CRANIAL NERVE DISORDERS

Nikki Rose Libarnes-Manalili, MD, FPNA

Internuclear Ophthalmoplegia
Is a disorder of conjugate lateral gaze
in which the affected eye shows
impairment of adduction.
Caused by injury or dysfunction in the
medial longitudinal fasciculus (MLF), a
heavily-myelinated tract that allows
conjugate eye movement by
connecting the paramedian pontine
reticular formation (PPRF) -abducens
nucleus complex of contralateral side
to the oculomotor nucleus of the
ipsilateral side.

Internuclear Ophthalmoplegia
When an attempt is made to gaze
contralaterally (relative to the affected
eye), the affected eye adducts
minimally, if at all. The contralateral eye
abducts, however with nystagmus.
Additionally, the divergence of the eyes
leads to horizontal diplopia. That is, if
the right eye is affected the patient will
"see double" when looking to the left,
seeing two images side-by-side.
Convergence is generally preserved.

Internuclear Ophthalmoplegia
In older people, the disorder usually results from a
stroke, and only one eye is affected.
In younger people, it usually results from multiple
sclerosis, and both eyes are often affected.
Less common causes include Lyme disease,
tumors, and toxicity due to a drug (such as tricyclic
antidepressants).

Horizontal Gaze Palsy

may be caused by lesions in the cerebral
hemispheres, which cause paresis of gaze
away from the side of the lesion,
or from brain stem lesions, which, if they occur
below the crossing of the fibers from the frontal
eye fields in the caudal midbrain, will cause
weakness of gaze toward the side of the
lesion.
Another way to remember this is that patients
with hemisphere lesions look toward their
lesion, while patients with pontine gaze palsies
look away from their lesions.

Vertical Gaze Palsy

Vertical gaze decreases gradually with aging, but
vertical gaze palsy is more severe than age-related
changes. Usually, upward gaze is affected. The
most common cause is damage to the top part of
the brain stem (midbrain), usually by a stroke or
tumor.

Oculomotor Nerve Palsy

Oculomotor nerve supplies the majority of the muscles controlling eye
movements (medial rectus, superior rectus, inferior rectus, and
inferior oblique). These muscles adduct, depress, and elevate the
eye.
In addition, the nerve also supplies the upper eyelid muscle (Levator
palpebrae superioris) and the muscles responsible for pupil
constriction (sphincter pupillae) .
Symptoms: down and out position of the affected eye, diplopia,
ptosis, and pupil dilation

Oculomotor Nerve Palsy

Etiology/ies:
Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm
(posterior communicating artery); Tumours (malignant and non-malignant); Inflammation
and Infection; Trauma; Multiple Sclerosis; Myasthenia Gravis; Post-op complication of
NSS; Cavernous Sinus Thrombosis

Diagnosis and Treatment:

diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR
angiography, CT angiography may be done.
Treatment depends on the cause. Emergency treatment is required if a life-threatening
disorder is the cause.

Trochlear Nerve Palsy

Fourth nerve palsy is a condition caused by
weakness or paralysis of the superior oblique muscle
(abducts, depresses, and internally rotates the eye).
Because the fourth cranial nerve is the smallest and
has the longest course of the cranial nerves, it is
particularly vulnerable to injury.

Symptoms: Palsy of the 4th cranial nerve causes

double vision, to compensate for the double-vision
resulting from the weakness of the superior oblique,
patients characteristically tilt their head down and to
the side opposite the affected muscle.

Trochlear Nerve Palsy

Etiology/ies:
Often, the cause cannot be identified. The most common identified cause is a head
injury, often due to a motorcycle accident. Occasionally, diabetes causes this palsy.
Rarely, the cause is a tumor, an aneurysm, or multiple sclerosis.

Diagnosis and Treatment:

diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR
angiography, CT angiography may be done.
Treatment depends on the cause. Emergency treatment is required if a life-threatening
disorder is the cause.

Abducens Nerve Palsy

CN VI, innervates the ipsilateral lateral rectus (LR), which functions to
abduct the ipsilateral eye.
It has the longest subarachnoid course of all the cranial nerves;
therefore, its syndromes are similar to those of the fourth nerve because
of their long intracranial courses.
The sixth nerve nucleus is located in the pons, just ventral to the floor of
the fourth ventricle and just lateral to the medial longitudinal fasciculus
(MLF).
About 40% of its neurons project into the ipsilateral MLF only to cross
over to the contralateral side and ascend to innervate that contralateral
medial rectus subnucleus to participate in contralateral eye adduction.

Abducens Nerve Palsy

Symptoms:
The affected eye cannot turn fully
outward and may turn inward when
people look straight ahead. Diplopia
occurs when people look toward the side
of the affected eye.
Other symptoms depend on the cause.
They include severe headache,
accumulation of fluid (edema) in the
conjunctiva, numbness in the face and
mouth, loss of vision, and inability to
move the eye in other directions.

Abducens Nerve Palsy

Etiology/ies:
Head injuries, Tumors, Multiple sclerosis, aneurysms, brain infections (meningitis, a
brain abscess or a parasitic infection), complications of an ear or eye infection, Blockage
of an artery supplying the nerve, as can result from diabetes, a stroke, a transient
ischemic attack, or vasculitis, Wernicke's encephalopathy(commonly due to chronic
alcoholism); benign intracranial hypertension, Respiratory infections (in children)

Diagnosis and Treatment:

diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR
angiography, CT angiography may be done. If symptoms suggest vasculitis, blood is

withdrawn to check for signs of inflammation, such as certain abnormal antibodies

(ANA, ESR, RF) in the blood.
Treatment depends on the cause. Emergency treatment is required if a life-threatening
disorder is the cause.

Trigeminal Neuralgia
Usually occurs in middle-aged and older people, although it
can affect adults of all ages. It is more common among
women.
Symptoms: The pain can occur spontaneously but is often
triggered by touching a particular spot (called a trigger point)
on the face, lips, or tongue or by an action such as brushing
the teeth or chewing. Repeated short, lightning-like bursts of
excruciating stabbing pain
Usually, unilateral.
The pain usually lasts seconds but may last up to 2 minutes.
Recurring as often as 100 times a day, the pain can be
incapacitating.
Because the pain is intense, people tend to wince, and thus
the disorder is sometimes called a tic.
The disorder commonly resolves on its own, but bouts of the
disorder often recur after a long pain-free interval

Trigeminal Neuralgia
Etiology/ies:
In most cases, the cause is unknown.
A common known cause is an abnormally positioned artery that compresses the trigeminal
nerve near where it exits the brain.
Occasionally in younger people, trigeminal neuralgia results from nerve damage due to
multiple sclerosis.
Rarely, trigeminal neuralgia results from damage due to herpes zoster (a viral infection) or
compression by a tumor.

Diagnosis and Treatment:

Distinguished from trigeminal neuropathy (due to compression caused by a tumor, stroke, an
aneurysm, or multiple sclerosis). Trigeminal neuropathy can be distinguished because it causes
loss of sensation and often weakness in parts of the face and trigeminal neuralgia does not.
Anticonvulsants (carbamazepine, phenytoin, gabapentin); Baclofen; antidepressant; Nerve block;
surgery

Bells Palsy
Symptoms: may feel pain behind the ear, then one side
of the face may become weak or completely paralyzed.
Wrinkling the forehead, blinking, and grimacing may be
difficult or impossible. For most people, the face feels
numb or heavy, even though sensation remains
normal.
The ear on the affected side may perceive sounds as
abnormally loud (hyperacusis) because the muscle that
stretches the eardrum is paralyzed.
Etiology/ies:
Bell's palsy may result from herpes simplex virus type
1, which causes herpes mouth infections.
But the cause is sometimes unknown.

Bells Palsy
Diagnosis:
no specific test, usually be diagnosed based on symptoms.
can be distinguished from a stroke because a stroke usually causes weakness only
in the lower part of the face rather than in the entire face.
EMG-NCV
x-rays, magnetic resonance imaging (MRI), or computed tomography (CT) tumors,
infection, skull fractures
A blood test may be done to check for Lyme disease, and a blood test and a chest xray may be done to check for sarcoidosis.
Treatment:
Corticosteroids may be used to reduce swelling of the nerve.
Artificial tears, eye patch, rehabilitation
With or without treatment, most people recover completely within several months.

Hemifacial Spasm
painless involuntary twitching of one side of the face
due to malfunction of the facial nerve.
affects men and women but is more common among
middle-aged and older women.
Symptoms: Muscles on one side of the face twitch
involuntarily, usually beginning with the eyelid, then
spreading to the cheek and mouth. Twitching may be
intermittent at first but may become almost continuous.
The disorder is essentially painless but can be
embarrassing.
Etiology/ies:
The spasms may be caused by an abnormally
positioned artery or loop of an artery that compresses
the 7th cranial nerve where it exits the brain stem.

Hemifacial Spasm
Diagnosis:
Magnetic resonance imaging (MRI) should be done to check for a tumor,
other structural abnormalities, and evidence of multiple sclerosis. Usually,
MRI can detect the abnormal loop of artery pressing against the nerve.
Treatment:
Botulinum toxin is the drug of choice. It is injected into the affected muscles.
The same drugs used to treat trigeminal neuralgiacarbamazepine,
phenytoin, gabapentin, baclofen, antidepressant may help
If drug treatment is unsuccessful, surgery may be done to separate the
abnormal artery from the nerve by placing a small sponge between them
(vascular decompression).

Vestibulocochlear Nerve Disorders

Symptoms: hearing loss, vertigo, false sense of
motion, loss of equilibrium (in dark places),
nystagmus, motion sickness, gaze-evoked tinnitus
Etiology/ies:
Vestibular neuritis, cochlear neuritis, and acoustic
neuromas/neurofibromatosis are relatively common conditions that
affect these nerves.

Vestibulocochlear Nerve Disorders

Diagnosis:
The diagnosis is made when doctors see the
spasms. Magnetic resonance imaging (MRI) should
be done to check for a tumor.
Treatment:
Treatment depends on the cause.

Glossopharyngeal Neuralgia
a rare disorder, usually begins after age 40 and occurs more often in men.
Symptoms: brief attacks of excruciating pain, affecting one side of the
tongue or throat and sometimes an ear.
Attacks may be triggered by a particular action, such as chewing,
swallowing, talking, coughing, or sneezing.
The pain may last several seconds to a few minutes and usually affects
only one side of the throat and tongue.
Etiology/ies:
cause is usually unknown but sometimes is an abnormally positioned
artery that compresses the glossopharyngeal nerve.

Glossopharyngeal Neuralgia
Diagnosis:
Test done by touching the back of the throat with a cotton-tipped
applicator. If pain results, apply a local anesthetic to the back of the
throat. If the anesthetic eliminates the pain, the glossopharyngeal
neuralgia is diagnosed.
MRI is done to check for tumors.
Treatment:
The same drugs used to treat trigeminal neuralgiacarbamazepine,
phenytoin, gabapentin, baclofen, antidepressant may help
If drug treatment is unsuccessful, vascular decompression may de
done

Accessory Nerve Disorders

Symptoms: often exhibit signs of lower motor neuron disease such as
diminished muscle mass, fasciculations, and partial paralysis of the
sternocleidomastoid and trapezius muscles.
Interruption of the nerve supply to the sternocleidomastoid muscle results
in an asymmetric neckline,
while weakness of the trapezius muscle can produce a drooping shoulder,
winged scapula, and a weakness of forward elevation of the shoulder.
Etiology/ies:
Medical procedures are the most common cause of injury to the spinal
accessory nerve (radical neck dissection and cervical lymph node biopsy).

Accessory Nerve Disorders

Diagnosis and treatment:
Eden-Lange procedure, in which remaining
functional shoulder muscles are surgically
repositioned, may be useful for treating trapezius
muscle palsy.
Failure to rapidly identify spinal accessory nerve
damage may exacerbate the problem, as early
intervention leads to improved outcomes.

Hypoglossal Nerve Disorders

Symptoms: The tongue becomes weak on the affected side and eventually
wastes away (atrophies). As a result, people have difficulty speaking,
chewing, and swallowing.
Damage due to amyotrophic lateral sclerosis causes tiny, subtle twitching
movements (fasciculations) on the surface of the tongue.
Etiology/ies:
Causes include a tumor or bone abnormality at the base of the skull, a
stroke, infection of the brain stem, or an injury to the neck, such as that
due to surgical removal of a blockage from an artery in the neck
(endarterectomy).
Amyotrophic lateral sclerosis (Lou Gehrig's disease) can also damage the
hypoglossal nerve.

Hypoglossal Nerve Disorders

Diagnosis and treatment:
Magnetic resonance imaging (MRI) is usually done
to look for a tumor or evidence of a stroke. A spinal
tap (lumbar puncture) may be necessary if cancer
or infection is possible.
Treatment depends on the cause.

PERIPHERAL NEUROPATHIES

Peripheral Neuropathy
Damage to nerves of the peripheral nervous system,
which may be caused either by diseases of or trauma to
the nerve or the side-effects of systemic illness.
The four cardinal patterns of peripheral neuropathy are
polyneuropathy, mononeuropathy, mononeuritis
multiplex and autonomic neuropathy.
The most common form is (symmetrical) peripheral
polyneuropathy, which mainly affects the feet and legs.

Mononeuropathy
Most common cause of is by physical compression of the
nerve, known as compression neuropathy (Carpal tunnel
syndrome, Meralgia Paresthetica).
The "pins-and-needles" sensation of one's "foot falling asleep"
(paresthesia) is caused by a compression mononeuropathy (a
temporary one which can be resolved merely by moving
around and adjusting to a more appropriate position).
Direct injury to a nerve, interruption of its blood supply
(ischemia), or inflammation can also cause mononeuropathy.

Mononeuritis Multiplex
Simultaneous or sequential involvement of individual noncontiguous nerve trunks,
either partially or completely, evolving over days to years and typically presents
with acute or subacute loss of sensory and motor function of individual nerves.
The pattern of involvement is asymmetric; however, as the disease progresses
deficit(s) becomes more confluent and symmetrical, making it difficult to
differentiate from polyneuropathy.
Therefore, attention to the pattern of early symptoms is important.
May also cause pain, which is characterized as deep, aching pain that is worse at
night, is frequently in the lower back, hip, or leg.

Mononeuritis Multiplex
It is caused by, or associated with, several medical conditions:
diabetes mellitus
vasculitides: polyarteritis nodosa, Wegener granulomatosis, and
Churg-Strauss syndrome
immune-mediated diseases like rheumatoid arthritis, lupus
erythematosus (SLE), and sarcoidosis
infections: leprosy, lyme disease, HIV
amyloidosis
cryoglobulinemia
chemical agents, including trichloroethylene and dapsone
rarely, the sting of certain jellyfish, such as the sea nettle

Polyneuropathy
Many nerve cells in different parts of the body are affected, without regard to
the nerve through which they pass. Not all nerve cells are affected in any
particular case.
In distal axonopathy, one common pattern, the cell bodies of neurons remain
intact, but the axons are affected in proportion to their length (Diabetic
neuropathy)
In demyelinating polyneuropathies, the myelin sheath around axons is
damaged, which affects the ability of the axons to conduct electrical impulses.
The third and least common pattern affects the cell bodies of neurones
directly, either the motor neurones (known as motor neurone disease) or the
sensory neurones (known as sensory neuronopathy or dorsal root
ganglionopathy).

Polyneuropathy
Effect of this is to cause symptoms in more than one part of the
body, often on left and right sides symmetrically.
The chief symptoms: weakness or clumsiness of movement
(motor); unusual or unpleasant sensations such as tingling or
burning; reduction in the ability to feel texture, temperature, and
impaired balance when standing or walking (sensory).
In many polyneuropathies, these symptoms occur first and most
severely in the feet.
Autonomic symptoms may also occur, such as dizziness on
standing up, erectile dysfunction and difficulty controlling urination.

Polyneuropathy
Usually caused by processes that affect the body as a whole.
Diabetes and impaired glucose tolerance are the most common
causes.
Other causes including inflammatory diseases such as lyme
disease, vitamin deficiencies, blood disorders, and toxins (including
alcohol and certain prescribed drugs).
Most types of polyneuropathy progress fairly slowly, over months or
years, but rapidly progressive polyneuropathy also occurs.
The treatment of polyneuropathies is aimed at eliminating or
controlling the cause, maintaining muscle strength and physical
function, controlling symptoms such as neuropathic pain.

Autonomic Neuropathy
Is a form of polyneuropathy which affects the non-voluntary,
non-sensory nervous system, affecting mostly the internal
organs such as the bladder muscles, the cardiovascular
system, the digestive tract, and the genital organs.
Most commonly autonomic neuropathy is seen in persons
with long-standing diabetes mellitus type 1 and 2.
In most but not all cases, autonomic neuropathy occurs
alongside other forms of neuropathy, such as sensory
neuropathy.

Autonomic Neuropathy
The signs and symptoms of autonomic neuropathy include the
following:
urinary bladder conditions: bladder incontinence or urine retention
gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting,
malabsorption, fecal incontinence, gastroparesis, diarrhea,
constipation
cardiovascular system: disturbances of heart rate (tachycardia,
bradycardia), orthostatic hypotension, inadequate increase of heart
rate on exertion
other: hypoglycemia unawareness, genital impotence, sweat
disturbances

Signs and symptoms of PN

Sensory function: negative symptoms (numbness, tremor, and gait abnormality) and positive
symptoms (tingling, pain, itching, crawling, and pins and needles)
Motor function: negative symptoms (weakness, tiredness, heaviness, and gait abnormalities)
and positive symptoms (cramps, tremor, and fasciculations)
There is also pain in the muscles (myalgia), cramps, etc., and there may also be autonomic
dysfunction.
During a neurological examination:
those with generalized peripheral neuropathies most commonly have distal sensory or motor
and sensory loss,
though those with a pathology (problem) of the nerves may be perfectly normal; may show
proximal weakness, as in some inflammatory neuropathies like GuillainBarr syndrome; or
may show focal sensory disturbance or weakness, such as in mononeuropathies.
Ankle jerk reflex is classically absent in peripheral neuropathy.

Etiologies of PN
The causes are broadly grouped as follows:
Genetic diseases: Friedreich's ataxia, Charcot-Marie-Tooth syndrome, Hereditary neuropathy with
liability to pressure palsy
Metabolic/Endocrine: diabetes mellitus, chronic renal failure, porphyria, amyloidosis, liver failure,
hypothyroidism
Toxic causes: Drugs (vincristine, metronidazole, phenytoin, nitrofurantoin, isoniazid, ethyl alcohol),
organic metals, heavy metals, excess intake of vitamin B6 (pyridoxine)
Fluoroquinolone toxicity: Irreversible neuropathy is a serious adverse reaction of fluoroquinolone drugs
Inflammatory diseases: Guillain-Barr syndrome, systemic lupus erythematosis, leprosy, Sjgren's
syndrome, Lyme Disease, sarcoidosis
Vitamin deficiency states: Vitamin B12 (cyanocobalamin), vitamin A, vitamin E, vitamin B1 (thiamin)
Physical trauma: compression, pinching, cutting, projectile injuries (i.e. gunshot wound), strokes
including prolonged occlusion of blood flow, electric discharge, including lightning strikes
Others: shingles, malignant disease, HIV, radiation, chemotherapy

Treatment of PN
Pregabalin is an anticonvulsant drug used for neuropathic pain. It has also been found
effective for generalized anxiety disorder. It was designed as a more potent successor to
gabapentin but is significantly more expensive
Duloxetine, a serotonin-norepinephrine reuptake inhibitor, is also being used to reduce
neuropathic pain.
TENS (Transcutaneous Electrical Nerve Stimulation) therapy may be effective and safe in
the treatment of diabetic peripheral neuropathy.
A recent review of three trials involving 78 patients found some improvement in pain scores
after 4 and 6 but not 12 weeks of treatment, and an overall improvement in neuropathic
symptoms at 12 weeks.
(Jin DM et al, 2010)
A second review of four trials found significant improvement in pain and overall symptoms,
with 38% of patients in one trial becoming asymptomatic. The treatment remains effective
even after prolonged use, but symptoms return to baseline within a month of treatment
cessation.
(Pieber K et al, 2010)

Thank You!

CEREBROVASCULAR
DISEASE

Nikki Rose Libarnes-Manalili, MD, FPNA

What is a Stroke?
STROKE IS A BRAIN ATTACK!!!
Rapidly developing clinical symptoms and or signs of focal and at
times global loss of cerebral function with symptoms lasting more
than twenty four hours or leading to death with no apparent cause
other than that of vascular origin.
(Hatano 1976)

Sudden onset of focal (or global) neurologic deficit due to an

underlying vascular pathology.
(SSP and PNA-SC 2009)

Transient Ischemic Attack (TIA)

Acute loss of focal cerebral function with symptoms lasting for less
than twenty four hours, which after adequate investigation, is
presumed to be due to embolic or thrombotic vascular disease.
(Warlow and Morris 1982)

A transient episode of neurological dysfunction caused by focal brain

or spinal or retinal ischemia, without evidence of acute infarction in
which clinical symptoms typically last less than an hour.
(SSP and PNA-SC 2009)

Frequency and Demographics

Ave. of 500,000 new strokes occur each year in the
USA. At current trends, this number is projected to
jump to one million per year by the year 2050.
Men are at higher risk than women for stroke.
Although stroke often is considered a disease of the
elderly, 25% of strokes occur in persons younger
than 65 years.

Frequency and Demographics

The incidence of hemorrhagic stroke in the
Japanese population is increased (it has been
associated with westernization of the Japanese diet
after World War II).
The WHOs Global Burden of Stroke in 2005
reported that the prevalence in the Philippines is 14
per 1,000 people, more than the average of <5 per
1,000 in the industrialized world.

Mortality and Morbidity

2nd most common cause of death worldwide and in
the Philippines.
WHO predicts an impending epidemic of diseases
of the vascular system including stroke in 2020. It is
predicted that there will be 6.5M deaths due to
stroke in 2015 and 7.8M in 2030.

Mortality and Morbidity

Of the 58 million global deaths in 2005, 5.7 million
were from stroke alone. Worldwide, 10% of all
deaths are attributed to strokes.
Leading cause of disability in adults with up to 32%
of all stroke survivors permanently disabled.

Mortality and Morbidity

Most disabling of all neurologic diseases worldwide.
In the Philippines, stroke remains to be a leading
cause of disability, afflicting 400,000 Filipinos yearly
(Manila Bulletin, 13 September 2004).

App. 50% of survivors have a residual neurologic

deficit.
Greater than 25% require chronic care.

Classification

80%
rebrovascular Disease

Acute Stroke
15%
85%
Infarction

Hemorrhage
Intracerebral
Subarachnoid

15%
Cardiogenic embolism

Atrial fibrillation
Atherothrombotic Hemodynamic/
Ischemic heart disease
cclusive artery to artery emboli
Valvular heart disease
mall artery lipohyalinosis lacunes
Prosthetic cardiac valves
Other mechanisms
Infective endocarditis
Other, less common

5%
Other, unusual

Dissections
Hypercoagulable stat
Vasculitis
Systemic hypotension

Types of Stroke

Types of Stroke

Pathophysiology of Ischemic Stroke

Ischemic cascade
Within seconds to minutes of the loss of perfusion to
a portion of the brain, an ischemic cascade is
unleashed,

Pathophysiology of Ischemic Stroke

Ischemic cascade
if left unchecked, causes a
central area of irreversible
infarction surrounded by
an area of potentially
reversible ischemic
penumbra.

Clinical Presentation
Clinically, symptoms depend on the area of cerebral
circulation affected and on the extent to which it is
affected.
1. Internal Carotid Artery (ICA) occlusion:
a. no characteristic clinical picture
b. may range from a TIA to infarction of a major portion
of the ipsilateral (on the same side) hemisphere
c. if adequate intracranial collateral circulation is
present, may see no signs or symptoms

Clinical Presentation
1. Internal Carotid Artery (ICA) occlusion:
d. Neurological symptoms:
1. monoparesis to hemiparesis with or without a defect
in vision
2. impairment of speech or language
3. transient monocular blindness

Clinical Presentation
2. Middle Cerebral Artery (MCA) occlusion:
a. opportunity for collateral circulation is restricted to
anastomotic blood flow from the anterior and
posterior cerebral arteries on the surface of the brain

Clinical Presentation
Middle Cerebral Artery (MCA) occlusion:
b. Neurological symptoms:
1. hemiplegia (paralysis of one side of the body)
2. hemisensory deficit
3. hemianopsia (blindness in 1/2 of the visual field)
4. aphasia (if infarct is in the dominant hemisphere)
.Since the MCA supplies the upper extremity motor
strip, weakness of the arm and face is usually worse
than that of the lower limb.
2.

Clinical Presentation
3. Anterior Cerebral Artery (ACA) occlusion:
a. Neurological symptoms:
1. weakness of the opposite leg with or without
sensory involvement
2. apraxia (particularly of gait)
3. primarily affect frontal lobe function, producing
cognitive impairment (altered mental status,
impaired judgment)

Clinical Presentation
4. Posterior Cerebral Artery (PCA) occlusions:
a. Neurological symptoms:
1. Affect vision and thought, producing homonymous
hemianopsia, cortical blindness, visual agnosia,
altered mental status, and impaired memory.

Clinical Presentation
5. Vertebrobasilar Artery occlusions:
a. are notoriously difficult to detect because they
cause a wide variety of cranial nerve, cerebellar,
and brainstem deficits.
b. Neurological symptoms:
1. vertigo, nystagmus, diplopia, visual field deficits,
dysphagia, dysarthria, facial hypesthesia, syncope,
and ataxia

Clinical Presentation
5. Vertebrobasilar Artery occlusions:
b. Neurological symptoms:
2. Loss of pain and temperature sensation occurs on
the ipsilateral face and contralateral body (In
contrast, anterior strokes produce findings on one
side of the body only).

Clinical Presentation

Risk Factors

HYPERTENSION (2-4x)
DIABETES MELLITUS (1.5-3x)
ATRIAL FIBRILLATION (6x)
VALVULAR HEART DISEASE
CORONARY ARTERY DISEASE (3x) AND MYOCARDIAL INFARCTION (5x)
HYPERLIPIDEMIA
SYMPTOMATIC CAROTID STENOSIS
TIA (24-29% during the next 5 years (4-8% in 1 st mo. and 12-13% during the 1st year)
CIGARETTE SMOKING (1.5x)
ALCOHOL
PHYSICAL INACTIVITY
LIFESTYLE FACTOR: DIET

Diagnosis
Having a stroke is an emergency situation!
Diagnosis includes:
Good clinical history
A brief physical and neurological exams
Diagnostics (blood tests, imaging scans, and other
tests to quickly determine the cause, location, and
amount of damage).

Diagnostics

Prioritize diagnostic exams as not

to delay treatment ..
IN THE ER, Must DO in all :
CBC with platelet count
CBG
PT-INR, PTT
12 L ECG
Plain Cranial CT scan

Imaging Studies
Cranial CT scan
Emergent noncontrast head CT scanning is mandatory for
rapidly distinguishing ischemic from hemorrhagic infarction
and for defining the anatomic distribution of stroke.

Dense Artery
sign

Insular Ribbon
sign (loss of insular
stripe)

Early signs of infarction on Cranial CT

Obscuration of lentiform
nuclei

Effacement of sulci

Cranial CT: Completed Infarction

Large cortical infarcts tend to be wedgeshaped, while small subcortical infarcts are
usually round or ovoid

Cranial CT: Chronic (Old) Infarct

Encephalomalacia (gliosis is
isodense to CSF)
Volume loss leading to ex
vacuo dilatation of ventricles

Common Sites of Hypertensive ICH

Common Sites of Hypertensive ICH

Computation of Hematoma Volume (Kothari

Method)
Hematoma volume (in cc) = A x B x C / 2

A = largest diameter in hematoma (in cm)

B = diameter perpendicular to A (in cm)
C = number of slices on CT scan X slice
thickness (cm)
Count slice as 1, if size of hematoma is
>75% of
largest hematoma
Count slice as .5, if size of hematoma is
25-75%
of largest hematoma
Disregard slice, if size of hematoma is
<25% of
largest hematoma

CT FINDINGS: SAH

CT FINDINGS: Epidural Hematoma

Usually secondary to damage of

Middle Meningeal Artery.
Lentiform or biconvex in shape.
Does not cross suture lines.
Clinically lucid period may follow
initial trauma.

CT FINDINGS: Subdural Hematoma

Damage to the bridging veins (e.g from

falls in elderly or alcoholics).
Cresentric shape.
Crosses suture lines.
Injury may be remote or relatively
minor.

Imaging Studies
Magnetic Resonance Imaging (MRI)
MRI is useful for patients with acute ischemic stroke
involving cerebellar or lacunar pathology.
Disadvantages include its high cost, lack of ready
availability at most centers, and insensitivity for
detecting early hemorrhages.

DWI: acute
infarct
appears bright

Slow flow (absence of

normal flow void) in involved
artery

Early signs of infarction on MRI

Parenchymal signal changes

(hypointense on T1, hyperintense on T2
and DWI)

T1

T2

medulla

T2
T1

MRI is superior to CT for imaging brainstem lesions

(example above: R lateral medullary infarction)

Magnetic Resonance Imaging in Acute Stroke

MRI is not sensitive for acute hemorrhage

Magnetic Resonance Imaging in Acute Stroke

MRI is not sensitive for acute hemorrhage

Imaging Studies
Noninvasive arterial studies
Carotid duplex scanning
Transcranial Doppler (TCD) ultrasound
Echocardiography

Other tests
Angiography
PET scan

Guidelines for Acute Stroke Treatment

rinciples :
Stroke is a brain attack
needing emergency management, including specific treatments
and secondary and tertiary prevention.
Stroke is an emergency
where virtually no allowances for worsening are tolerated.
Stroke is treatable
optimally, through proven, affordable, culturally-acceptable and
ethical means.
Stroke is preventable
in implementable ways across all levels of society.

 The therapeutic approach to patients with cerebrovascular

disease involves multiple phases, including:
(1) preventive measures against stroke and vascular
disease in general,
(2) supportive and medical management during the acute
phase of stroke,
(3) measures to mitigate the pathologic or atherothrombotic
process, and
(4) appropriate rehabilitative and physical therapy programs
during the poststroke period.

Rationale for Drugs in Acute Ischemic Stroke

Recanalization

Thrombolysis (rTPA)

Prevent neurologic worseningAntithrombotics

Prevent early recurrent strokeAntiplatelets
Prevent complications (e.g. Anticoagulants
DVT)

Preserve ischemic tissue

Neuroprotection
(penumbra)

ELIGIBILITY CHECKLIST
INCLUSION:
Screening NIH
Onset < 3 hrs
CT no hemorrhage

EXCLUSION:
SBP > 185, DBP > 110

Rapidly improving / minor

symptoms
Seizure at onset

Head trauma within 3 mos

GI or Urinary tract hemorrhage

within 21 days
On anticoagulants / heparin within
48 hrs
Elevated PTT / PT > 1.5

Platelet count < 100,000

Glucose < 50, > 400

Intravenous rTPA
Properly selected patients
within 3 hours
Dose : 0.9 mg / kg IV
10 % as bolus, 90% as drip for 1 hr
56 kg, female
Total dose = 50 mg
5 mg bolus (within 3 hrs of ictus)

30 % MORE LIKELY to have 45 mg as drip for 1 hour

minimal or no disability at 3 months

NTI-PLATELETS
ASPIRIN
In 48 hours works!
Fewer recurrent strokes within 14 day
Fewer deaths / dependency at 6 months (IST and CAST
data, 1997)
Dose: 80 325 mg / day
Antiplatelet Trialist Collaboration:
145 trials with almost 100,000 patients showed
23% risk reduction for stroke, MI, and vascular death.

NTI-PLATELETS
Clopidogrel
Clopidogrel vs. Aspirin in Patients at Risk of
Ischemic Events (CAPRIE):
19,185 patients with prior stroke, MI, or PVD given
Clopidogrel 75mg/day vs. ASA 325 mg/day showed
8.7% RRR in stroke, MI, and vascular death over
ASA.

NTI-PLATELETS
Cilostazol
Cilostazol Stroke Prevention Study (CSPS):
1,095 patients with cerebral infarction at 1-6 months
were given Cilostazol 100 mg BID vs. Placebo,
showed RRR of 41.7%.

NTI-PLATELETS
Dipyridamole
European Stroke Prevention Study 2:
6,602 patients randomized to ASA 25 mg BID,
Dipyridamole 200 mg BID, ASA 25 mg BID +
Dypiridamole 200 mg, and placebo
Results: ASA better than placebo, Dipyridamole
better than placebo, combination of ASA and
Dipyridamole better than either one alone

NTI-PLATELETS
Ticlodipine
Canadian American Ticlodipine Study (CATS):
23% RR vs. placebo for stroke, MI, or vascular
death.
Ticlodipine Aspirin Stroke Study (TASS)
12% RR vs. ASA for stroke or death at 3 years.

NTI-COAGULANTS
Anecdotal evidence suggests that heparin may
benefit some patients with progressive stroke,
especially in the vertebrobasilar system, or strokes
involving only a small area of the brain that are
associated with an arterial or cardiac mechanism.

NTI-COAGULANTS
Anticoagulation is not without risk. Overall,
intracranial hemorrhage occurs in 1-4% of patients
who receive an anticoagulant for TIA or acute
stroke.
Accordingly, uncontrolled hypertension, intracranial
hemorrhage, and uncontrolled bleeding at another
site are contraindications to anticoagulation.

NTI-COAGULANTS
Patients with cardioembolic strokes also may be at
risk for hemorrhagic transformation.
Although some evidence indicates that early
heparinization is beneficial, some authors believe
that patients with cardioembolic stroke should not
be given anticoagulants until at least 48 hours after
symptom onset because of the risk of hemorrhagic
transformation (5-7 d for large cardioembolic
strokes).

NTI-COAGULANTS
Immobilized stroke patients who are not receiving
anticoagulants, such as IV heparin or an oral
anticoagulant, may benefit from low-dose
subcutaneous unfractionated or low-molecularweight heparin, which reduces the risk of deep vein
thrombosis.
The use of low-molecular-weight heparin as
treatment for acute ischemic stroke has not yet
been studied adequately.

EUROPROTECTANTS
Since the ischemic cascade is a dynamic process,
the efficacy of interventions to protect the ischemic
penumbra also may prove to be time dependent.
Citicoline (cytidine-5-diphosphate
choline) is an essential intermediate in the
biosynthetic pathway of structural
phospholipids which are important
constituents of all biological membranes,
including neuronal membranes

EUROPROTECTANTS
Data Pooling Analysis of Trials on Citicoline
Treatment of patients with moderate to
severe stroke with Citicoline within 24
hours resulted in 33% odds of complete
recovery at 3 months.

Davalos, et al. Stroke 2002;33: 2850 - 2857

P Management in Acute Ischemic Stroke

1. Treat if with any of the ff:
SBP > 220 or DBP > 120 or MAP > 130mm Hg
2. Avoid precipitous drop in BP
Not > 15 - 20% of baseline MAP
3. Do not use rapid acting sublingual agents
e.g. SL Nifedipine
4. Use easily titratable IV anti-HPN medications
e.g. Nicardipine, Hydralazine,
Labetolol, Esmolol

Bring down the BP to not lower

than 20% of the baseline MAP.
BP = 210/120
MAP = 150 mmHg
20% of 150 = 30
Compute for the desired MAP:
150 30 = 120
The desired BP:
180/90 or 160/100

MAP = systolic + 2
(diastolic)
3

ACUTE STROKE
MANAGEMENT
Recognize stroke : History, PE and focused Neuro exam should be
done immediately
Prioritize diagnostic exams in the ER

Screen for eligibility for rTPA

Plain Cranial CT scan remains as the most important

neuroimaging study of choice

Ascertain stroke subtype because management is different

ACUTE STROKE
MANAGEMENT
IV rTPA is strongly recommended in carefully selected patients with
acute ischemic stroke who can receive the medication within 3 hrs
ASA (80 325 mg) should be given to acute ischemic stroke
patients within 48 hrs of symptom onset
Do not forget NEUROPROTECTION: Avoid hypoxemia, hypohyperglycemia, hyperthermia, hypotension, hyponatremia

Rehabilitation
Physiotherapy
Optimize muscle function: e.g., mobility, balance,
coordination.
Help patients deal with disabilities: e.g., correct use
of a cane, walker, or brace.
Supplementary devices are indicated: e.g., for
feeding, dressing, and writing.

Rehabilitation
Speech therapy
Assists in improving verbal, written, or nonverbal communication skills:
e.g., for those with aphasia.
Diagnose and handle swallowing deficits to minimize complications.
Occupational therapy
Optimize functional capacities: e.g., writing and other functions to assist
in daily living (ADL)

Complications
Problems due to loss of mobility (joint Reduced ability to
contractures, pressure sores)
function or care for
self
Permanent loss of movement or
Decreased life span
sensation of a part of the body
Side effects of
Bone fractures
medications
Muscle spasticity
Aspiration
Permanent loss of brain functions
Malnutrition
Reduced communication or social
interaction

Prognosis
The long-term outcome from a stroke depends on the extent of
damage to the brain, the presence of any associated medical
problems, and the likelihood of recurring strokes.
22% of men and 25% of women who have an initial stroke die
within a year.
51% of men and 53% of women under age 65 who have a
stroke die within 8 years.

Prognosis
Some survivors experience depression following a stroke;
early treatment for depression can positively impact
rehabilitation.
Between 50 and 70% of stroke survivors regain functional
independence; the sooner rehabilitation begins, the greater
the chance of leading a productive life.
Between 15 and 30 percent of stroke survivors experience
permanent disability.
20% require institutional care at three months after onset.

 Last September 1999, the former Health Secretary

Alberto G. Romualdez said in a press release that
the cost of treating uncomplicated stroke for 5-7
days range from Php 15,000 to Php 20,000 making
it not only a burden emotionally but also
economically to the family and community.

Thank You!

Treatment and
Prevention

of Stroke

 Infarct
Thrombotic
Embolic
Hemorrhage
ICH
SAH

Temporal Profile
Risk Factors
HPN
DM
Smoking
Hyperlipidemia
Age
Heart Disease

ACUTE STROKE MANAGEMENT

CATEGORIES

1. MEDICAL SUPPORT
2. THROMBOLYSIS
3. ANTI-COAGULATION
4. ANTI- PLATELET AGENTS
5. NEUROPROTECTION

I. MEDICAL SUPPORT

*BP control

SBP > 220

DBP > 120
MAP > 130

MAP = S + 2D / 3
not > 20 % of MAP
Exceptions:
LVF
AMI
Aortic Dissection

*Drugs
Nicardipine
Nitroprusside
Esmolol / Labetolol
Hydralazine (?)

*Fever
Increase brain damage
Treat the source
Paracetamol

 Blood Sugar
Treat Hyperglycemia > 180

II. THROMBOLYTIC THERAPY

Thrombolytic Therapy

rTPA
Streptokinase
Golden period 3 hours
Guidelines:
BP < 180 / 220
CT no bleed
mild and severe are not treated

III.ANTI-COAGULATION

ANTI- COUAGULATION
Heparin
- carotid a occlusion
- basilar a thrombosis
- fluctuating exam
LMWH
ASA

IV. ANTI-PLATELET AGENTS

ANTI-PLATELET AGENTS
ASA 80 325 mg
Dypiridamole
ESPS 2 results
ASA > placebo
Dypiridamole > placebo
ASA + Dypiridamole > than each alone

 Clopidogrel
Caprie
Claire
Cilostazol
Triflusal
TACIP
Embolic
Coumadin
INR 2 to 3
metal values 3 to 4.5

V. NEUROPROTECTION

Neuroprotectors
Dexa NO

Mg SO4
Hypothermia

Barbiturate Coma

Citicoline

Piracetam

Surgical Management
Carotid NASCET
Craniotomy
Ventriculostomy

OTHER MODES OF MGT.

Statins
SPARCL
80mg Atorvastatin
Stroke and TIA
for 4731 patients
LDL-C
Results: 16% reduction in stroke; 20% reduction in
cardiovascular events

OTHER MODES OF MGT.

Side Effects:
1. Myopathy
2. > liver enzyme
3. Hemorrhage
Dose

ACE inhibitors
ARBI

 ICH
- HPN
- Location
- Size
a x b x c / 3 (mm)
Golf ball = 30 to 40 cc

 Increase ICP
Mannitol
Hyperventilation
Raise Head

RICH trial

 Surgical Immediate Cerebellar Hemmorhage > 3

cm
Brainstem comprssion
Ventricular obstruction
Large lobar

Poor outcome
Age
Deep hemorrhage
Ventricular extension
Large volume
Coexisting disease

SAH

Headache
Nape pain
Prognosis: vasospasm
re-rupture
MEDICAL MANAGEMENT:
MANNITOL
DEXAMETHASONE
TRIPLE H hypertension, hemodilution, hypo-volemic
therapy
NIMODIPINE

SAH
SURGICAL MANAGEMENT:
CLIPPING
COILING

Prognostication
Prognosis by Neuro Exam
a. Day of Presentation: corneal, pupillary, and
occulocephalic responses
1) Absence of 1 of the 3: 95% vegetative / severely
disabled
2) Absence of 2 of the 3: 99% vegetative / severely
disabled

Prognostication
b. Day 1:
1) Spontaneous Eye Movements: 99% w/o will be vegetative
/ severely disabled
2) Motor Withdrawal to pain: 90% w/o will be vegetative /
severely disabled
c. Day 3:
1) Motor Withdrawal: 100% w/o will be vegetative /
severely disabled
2) Spontaneous Eye Opening: (+) withdrawal but eyes
closed 80% will be vegetative / severely disabled

Prognostication
Day 7:
1) Spontaneous Eye Opening: (+) withdrawal
but eyes closed 100% will be vegetative /
severely disabled
2) Obeying Commands: (+) eye opening, dont
follow commands 80% will be vegetative /
severely disabled

Thank you!

HEADACHES

Pain-Sensitive Structures
of the Head
Venous sinuses
Dural arteries
Proximal 50% of the larger
arteries of the circle of Willis
Dura at the base of the
brain
All extracranial structures

Pain-Insensitive
Structures
of the Head

Brain parenchyma
Ependyma
Choroid
Pia
Arachnoid
Dura over convexity
Skull

General Mechanisms of
Headache

Traction on major intracranial

vessels
Distention and dilation of
intracranial arteries
Inflammation near pain sensitive
structures
Direct pressure on cranial or
cervical nerves
Sustained contraction of scalp or
neck muscles
Stimulation from disease of eye,
ear, nose and sinuses

Epidemiology

60-75% of adults have at least one

headache / year

5-10% will seek physician evaluation

2.8 million annual emergency room

visits for headache (U.S. statistics)

Less than 10% of emergency room

patients with chief complaint of
headache will have emergent
secondary cause

Classification of
Headaches
Primary headache
disorders
Secondary headache
disorders

Epidemiology
Primary Headache
h
h
h

Lifetime Prevalence

Tension
Migraine
Cluster

69%
15%
0.1%

Secondary Headache
h
h
h
h
h
h
h

Hangover
Fever
Metabolic disorder
Disorders of nose/sinuses
Head trauma
Disorders of eyes
Vascular disorders

72%
63%
22%
15%
4%
3%
1%

Approach to a
Patient with
HEADACHE

How to approach the patient

with a headache
Need to distinguish primary from
secondary headache disorders
This can be done by obtaining an
accurate history and performing a
focused physical exam.

Questions to Ask in Obtaining a

Headache History
Is this your FIRST or WORST
headache?
How bad is your pain on a scale of 1
to 10?
Do you have headaches on a regular
basis?
When did this headache begin?
How did it start (gradually, suddenly,
other)?

Questions to Ask in Obtaining a

Headache History
Where is your pain?
Does the pain seem to spread to
any other area? If so, where?
What kind of pain do you have
(throbbing, stabbing, dull,
other)?

Questions to Ask in
Obtaining a Headache
History
Do you have other medical
problems? If so, what?
Do you take any medicines?
If so, what?
Do any of your family
members have headaches?

Performing the
physical exam
The primary purpose of the
physical examination is to
identify causes of secondary
headaches
Only a minority of
headaches are secondary,
but this category contains
the most life -threatening
conditions

Performing the physical

exam

PE should include vital signs,

cardiovascular, head, and neck
examinations
A complete neurologic
examination is essential
(including funduscopic exam)

Performing the
neurological exam
mental status
level of
consciousness
cranial nerve
testing
pupillary
responses
funduscopic exam
motor strength
testing

sensation
pathologic reflexes
(e.g. Babinski's
sign)
cerebellar function
and gait testing
signs of meningeal
irritation (Kernig's
and Brudzinski's
signs)

Funduscopic exam

Papilledema

Diagnostic Alarms

Onset after age 50

Sudden onset

Increased frequency
and severity

New onset with risk

factors for HIV or
cancer

Associated with
systemic illness
(fever, meningismus,
rash)

Altered
consciousness or
focal neurologic
deficits

Papilledema

Significant trauma

Warning Signs
Suspected recent
subarachnoid hemorrhage or
meningitis
Other abnormal neurological
signs
hemiparesis
diplopia
ataxia

Decrease in visual acuity or

temporary loss of vision

Warning Signs
Persistent or increasing
vomiting
Seizures
Endocrine disturbances (e.g.
acromegaly, diabetes
insidipus, amenorrhea,
galactorrhea, impaired male
sexual function or beard
growth and poor growth in

Overall Approach
Chief Complaint: HEADCHE
Headache Alarms
Evidence of serious headache disorder
by history or physical exam
NO
Diagnosis of
Primary Headache Disorder
YES
Treat Primary
Headache

YES
Work-up to identify/exclude
Secondary Headache etiology
NO
Consider work-up for
secondary headache

Primary headache is
the illness itself

Primary headaches

Most common type

Have no organic cause
Usually recurrent
Normal neurologic exam
Key to correct diagnosis is the
history

The Primary
Headache Disorders
I.
II.

Migraine
Tension-type
headache
III. Cluster headache

Primary headaches
Differentiated by
Duration
Frequency
Location
Severity
Quality of pain

MIGRAINE
HEADACHE

Migraine headaches

Unilateral
Throbbing pain
Moderate to severe
Aggravated by
movement
4-72 hours
Nausea +/vomiting
Photophobia

Types of Migraine
Migraine without aura
(common migraine)
Migraine with aura
(classical migraine)

Migraine Variants
Ophthalmoplegia
Hemiplegia
Complicated

Phases of Migraine
Premonitory phase
Aura phase
Headache phase
Resolution phase

Migraine
Premonitory
Occurs in more than 50% of cases
Phase

Occurs hours to days before the

headache
The features are psychological,
neurological and autonomic
Reflects limbic/hypothalamic
dysfunction

Migraine

Premonitory
Psychological Neurological
Phase

Depression
Sluggishness
Euphoria
Hyperactivity
Hypertalkativ
e-ness
Drowsiness

Stiff neck

Autonomic

Anorexia

Photophobia

Food craving

Phonophobia

Thirst

Osmophobia

Constipation

Concentration
difficulty

Urination

Cold feeling

Yawning

Migraine
Aura Phase
Present in classical migraine
Develops in > 4 minutes, lasts
less than one hour
Characterized by visual,
sensory, motor, language and
brainstem dysfunctions
Develops headache within one
hour after end of aura

Migraine
Headache Phase

Hemicranial
Gradual onset
Throbbing
Moderate-severe
Duration of 4 72 hours
Aggravated by physical activity
Associated features
Related to trigeminovascular events

Migraine
Resolution Phase
The patient feels bad or
good after disappearance
of the headache

The Modified
Diagnostic
Criteria of
Migraine
of the
International

Migraine without aura

A. At least 5 attacks fulfilling B-D
B. Headache lasting 4-72 hours
C. At least two of the following:
1.
2.
3.
4.

Unilateral location
Pulsating quality
Moderate to severe intensity
Worsened by physical activity

D. At least one of the following: nausea,

vomiting, photophobia, phonophobia
E. Secondary headache is ruled out

Migraine with aura

A. At least 2 attacks fulfilling B
B. At least 3 of the following:

1. One or more fully reversible aura

2. At least one aura symptom develops
gradually over more than 4 minutes
3. No single aura lasts longer than 1 ho
4. Headache follows aura within 1 hour
of the end of aura

C. Secondary headache is excluded

Trigger Factors of
Migraine
Psychological

Physical

Stress

Hormonal Changes

Tension

Sexual activity

Anxiety

Letdown

Changes in sleep
Fatigue

Trigger Factors of
Migraine
Dietary

Environmental

Temperature/
weather changes
Bright light

Odors

High altitude

Alcohol

Certain foods

Missed or
delayed meals

Management of
Migraine
Behavioral modifications
Headache treatment

A. Abortive

B. Preventive

Migraine management

Behavioral Modifications
Regularization of meals, sleep,
exercise
Avoidance of migraine triggers
Avoidance of overuse of analgesics
Stress management

Migraine management
Abortive Pharmacotherapy
Starting doses

Maximum
doses
6 mg

Ergotamine

1-2 mg PO

Sumatriptan

25-100 mg PO

300 mg

Zolmitriptan

6 mg SC

12 mg

Chlorpromazin
e

25-50 mg
IV/IM

400 mg

Prochloperazi
ne

5-10 mg IV/IM

Dexamethaso
ne

40-100 mg PO

120 mg

30-60 mg IM

1500 mg

Prednisone
Ketorolac
Naproxen

4-8 mg PO

250-750 PO

40 mg
32 mg
200 mg

Migraine management
Preventive Pharmacotherapy
Starting doses

Maximum doses

Propranolol

40 mg PO

320 mg

Metoprolol

50 mg PO

450 mg

Flunarizine

5 mg PO

10 mg

Divalproex

250 mg PO

3,000 mg

Methysergide

2mg PO

40 mg

Tolfenamic
acid

100 mg PO

600 mg

25 mg PO

200 mg

Topiramate

Migraine
management
Indications of Preventive
therapy
Diagnosis of migraine
Acute therapy is needed more
than 2x per week
Acute therapy is ineffective,
intolerable, contraindicated
2 or more attacks/month that
produce disability for > 3 days
Headache is associated with
neurologic deficit

TENSION-TYPE
HEADACHES

Tension-Type
Headaches

Band-like, bilateral
Tightness/pressure/ dull ache
Radiates to neck and shoulders
Mild to moderate
Not aggravated by movement
30 min to several days

Tension-Type Headache
(TTH)
Previous Labels
Tension headache
Psychogenic headache
Muscle contraction headache

Tension-type headache
Types
Episodic tension-type headache
Chronic tension-type headache
TTH associated with disorder of
pericranial muscles
TTH unassociated with disorder of
pericranial muscles

Tension-type headache

IHS Diagnostic Criteria

A. At least 2 of the following:

1. Pressing, tightening
2. Mild to moderate severity
3. Bilateral location
4. No aggravation by routine physical
activity
B. Both of the following:
1. No nausea or vomiting
2. No photo/phonophobia, or one of them is
present
C. At least one of the following:
1. No cause for secondary headache
2. If one is present, the onset of the TTH is
not in close
temporal relation to it

Tension-type headache

Management
A. Pharmacological therapy
1. Abortive
2. Preventive
B. Non-pharmacologic therapy
1. Psychophysiologic
2. Physical

Management of TTH
Abortive Pharmacotherapy
Analgesics: paracetamol
NSAIDs : aspirin, indomethacin,
naproxen, ketorolac
Combination: analgesic + caffeine +/butalbital
Muscle relaxants : no proven value

Management of
TTH

Indications for preventive

pharmacotherapy

Headache frequency of > 2x per week

Headache duration of > 3-4 hours
Headache severity that leads to
disability and overuse of abortive drugs

Management of
TTH

Preventive Pharmacotherapy

Tricyclic antidepressants
Selective serotonin re-uptake
inhibitors
Migraine preventive drugs

CLUSTER
HEADACHES

Cluster headaches
Unilateral
Hot poker/
stabbing pain
Excruciating
Autonomic
dysfunction
Restless
15 min to 3 hours

Clinical Features of
Cluster Headache
Striking periodicity: cluster starts in
the same season; headache starts at
the same time
Stereotypical features: same side,
same location
Pain : excruciating, deep, boring
Associated features: autonomic
Headache frequency: usually 1-2/day
Headache duration: 30-180 minutes
Cluster periods: 1-2/year
Cluster duration: 1 week 1 year

Management of
Cluster Headache
Abortive treatment
Preventive treatment
Avoidance of triggers
Surgery of the trigeminal
ganglion

Cluster Headache
Abortive treatment
100% O2 at 7-10 L/min. for 15
mins
Sumatriptan 6 mg SC
Dihydroergotamine 1mg IV/IM
4-6 % Lidocaine, nasally

Cluster Headache
Preventive treatment
Verapamil 120-480 mg
Ergotamine 3-4 mg/day
Lithium carbonate 300 mg BID
Methysergide
Valproate
Corticosteroids

Secondary headache
is the symptom

Secondary Headaches
Certain features of the history
will make you suspect
secondary headache
Physical exam will be abnormal
Focal neurologic findings
Signs of infection
Evidence of head trauma

Secondary Headaches
Findings on history
First or worst HA ever
Sudden-onset headache
Increase frequency & severity of
usual HA
Age > 40 years old
Increase in pain with coughing,
sneezing, straining
Wakes patient from sleep or
disturbs sleep

Secondary Headaches
Findings on history
HIV +
History of cancer
History of head trauma
Symptoms of infection
Fever, nausea, and vomiting
Photophobia
Stiff neck

Secondary Headaches
Findings on PE
unilateral loss of sensation
unilateral weakness
unilateral hyperreflexia
signs of infection

Secondary Headaches
Findings on PE
Head trauma
Papilledema
Changes in mental status
Ataxia

Red Flags on history

Onset after age 40
Temporal arteritis
Mass lesion

Increase frequency and

severity
Subdural hematoma
Mass lesion
Medication overuse

Red Flags on history

Sudden onset of headache
Subarachnoid hemorrhage
Vascular malformation
Mass lesion or hemorrhage
into mass lesion

Red Flags on history

History of head trauma
Intracranial hemorrhage
Subdural hematoma
Epidural hematoma
Post-traumatic headache

Red Flags on history

History of HIV or cancer
Meningitis
Brain abscess
Metastasis
Opportunistic infection

Red Flags on PE
Papilledema
Meningitis
Mass lesion
Pseudotumor cerebri

Diagnostic Studies

Computerized tomography
Hemorrhage, tumor, abscess, AVM

Lumbar puncture
Hemorrhage, infection, increased CSF pressure

MRI, MRA, or Angiography as indicated

Laboratory studies based on
suspected etiologies
ESR: Temporal arteritis
Carboxyhemoglobin: Carbon monoxide

HEADACHES
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