruction to airflow and absorption of CSF
c. Abscess
d. Mass lesion / localized mass VI. Expansion of CSF Volume
e. Focal swelling – swelling causing localized - Meningitis
pathology - Subarachnoid Hemorrhage
2) Generalized brain swelling
3) Increase in venous pressure VII. Increase in CSF production
a. Venous sinus thrombosis - Choroid plexus tumor
 If there is blockage in the venous
sinuses, there will be an increase in Flow of CSF
pressure. There is a generalized
increase ICP, it is not focal because
there is a decrease in CSF resorption.
A decrease in CSF resorption will result
to increase in CSF fluid hence
increased ICP.
4) Idiopathic
5) Obstruction to the flow and absorption of CSF
6) Expansion of CSF volume
7) Increase in CSF production

Note: A localized swelling is more fearsome than a generalized

swelling because a localized swelling causes herniation. In
generalized swelling the pressure is usually equal so there will be no
herniation from the right to the left or vice versa. All herniations
usually occur in between. Herniation only occurs when there is a
higher pressure on one side and a lower pressure on the other side
so the net effect is that it will go to the side with the lower pressure.
But there is a possibility that in generalized swelling, it may herniate
into the foramen magnum.

8|JKCP V illar am a
 7o’clock, arrived at ER – 12mn, papilledema is negative because you
will never see a papilledema in that short period of time. Papilledema
occurs several days to weeks after. If a patient has papilledema, you
can say that the lesion has been there for quite some time. It may be
a mass lesion that bled suddenly that is why there is sudden altered
sensorium but the pressure was there even before. This is why
fundoscopy is of big help because you can diagnose.

Pressure Headache
- Often exacerbated by any factors that further increase ICP
such as coughing, sneezing, recumbency or exertion
- Tends to be worse in the morning attributed to a rise in ICP
during the night as a consequence of recumbency , a rise
in PCO2 during sleep caused by respiratory depression ,
and probably a decrease in CSF absorption

Papilledema
- A reliable sign of raised ICP but can require several days of
or raised pressure to develop
- Due to pressure differential applied to the optic nerve by
the increase in ICP

Herniation syndromes
- The cranial vault is divided into compartments by the dural
reflections of the falx cerebri and tentrorium cerebri
- Raised ICP frequently results in pressure gradient
between compartments (separated by dural reflections)
and a shift of brain structures
- Many of the clinical counterparts of raised ICP are the
consequence of such shifts rather than the absolute level
of ICP
- Herniation syndromes:
 Subfalcine Herniation
 Uncal Herniation
 Central Transtentorial Herniation
 Tonsillar Herniation
Clinical Manifestations of increased ICP  Upward Brainstem Herniation
1. Headache
2. Nausea and vomiting Note: The brain is divided into falx (into dural reflections). The dural
3. Altered Sensorium reflection forms falx (falx cerebri, tentorium cerebeli). When there is
4. Ocular palsy herniation, the brain parenchyma that should be in one side
5. Papilledema (enclosed by the dural reflection) now goes to the other side. This is
o Seen during fundoscopy what you call herniation. Example: With falx in the middle, if the
o The earliest sign of increased ICP is loss of right side of the frontal lobe goes to the right side = herniation.
venous pulsation.
o Papilledema is a marker of a subacute to chronic Subfalcine Herniation (rare; not fatal)
increase in ICP. - Occurs when an expanding lesion presses the cerebral
6. Cushing’s triad hemisphere medially against the falx
a. Hypertension - The cingulated gyrus and the pericallosal and
b. Bradycardia callosomarginal arteries are compressed against the falx
c. Irregular respiration and may be displaced under it
- Believed to be a precursor of other types of herniation.
Note: The ocular palsy noticed in patients with increased ICP is - Symptoms are not well-defined but compression of
lateral rectus palsy. Lateral rectus palsy, which is abducens nerve parafalcine cortex may lead to contralateral leg weakness.
palsy, is a non localizing sign. It is a sign that there is increased ICP It leads to contralateral leg weakness because in
but it is never a sign of focal neurologic problem in the pons. There is homunculus, the medial side is the lower extremities.
inward squinting in lateral rectus palsy (medially located).

Case: Patient with sudden altered sensorium with bilateral lateral

rectus paralysis. Check for the presence of papilledema. Dictus –

9|JKCP V illar am a
Note: What is involved in subfalcine herniation is “under the falx”.
Falx divides that frontal and parietal (fronto-parietal) so what usually
herniates is the one medially located which is near the falx. This is
the cingulate gyrus (for memory) which may herniated to the other
side. Patients with subfalcine herniation are usually asymptomatic
and are rarely fatal. But there is a pending herniation that may occur
either a tonsillar or uncal herniation.
Uncal Herniation
- Occurs when an expanding mass lesion usually located
laterally in one cerebral hemisphere forces the medial edge
of the temporal lobe to herniated medially and downward
over the free tentorial edge into the tentorial notch
- The key sign associated with uncal herniation is an
ipsilateral fixed and dilated pupil
o The earliest and most subtle sign
o due to compression of the dorsal surface of the
oculomotor nerve
o Not all patients with dilated pupils have increased
ICP especially if there is no loss of
consciousness. It may be a localized pathology
or aneurysm that is impinging the 3rd nerve.
- Second key feature is impaired level of consciousness
o may be due to distortion of the ascending arousal
systems
- Therefore a patient with a unilateral fixed and dilated pupil
and normal level of consciousness, the examiner must look
for another cause of pupillodilation
Note: What herniates in uncal herniation is the uncus of the
temporal lobe. Manifestations include ipsilateral pupillary
dilatation iand contralateral hemiparesis. There is ipsilateral
pupillary dilatation because of 3rd nerve compression which functions
for pupillary constriction. Impingement of 3rd nerve leads to
constriction. 3rd nerve is located in the midbrain near the uncus. The
temporal lobe is supratentorial (above tentorium cerebella) and the
midbrain has tentorial notch. It herniates from supratentorial down to
the infratentorial via the tentorial notch (which is the cerebral
peduncle where midbrain goes out; provides connection between
supra and infratentorial). Inverted pajama or inverted shorts
appearance. Uncus herniates downwards. Midbrain contains nuclei
of CN III and CN IV.
3rd nerve functions:
o Extraoccular muscles
o Pupillary constriction
o Levator palpebra (So check for presence of
ptosis)
Papillary constriction is the only one affected. The nerve is arranged
in such a way that the outermost is the pupillary constriction and the
innermost is the extraocular muscles. If the problem started inwards
going outwards then the first manifestation is CN palsy with normal
pupils. If the problem is outside impinging on the nerve, the first
manifestation is pupillary constriction. This is the reason why it is
the pupillary constriction that is first affected but will eventually
involve all 3rd nerve functions (EOM) if it is severely impinged.
Case: Presence of anisocoria – 3rd sign that there is herniation in the
patient. With this finding, management will be to lower the ICP. If no
management is done in the next few hours, the patient will die.
Pupillary constriction is an important parameter for checking
herniation problems.
Why is there ipsilateral pupillary dilatation and contralateral upper
and lower extremities weakness?
- This is because of the corticospinal tract decussating in the
medulla. The problem is in the midbrain and it has not
decussated yet so the problem will be ipsilateral pupillary
dilatation and contralateral upper and lower extremities
weakness.
What if there is herniation and the weakness is on the same side of
the pupillary dilatation?
- This is called Kernohan’s notch or Kernohan’s
phenomenon
Note: The most important parameter when you localize the
herniation side is not the weakness but the dilated pupil. The problem
is always on the same side of the dilated pupil.
Hemiparesis
- Due to compression of cerebral peduncle by the uncus
- Contralateral ( if the advancing uncus impinges upon the
adjacent cerebral peduncle)
- Ipsilateral (if the uncus pushes the midbrain so that the
opposite cerebral peduncle is compressed against the
incisural edge---Kernohan’s notch)
- Hence, the side of the paresis is not helpful in localizing the
lesion , but the side of the enlarged pupil accurately
identifies the side of the herniation over 90% of the time
Note: Inverted shorts appearance; compression of midbrain.
10 | J K C P V i l l a r a m a
Central Transtentorial Herniation
- Due to pressure from an expanding mass lesion on the
diencephalon
- The earliest and most subtle signs of impending central
herniation tend to begin with compression of the
diencephalon
- The first evidence of beginning impairment of the
diencephalon is usually a change in alertness and behavior
o difficulty to concentrate and unable to order
details of recent events
- As the compression of the diencephalon progresses, the
patient lapses into torpid drowsiness, and finally stupor and
coma
- The clinical importance, therefore, of the diencephalic
stage of central herniation, is that it warns of potentially
reversible lesion that is about to encroach on the brainstem
and create irreversible damage
- The patient suddenly stops breathing and blood pressure
rapidly increases as the vascular reflex pathways in the
lower brainstem attempt to perfuse the lower medulla
against the intense local pressure
Note: Usually with altered sensorium
Tonsillar Herniation
- Occurs in cases in which the pressure gradient across the
foramen magnum impacts the cerebellar tonsils against the
foramen magnum, closing off the 4th ventricular outflow
compressing the medulla
- Patient stops breathing
Note: The problem is in the tonsils which is located in the
cerebellum. It will herniate downwards to the foramen magnum. The
patient will go into respiratory arrest because of the compression of
the medulla. If you have tonsillar herniation, it will never cause
pupillary anisocoria. It will always have normal size pupils but there
are problem with sensorium and respiratory arrest.
Upward Brainstem Herniation
- Occur through the tentorial notch in the presence of a
rapidly expanding posterior fossa lesion
- The superior surface of the cerebellar vermis and the
midbrain are pushed upward, compressing the dorsal
mesencephalon
Treatment for increased ICP
- Head elevation
o elevation of the head of the bed to 30◦ improves
jugular venous outflow and lowers ICP
Note: Head elevation might help because it will allow drainage of the
CSF and lowers ICP.
- CSF Drainage
o when an intraventricular catheter is used to
monitor ICP, CSF drainage is an effective
method for lowering ICP
o this can be accomplished by intermittent
drainage for short periods in response to
elevations in ICP
o the principal risks of ventriculostomy are infection
and haemorrhage
Note: CSF drainage is surgical.
- Osmotic agents and loop diuretics
o Mannitol: establishes an osmotic gradient
between the brain and the intravascular
compartment
o Furosemide: Inhibit sodium and chloride
reabsorption in the loop of Henle, resulting in
contraction of the blood volume which may
mobilize cerebral edema
Note: Osmotic diuretic agents: Mannitol is sugar and if ti runs
through the blood vessels the water will be absorbed from the
extracellular going to the intravascular space leading to a decrease in
ICP. The downside is that eventually the blood vessels will be
saturated (equal between intra and extra). It is only effective during
acute stages.
- Hyperventilation
o Lowers ICP by inducing hypocapnoiec
vasoconstriction mediated through metabolic
autoregulation
Note: Hyperventilation works because it is one of the fastest ways to
lower down ICP. The blood vessels will constrict in hyperventilation.
Remember, intracranial components involve blood, CSF, and brain.
Reducing the blood flow will lead to”more space”  less ICP. The
problem with hyperventilation is that it cannot be done for a long
period of time because it may induce alkalosis leading to
complications. Prolonging the vasoconstriction will lead to ischemia
which may lead to stroke.
11 | J K C P V i l l a r a m a
 BRAIN TUMORS  Pilocytic astrocytoma which usually
Outline: involves the cerebellum is common in
1. Gliomas children and rare in adults
2. Meningiomas o Supratentorial
 40%
Brain Tumors
- Primary Brain tumor Clinical Presentation
o Causes an increase in ICP  Depends on location of the tumor and rate of growth of
o Examples: tumor
 Primary Glioma  Insidious onset
 Meningioma  Slowly progressive course
- Secondary Brain tumor (Metastatic) o slow growing tumors usually present with:
o Involves the following:  Headache
 Brain parenchyma  Seizure
 Leptomeninges  Mental, behavioral and personality changes
 Dural space  Lateralizing or focal neurologic deficit
 Increased intracranial pressure
Note: The most common brain tumor is a secondary type of tumor  Due to adaptation of the tumor
which is metastasis. A lot of patients will be secondary to metastatic
brain tumor. Primary brain tumors are not common. Note: Seizures are common in slow growing tumors. This is why
metastasis cases do not usually present with seizures. Example:
- Benign Lung cancer with brain mets do not present with seizures but shows
- Malignant focal neurologic deficit. In cases of meningioma which is insidious,
- Location of brain tumor: the first reason of patients for coming to the clinic will be seizures.
o Extramedullary (Extraaxial)
o Intramedullary (Intraaxial) Cerebral Dysfunction
o Intraventricular - Seizure
- Language Disorder – Aphasia
Intraaxial (Intramedullary) - Organic mental, behavioral & personality changes
- Located within the brain parenchyma - Contralateral
- Examples: o Hemiparesis with Babinski and cranial nerve
o Glioma deficits
 Arises from the white matter of the o Hemisensory deficits
brain; astrocytes o Homonymous hemianopsia/ quadrantanopsia
o Primary CNS Lymphoma
o Metastatic I. GLIOMAS (Intramedullary)
- Most common primary brain tumor
Extraaxial (Extramedullary) - 50% of all symptomatic brain tumors
- Located outside the brain parenchyma - Incidence increases with advancing age
- Examples: - Originates from glial cells (white matter of the brain) or
o Meningioma their precursor
 Arises from the meninges o Glial cells is where the astrocytes,
o Pituitary Adenoma oligodendrocytes, and ependymas come from
o Vestibular Schwannoma - Includes
 Arises from the 8th nerve o Astrocytoma
o Oligodendroglioma
Age Incidence o Ependymoma
 Adults
o Supratentorial 1. Astrocytoma
 80-85% - Most common glioma
 most common in adults - May be benign or malignant
o Infratentorial o Most malignant – GBM (Glioblastoma multiforme)
 15-20% - Maybe found in any age group
 Children - May affect any part of the brain
o Infratentorial o Cerebrum in adults
 60% o Cerebellum and brainstem in children
 most common in pediatric cases - 25-30% of cerebral gliomas are low grade
 Involves the midbrain, cerebellum (occurs mainly in 3rd and 4th decades)
 Examples: o High grade cerebral gliomas are the most common
 Medulloblastoma which is common in - Infiltrative (complete resection is difficult)
children and rare in adults - Latent potential for malignant transformation
12 | J K C P V i l l a r a m a

Note: Astrocytoma has grade 1 to grade 4
Grade 1 is the pilocytic astrocytoma (benign tumors)
Grade 2 is the diffuse astrocytoma
Grade 3 is the anaplastic astrocytoma
Grade 4 is the glioblastoma multiforme
Management depends on the grade of the tumor
Grade 1 – surgical removal
Grade 4 – Gold standard for GBM: surgical removal, concomitant
chemotherapy and radiotherapy, and adjuvant chemotherapy
Before, GBM is just treated with radiotherapy and surgery
2. Glioblastoma Multiforme
- Malignant astrocytoma
- 20% of all intracranial tumors
- 80% of cerebral gliomas in adults
o Most are high grade/malignant rather than low
grade
- Predominantly cerebral
- Peak incidence in middle adult life
o Mean age of 56-60years
- Males > Females (1.6:1)
o Also, meningiomas are most commonly benign
when it occurs in females.
o Malignancy common in males
o Germinomas, GBM, etc common in males
- Occurs sporadically without familial predilection
- Infiltrative, rapidly progressive
- Commonly solitary but may be multiple in 3-6%
(simulating metastatic cancer)
- May cross the midline
o BUTTERFLY PATTERN
o Since it is infiltrative, it crosses the midline
o When you do an imaging study and it shows
crossing of the midline, it is possible that it is a
high grade glioma.
- CSF seeding
Note: There is no treatment for grade 4 astrocytoma. Surgery is
possible if you can remove everything which rarely happens. Total
resection is not possible because it is an infiltrative tumor. If resection
is possible, radiotherapy must be given after at least 2cm from point
of resection.
- Diagnosis
o Stereotactic biopsy
o Craniotomy – for diagnosis and debulking
- Treatment (Palliative)
o Radiotherapy
o Chemotherapy – oral TEMOZOLOMIDE
o Corticosteroid
 Given to decrease the pressure
 Steroids are best given in cases of brain
tumors because brain tumors have
vasogenic edema
 Effect of steroids is only temporary so
there is a need to address the tumor
 Best steroid for vasogenic edema:
 Dexamethasone - because it has low
mineralocorticoid activity
o Anticonvulsants – if with seizures
Note: If there is a tumor, you expect an increase in ICP. Steroid
therapy is also applicable for cases of increase in ICP. Mannitol
should not be given because edema in brain tumor is called
vasogenic edema (Edema in stroke is called as cytotoxic edema). It
depends on the type of edema. If there is vasogenic edema, it will
work best with steroids. But if it is a cytotoxic edema, it works best if
you give mannitol (osmotic diuretic). But, mannitol can still be given
as back-up to steroids. Example: A very large tumor with increased
ICP  there is a need to lower it down by which way possible.
- Prognosis
o Without treatment: 7-9 months
o With aggressive surgical removal and
radiotherapy
 Mean survival of 12 months
o With surgery, radiotherapy and chemotherapy
 Mean survival of 14.6 months
o Almost all glioblastomas recur within 2cm of
their original site
o Cerebral edema and increased ICP
 Causes death
3. Oligodendroglioma
- Derived from oligodenrocytes or their precursor
cells
- 5-7% of all intracranial gliomas
- Most often in 3rd and 4th decades
- Male > Females (2:1)
- Found primarily in cerebral hemispheres
(frontal and temporal lobes)
- Calcification common
- CSF Seeding
- Radiosensitive
- Somatic mutations within the tumor:
o Loss of certain alleles on
 Chromosome 1p
 Chromosome 19q
- Conventional treatment
o Surgical excision followed by radiation therapy
Note: Oligodendroglioma also has anaplastic type. It will depend on
what type. Prognostic markers:
Chromosomal mapping is now available:
- Oligodendroglioma
o Chr. 1p and Chr. 19q
o These two chromosomes are important because if
these are positive they are more likely to be
radiosensitive. These tumors are responsive to
radiotherapy.
- GBM
o IDH – presence of this signifies a good prognosis
o MGMP – hypermethylation of MGMP signifies a
good prognosis
II. MENINGIOMA (Extramedullary)
13 | J K C P V i l l a r a m a
  2nd most common primary brain tumor in adult
 Originate from arachnoid cells
(meningoepithelial cap cells normally seen in arachnoid villi)
 20% of all intracranial tumors (with asymptomatic cases –
40% or more)
 7% of all posterior fossa tumors
 3 – 12% of cerebellopontine angle tumors
 Most diagnosed in 6th and 7th decades
 Female > Male (3:2 to 2:1)
o If it occurs in females it is usually benign
o If it occurs in males it is usually malignant
 Multiple in 5 – 15% (NF – 2)
 90% Intracranial
10% Intraspinal
Spinal Meningioma – 10x in women

Note: All familial meningiomas occurs with NF2

 Etiology
o Radiotherapy – only established risk factor
 Radiation-induced tumors tend to occur
over convexities
 Multiple
 Histologically Malignant
 More likely to recur
o Head trauma
 Not confirmed risk factor
o Molecular Genetic Studies of men with
meningiomas
 Loss of 22q in 80% of sporadic
meningiomas
(deletion of NF – 2 tumor suppresor gene at
22q11 and lack of protein product Merlin)
 All familial meningiomas occur with NF
–2
 NF – 2 patients at increased risk of
meningiomas, vestibular schwannomas,
both frequently multiple

 Clinical Manifestations
o Asymptomatic - found incidentally by MRI
o Symptoms
 Tumor location
 By compression of underlying neural
structures
o Sites of Predilection
 Cerebral convexity
 Falx Cerebri
 Skull base

 Treatment for Meningiomas

o Since it is extracranial, the best treatment for
meningiomas is surgery
o After surgical removal, do a biopsy to determine
if it is positive for estrogen and progesterone or
not and then treat accordingly.

14 | J K C P V i l l a r a m a
 CNS INFECTION
Lumbar puncture
- LP is done to get a sample of the CSF for analysis
- It has a lot of uses. It is not just diagnostic, it is also
therapeutic.
o Example: Chemotherapy can be given intrathecal
via LP (Intrathecal chemotherapy)
- LP is done usually in patients with slight edema in the
brain. Patients are usually groggy, drowsy, and with signs
of increased ICP.
Position
- The patient is in fetal position.
- The needle is inserted where the spinal cord ends
o Adults = spinal cord ends at the lower border of
L1 and upper border of L2 vertebrae
o Children = spinal cord ends at the lower border of
L2 and upper border of L3
- The guide for LP is the ASIS (Anterior Superior Iliac Spine)
Indications for LP
- Administration of anesthetics, antibiotics, or chemotherapy
treatment
- Examination of the CSF is the single most important
diagnostic test in patients with suspected CNS infection
Contraindications to LP:
Absolute Relative
Skin infection over site Increased ICP with or without
papilledema
Focal neurologic deficit
Suspicion of mass lesion
Spinal cord tumor
Spinal epidural abscess at site
Bleeding diathesis
Note: Increased ICP is NOT an absolute contraindication to LP
because nothing will herniate in cases of generalized edema where
the pressure in equal in the entire brain. The development of
herniation is considered as a risk in LP which may cause death of
the patient. Focal ICP is a contraindication to LP. If it is a purely
increased ICP and there is no focal increase in ICP, there is no risk
for herniation therefore LP can be done. Infection over the site is a
contraindication for LP because of possible dissemination of the
infection (example: bed sore). If there is a mass lesion, do not
perform a LP especially if the mass lesion is causing the increased
ICP. Patient with increased ICP secondary to a focal mass lesion
and there is already a sign of herniation. DO NOT PERFORM LP ON
THE PATIENT.
- Once you insert the needle, get the opening pressure. It is
not just getting a sample of the CSF but also getting the
opening pressure.
- After getting the opening pressure, also note for the color
and the characteristic of the CSF.
- Get samples for work-up
Case: Patient had sudden onset of severe headache for 3-4 days +
sleepiness. Upon neurologic examination there is no focal neurologic
deficit, there is no prerequisite in doing LP. But it is advisable to do a
CT scan for confirmation.
Prerequisite before doing LP
- CT scan – it is always good to have back-up evidence that
there is no focal mass that might cause herniation upon
doing LP.
o Signs of increased ICP:
 Altered sensorium
 Lateral rectus palsy
 Focal neurologic deficit
- PT, PTT, INR – Make sure that there are no bleeding
problems. Not routinely requested unless there is an
indication.
- Neurologic examination – if the procedures above are not
available, this simple examination could be done to
confirm for focal neurologic deficit.
15 | J K C P V i l l a r a m a

Note:
- CNS infections:
o Viral
o Bacterial
o Fungal
o Tuberculosis
o Parasite (US only, not common in the Philippines)
- From CSF analysis alone, you may have an idea what the
problem and etiology of the infection is. This is very
important because you cannot diagnose a disease by
neuroimaging alone. Most of these have normal CT scan
findings except for Leptomeningeal enhancement. You
can only find out what caused the disease by doing an
LP. Therefore, LP, unless contraindicated, should be
done in all patients suspected of CNS infection.
- LP gives an idea what the pathogen is so you can treat the
patient accordingly. Treatment is available for all types of
CNS infections except for viral.
Opening pressure
- Normal is up to 180 (some is up to 200). Above 180 means
that there is an increase in ICP. LP may help in
decreasing the pressure  less headache.
Characteristic color
- Normal CSF – clear, transparent, colorless CSF
- Infected CSF, Hemorrhage (subarachnoid) – xanthocromic
CSF
o When blood mixes with the CSF it becomes
yellowish
Protein
- Bacterial – increased
- Tuberculosis – increased
- Fungal – increased
- Viral – usually normal or somehow increased
Glucose
- Bacterial – decreased
- Tuberculosis – decreases
- Fungal – decreased
- Viral – normal
Note: Always compare CSF glucose finding with serum glucose. It
doesn’t always mean that if there is a decrease in the glucose in the
CSF, there is already hypoglycorrhachia because it is possible that
the patient is already hypoglycemic. Definitely, CSF and serum
sugars are correlated with each other. RBS should always be done
along with LP and then look at the ratio.
Case: 25 y/o male with questionable sexual activity comes in the
hospital with a 3-week history of pain that is frontal, constricting,
bilateral, occurring throughout the day not accompanied by fever but
claim that sometimes there is blurring of vision. There is no vomiting,
focal neurological deficit.
What else would you like to do to rule out a CNS infection?
- Initial neurologic exam: Meningeal signs  no nuchal
rigidity
- Repeated meningeal sign exam  unequivocal because
there is resistance in passive neck flexion, extension, and
left and right lateral rotation

Four very important tests to do: Is this a sign of infection?

- Cell count
- Differential count - Nuchal rigidity is positive only if there is neck flexion. It is
- Protein never extension and lateral rotation.
- Sugar/Glucose - If it involves extension, flexion, and lateral rotation it is
usually a musculoskeletal problem.

Cell count Unfortunately, an LP was done

- Bacterial – increased (highest)
- Viral – increased (lowest) - LP result: 175 (normal)
- Tuberculosis - increased - WBC count of 5 with 25% lymphocytes
- Normal protein
Note: The cell count MAY not increase if there is only one infection - Normal sugar
 aseptic meningitis. It is usually secondary to a viral pathology.
But, it usually increases even slightly around +10 from normal. There Interpretation: NORMAL
is also no increase in cell count in cases of patients who are
immunocompromised with very low CD4 count. It is still considered What if the WBC count is 5 with 25% neutrophils?
as a CNS infection even if there is only +10 increase in cell count
plus a yellowish CSF. - A WBC count of 5 and a 25% lymphocyte are still normal
but never normal if there are neutrophils present.
Differential count (neutrophils versus lymphocytes) - Check if the patient is immunocompromised which is why
- Bacterial – Neutrophils the WBC count is non-responsive with 25% neutrophils.
- Viral – lymphocytes
- Tuberculosis - lymphocytes Pateint is with normal LP findings, what is the diagnosis?
- Fungal – lymphocytes
- Partially treated bacterial meningitis – lymphocytic - Tension headache
predominance o Common in a 25 y/o individual

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Note: It is very important to look at the patient’s history. The patient
has no fever and there is no prominent nuchal rigidity. Common
presentation of patients with CNS infections: fever + nuchal rigidity.
Case: Patient without fever but with sudden or acute onset of
headache + nuchal rigidity
- Treatment of S.aureus is different from the treatment of
other bacterial meningitis
- Most commonly, the Strep and gram negative bacilli will
respond to ceftriaxone which does not work for S.aureus
- Vancomycin is used for S.aureus (methicillin resistant) or
oxacillin if not resistant

Diagnosis: Subarachnoid hemorrhage Group B Streptococcus

Case: Patient with fever + nuchal rigidity + acute to subacute onset Listeria monocytogenes
of headache
H. influenza
Diagnosis: CNS infection
What is causing the symptoms in a patient with CNS infection?
- The inflammatory cytokines are the cause of the symptoms
and not the bacteria itself. The bacteria start the cascade.
- Production of inflammatory cytokines will alter the BBB that
will lead to presence of vasogenic edema (cerebral
ischemia, obstructive hydrocephalus)
INFECTION OF THE NERVOUS SYSTEM Determination of Pathogen
(READ HARRISONS) - Gram stain
- Culture and sensitivity – 3-7 days release
Difference between Meningitis, Encephalitis, and - PCR – expensive; not routinely requested
Meningoencephalitis - Latex agglutination test (PHADEBACT) – usually
- Meningitis – involves the meninges requested; cheaper than PCR, released in 1 day
- Encephalitis – involves the brain parenchyma o Five common organisms:
- Meningoencephalitis – involves both the meniges and  S.pneumoniae
brain parenchyma  Neisseria
 Haemophilus
Symptoms:  E.coli
- Meningitis:  S.agalactiae
o Altered sensorium
- Encephalitis Treatment
o Loss of consciousness, seizures, increased ICP, - The best empiric therapy is 3rd generation cephalosporin
and stroke given as double dose to be able to penetrate the BBB (2g
- Meningoencephalitis 2x/day)
o The meninges and the subarachnoid are involved - If positive for TB, add anti-Kochs medication
in the inflammatory reaction
Note: Memorize CSF findings, treatment, and presentation (bacterial
ETIOLOGIC AGENTS and viral are usually acute while the TB and fungal are usually
subacute to chronic)
Step.pneumoniae
- Most common Case: Patient comes to you with 3 day history of high grade fever,
nuchal rigidity  bacterial and start with antibacterial regimen. If
Neisseria meningitides viral, it usually does not present with high grade fever. There is no
- is life-threatening and is highly infectious. specific medication for viral except if it is Herpes (acyclovir)
- Its colonization is nasopharyngeal.
- The typical symptoms of patients with meningococcemia: Case: 2-3 week history of headache, progressive in nature, with on
typical skin lesions (violaceous skin lesions). and off fever, altered sensorium  subacute to chronic type of
- The presence of petechial or purpuric lesions can provide meningitis  TB and fungal
an important clue to this diagnosis.
- The prophylactic medicine for meningococcemia are
ripamficin and and ciprofloxacin.

Enteric Gram negative bacilli

- Usually present in chronic UTI, complications of urosurgical
procedures, etc

Staph. aureus
- Common in patients who have catheter post-surgical

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 VIRAL MENINGITIS
(Hand-out)

VIRAL ENCEPHALITIS

- Commonly presents with altered sensorium and seizures.

- If you suspect encephalitis which is viral in origin, MRI
should be done because in MRI, approximately 80% of
patients with proven HSV encephalitis have MRI
abnormalities involving the temporal lobes
- This percentage likely increase to 90% when FLAIR and
DWI sequences are also utilized.
o MRI has a lot of sequences: GRE, DWI, FLAIR,
ABC, etc
o DWI is the best imaging if you are thinking of
stroke
o DWI further enhance diagnostic acuity in HSV
(usually centered at the temporal lobe)
- In general, if you have a patient with meningitis MRI is
better.
Note: In Japanese encephalitis, it involves the basal ganglia thalamic
area. MRI with contrast really helps in viral encephalitis diagnosis.
SUBACUTE MENINGITIS
- Typically have an unrelenting headache, stiffness, low
grade fever, and lethargy for days to several weeks
before they present for evaluation
Note: Patients with TB or Fungal meningitis will only seek consult
after 1-2 weeks with alteration in sensorium, on and off fever, nuchal
rigidity, etc. The patients are usually in the end-stage of the disease
with focal deficits and are near death. The treatment should be fast
and aggressive. Do an LP at once.
Tuberculous meningitis
Bacterial seeding of the meninges and subpial region of the brain
Formation of tubercles
Note: This is a communicating type of hydrocephalus because
there is an enlarged lateral, 3rd ventricle, 4th ventricle, and lateral
horns of lateral ventricles. No part was spared. If it is a non-
communicating type, it is either the right lateral ventricle is enlarged
or the left lateral ventricle is enlarged.
- In TB, the infiltrates will go downwards in the basal area.
There are whitish materials seen with contrast
enhancement. It goes down to the basal area where the
midbrain and pons are so you will expect cranial nerve
deficits (common) – medial rectus palsy, anisocoria,
facial asymmetry.
- Usual presentation is diplopia. If you have a patient with
diplopia with only slight drowsiness, it is not usually
considered as an increase in ICP.
Clinical Features:
o Low grade fever
o Malaise
o Headache
o lethargy
o Cranial nerve deficits
o Nuchal rigidity

- Small discrete white tubercles are scattered over the base Staging:
of the cerebral hemisphere o Stage I
- Meningeal tubercles o Stage II
o Central zone of caseation surrounded by o Stage III
epitheloid cells and some giant cells, lymphocytes, - Depends on what the symptoms are
plasma cells, and connective tissue.
CSF Finding:
Note: It s actually the seeding of the bacteria and the rupture in the o Increased pressure
subarachnoid space that causes the symptoms. The type of o WBC: 50-500/cu mm
hydrocephalus in this patient with CNS infection is expected to be a  Predominance of lymphocytes
communicating which is the non-obstructive type. There are two o Elevated protein: 100-200 mg/dL
types of hydrocephalus: communicating and the non-communicating. o Low glucose: <40 mg/dL
If it is non-obstructing, the pathology is in the resorption from the o (+) AFB stain
pacchionian bodies to the venous sinuses. o Culture and sensitivity
o TB bactec

Note: The best tool is TB culture because eventhough AFB stain

gives fast results it is very low yield. The result of culture usually
comes out after 42 days.

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Treatment for TB meningitis: Anti-Kochs oral medication meningitis, the cell count, diff count, protein, and sugar tests cannot
be solely relied on because it cannot differentiate between TB and
Drugs Doses Adverse effects fungal causes of subacute meningitis. Neuroimaging like CT scan
Isoniazid Hepatic toxicity, peripheral can be requested because there is basal infiltrates in TB meningitis.
neuropathy (can be prevented with
pyridoxine), phenytoin toxicity Treatment
Ripamficin Hepatic toxicity, interstitial nephritis - Immunocompetent patients
Pyrazinamide Optic neuropathy o Induction course: 2 weeks
Ethambutol Hepatic toxicity, arthralgia with  Amphothericin B (0.5-1mg/kg/d)
hyperuricemia  Flucytosine (100mg/kg/d)
Streptomycin Vestibular toxicity o Consolidation therapy (8-10%)

Note: The difference of pulmonary TB from TB meningitis treatment Note: The treatment usually is fluconazole. It has a lot of side effects.
is the duration of treatment. The dosage is the same. The only drugs given for this case are Amphotericin B and
Pulmonary TB (6 months) Fluconazole.
o Intensive phase – 2 months
o Maintenance phase – 4 months Neurosyphilis
TB meningitis (1 year) - Can remain untreated  Tabetic neurosyphilis (incurable)
o Intensive phase – 2 months
o Maintenance phase – 10 months Note: This can remain untreated for several years until the patient
acquires the Stage III type of syphilis or Tabetic neurosyphilis which
Corticosteroid is incurable. It is very important to detect the asymptomatic
- Dexamethasone 0.4mg/kg for a week and then taper in meningitis and meningovascular neurosyphilis. Meningovascular
doses for 3 weeks (0.40.30.20.1 tapered every neurosyphilis are patients who had stroke at a very young age.
week) They usually present with stroke-like manifestations. It is treated with
syphilis medications.
Note: If there is already a focal deficit and you cannot risk waiting for
the drugs to take effect you can give steroids. Chronic Encephalitis (READ)
- PML
Prognosis - SSPE (Subacute Sclerosing Panencephalitis)
- Overall mortality rate is 10% o This is a rare chronic progressive demyelinating
disease chronic nonpermissive infection of the
Note: The mortality rate is increasing because patients usually come brain with previous infection of measles virus
in the hospital in the late stage of the disease. o Manifestations:
 Poor school performance
Cryptococcal Meningitis  Personality changes
- Cryptococcal neoformans  As the disease progresses, the patient
- Stained with india ink develops progressive intellectual
- Usually found in immunocompromised patients deterioration, focal or general seizures,
and myoclonus (with movement problems)
Note: Always ask for the patient’s TB exposure, occupation, sexual  This is a differential for normal patients that
history, and exposure to bird droppings. deteriorates progressively
 No treatment
Clinical Features - MRI is often normal early
- Mental changes - EEG may initially show only non specific slowing but with
- Headache disease progression, the patient develops a characteristic
- Confusion periodic pattern with bursts of slow wide voltage slow
- Fever wave every 3-8 seconds followed by period of flat
attenuated background. (Burst  suppressed  burst
CSF Findings:  suppressed). Burst suppression pattern in typical of
- (+) CALAS (Cryptococcal Antigen Latex Agglutination SSPE
System)
- Increase pressure Brain abscess
- Lymphocytic pleocytosis - Predisposing conditions:
- Reduced glucose o Otitis media and mastoiditis
- Elevated protein  Ears – it is usually located in the temporal
- (+) India ink area
- Sabouraud glucose agar  Mouth – it is usually located in the frontal
area
Note: It is hard to differentiate between TB and fungal. So ask for
more tests to confirm. If the patient presents with subacute
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- Etiology:
o By direct spread from a contiguous cranial
infection site
o Hematogenous spread
o Following a surgical procedure after a head
trauma
- Radiographic features:
o It is necessary to ask for a contrast-enhanced
study in cases of brain abscess.
o Both CT and MRI demonstrate similar features,
although MRI has the ability to better distinguish
cerebral abscess from other ring enhancing
lesions.
 Early cerebritis stage
 Stage wherein when a CT scan is
done it is still negative.
 It is important to treat for brain
abscess even though it is still
negative in CT scan
 Cerebritis is still not encapsulated
compared to an abscess.
 Early capsular stage
- Treatment:
o Optimal therapy of brain abscesses is surgical
drainage especially if it is already encapsulated.
o If non-encapsulated, the patient can be given
antibiotics.

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