Prim Care Clin Office Pract

31 (2004) 381–393

Secondary headache and head pain

emergencies
Kenneth S. Peters, MD
Northern California Headache Clinic, 515 South Drive, Suite 15, Mountain View,
CA 94040, USA

The vast majority of patients presenting to primary care physicians

complaining of headache have primary headaches, such as migraine, tension,
or cluster. The Landmark study [1], which evaluated headache patients
presenting to a primary care physician, found that most have migraine.
Secondary or organic headaches, however, always need to be considered,
because when present they require prompt diagnosis and intervention.
Approximately 10% of patients [2] presenting to the emergency department
complaining of headache have a secondary headache, and as many as one in
three sudden severe headaches in patients presenting to a general practition-
er’s office can be attributed to an urgent neurologic condition that requires
rapid evaluation and management [3].
There are several diagnostic headache features that differentiate primary
from secondary headaches [4]. The primary headache features are comfort
signs and strongly suggest a diagnosis of migraine. These include:
A stable pattern
A positive family history of migraine
Head pain that improves with sleep
Head pain that is worsened during the menstrual cycle
A normal physical and neurologic examination
Uncomfortable features caused by secondary headache that can serve as
red flags include:
The first or worst headache
An abrupt new headache or change in headache pattern
Onset of headache after the age of 50 years
A headache that disrupts sleep or is present on awakening
Headache brought on by exertion

E-mail address: kpeters@pacbell.net

0095-4543/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2004.02.009
382 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

Headache that is brought on by coughing or is positional (ie, brought on

by straining, bending over, or lifting)
History of recent head trauma
History of associated chronic illness, such as cancer or HIV
History of systemic illness, such as fever
Association of headache with neck stiffness
Association of headache with change in personality, behavior, or
alteration in consciousness
Abnormal neurologic examination
The major causes of secondary headache include:
Infection, including meningitis, sinusitis, encephalitis, HIV, and Lyme
disease
An underlying structural abnormality, such as brain tumor
Cerebrovascular ischemia
Hemorrhage (subarachnoid or parenchymal)
Head trauma
Cerebral vein thrombosis
Malignant hypertension
AV malformation and aneurysm
Intraocular disease, such as glaucoma
Temporomandibular joint disorders
Dental disease
Cervical spine disease
Diseases of the occipitocervical junction, including Arnold-Chiari type I
malformation
Metabolic or toxic causes, such as headache caused by carbon monoxide
poisoning
CNS disturbance of intracranial pressure, either high or low
Vasculitis or connective tissue disease
The diagnosis of secondary headache is based on obtaining a careful
history, physical, and neurologic examination [5,6]. Appropriate laboratory
studies may include blood and CSF evaluation and radiologic examination
when indicated.

History
The important features of a headache history include:
Number and types of headaches present
Age and circumstances of onset
Family history of headaches
Characteristics of the pain
Location
Frequency of attacks
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 383

Duration of pain
Description of pain
Time of onset of the attack
Whether there are any prodromal symptoms or aura
Associated systemic symptoms, such as
Nausea, vomiting, or sensitivity to light, sound, and worsening of pain
with exertion, postural change, straining, or coughing
Neurologic symptoms consisting of weakness of arms or legs,
coordination problems, speech problems, cognitive changes,
seizures, or alteration of consciousness
History of head trauma
Precipitating factors of the headache
Environmental
Psychologic
Nutritional
Hormonal
Postural: do the headaches change with body position or bending over,
are they worsened with exertion, coughing or straining?
Temporomandibular joint symptoms, such as jaw pain, clenching, or
grinding
Previous diagnostic tests, including MRI, CAT scans, and pertinent
laboratory data
Response to medication, past and present [7]

Physical examination
Physical examination should include [8]:
Vital signs: a fever could suggest meningitis, especially if it is associated
with neck stiffness. Fever also can be seen in a patient with brain abscess
and encephalitis. A blood pressure should be obtained. Headaches
caused by hypertension are rare unless the diastolic pressure is greater
than 110 mm/Hg or there is other evidence of malignant hypertension.
The head should be examined carefully. If there is a prominent temporal
artery that is erythematous, tender, or has a decreased pulse, this is
highly suggestive of temporal arteritis. The eyes should be examined
carefully. If the eye is red and there is associated decreased visual
acuity, tonometry should be performed to rule out acute closed angle
glaucoma. The presence of unilateral ptosis could be suggestive of
a carotid dissection. Examination of the sinuses and nose should be
done to rule out acute sinusitis causing headaches. If one is considering
trigeminal neuralgia, one should check for trigger points in the face. If
the history is suggestive, look for signs of head trauma.
The neck should be evaluated for decreased range of motion, muscle
spasm, and tenderness. It is important to remember that neck pain is
384 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

seen in approximately 75% of migraineurs and can occur during the

prodrome headache or the postdrome phases of migraine [9]. If there
are abnormalities on physical examination and radiographic evidence
of cervical disk disease, one should consider cervicogenic headache.
Careful neurologic examination should include evaluation of the patient’s
level of alertness and orientation and evaluation of the cranial nerves,
evaluation of sensorimotor functioning, and tests of coordination,
including gait, Romberg test, tandem walk, finger-to-nose and heel-to-
shin tests.

Neuroimaging
See Box 1 for indications for neuroimaging [10]. Noncontrast CT head
scans should be done for evaluating acute onset headaches to evaluate for
bleed, such as subarachnoid hemorrhage. MRI brain scan is the procedure
of choice in patients coming in with subacute or chronic headaches. The
more common secondary headaches are covered in greater detail later [11].
Magnetic resonance angiogram (MRA) is helpful in diagnosing
aneurysms that are greater than 3 mm. If the MRA is suggestive of an

Box 1. Indications for neuroimaging

 Any unexplained abnormality on the neurologic examination
 Rapidly increasing headache frequency
 History of being awakened by headache
 Severe vertigo or lack of coordination
 Subjective numbness or tingling
 History of intravenous drug misuse, other intravenous risk
factors, or exposure to active tuberculosis
 History of recent head trauma or falls in elderly patients
 New-onset headache after age 50 years
 Constant headache, worsening in horizontal position
 Headache precipitated by coughing, sexual activity, or
exercise
 Headache associated with fever, personality change, or
transient altered consciousness
 Thunderclap headache
 Trigeminal neuralgia in a young adult (MRI to rule out
multiple sclerosis)

From Silberstein S. Evaluation of the Headache patient. In: Silberstein S, editor.

Clinician’s manual on migraine 2nd edition. Philadelphia: Current Medicine, Inc.,
2002. p. 9.
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 385

aneurysm, one should proceed to a cerebral arteriogram for confirmation.

MRA is also the best test for diagnosing carotid or vertebral dissections.
Magnetic resonance venography is best used for diagnosing central venous
sinus thrombosis. Other diagnostic tests obtained from blood include CBC
to rule out anemia. Hypothyroidism also has been associated with
headaches and therefore a free T4 and TSH should be obtained. Erythrocyte
sedimentation rate (ESR) and C-reactive protein are helpful screening tests
for evaluation of patients when temporal arteritis is considered.
Other diagnostic studies include lumbar puncture, which is necessary to
diagnose meningitis. Lumbar puncture also is performed in patients with
possible subarachnoid hemorrhage to evaluate for xanthochromia and to
diagnose disturbance of intracranial pressure.

Secondary headaches
Secondary or organic headache can be divided into three categories that
present as:
Acute sudden onset
Subacute, rapid but not sudden buildup; these headaches can be
intermittent or persistent
Headaches that have an insidious, gradual, progressive course, with
chronic buildup
Causes of headaches that present with an acute, sudden onset include:
Intracranial hemorrhage, including subarachnoid hemorrhage, intrace-
rebral hemorrhage, acute subdural or epidural hematoma, and
pituitary hemorrhage
Acute closed angle glaucoma
Acute severe hypertension
Internal carotid or vertebral arterial dissection
Head trauma causing a hemorrhage or cavernous sinus thrombosis
Spontaneous low CSF pressure headaches
Acute obstructive hydrocephalus from a tumor
Headaches that have a subacute onset that may have rapid but not
sudden buildup include:
Meningitis/encephalitis
Sinusitis
Cerebral vein thrombosis
Ischemic cerebrovascular disease
Cerebral vasculitis
Those headaches that have a more gradual buildup include:
Brain tumor
Chronic subdural hematoma
386 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

Brain abscess
Temporal arteritis
Idiopathic intracranial hypertension (pseudotumor cerebri)
Intracranial infection such as Lyme disease, AIDS, or other systemic
infections, and chronic sinusitis

Headaches presenting with acute sudden onset that require a rapid

diagnosis and treatment
Subarachnoid hemorrhage
In patients without a history of previous headaches who present with
their first or worst headache, the physician should consider a diagnosis of
subarachnoid hemorrhage. Subarachnoid hemorrhage usually results from
a rupture of a pre-existing aneurysm or arterial–venous malformation.
Rarely it can occur secondary to a hypercoagulable state, and even less
commonly from an intracranial tumor or vasculitis. The quality of the
headache is usually violent and sudden in onset, with maximum intensity
reached within a few seconds to minutes. These types of headaches are
commonly called thunderclap headaches. The headache often is accompa-
nied by nausea, vomiting, and alteration in level of consciousness, including
syncope, and severe hypertension and nuchal rigidity. Focal neurologic
symptoms are rare. Nuchal rigidity is seen in most patients with
a subarachnoid bleed; however, it can take several hours to develop. Its
absence therefore should not be used to exclude a diagnosis. Patients also
can complain of a sentinel headache of sudden onset that is less intense and
severe than thunderclap headaches. These types of headaches can represent
a warning leak of impending catastrophic bleed and can occur days to weeks
before the aneurysm rupture. The definitive diagnosis of subarachnoid
hemorrhage is obtained by performing a noncontrast head CT scan. The
sensitivity of the CT scan is approximately 90% within the first 12 hours
after hemorrhage. If one suspects subarachnoid bleed with a normal CT
scan, one therefore should proceed with a lumbar puncture evaluating for
xanthochromia. Once a diagnosis is made the physician should proceed with
prompt neurosurgical consultation [12].

Spontaneous parenchymal hemorrhage

The patient can present with sudden onset headaches that are similar to
the pain of a subarachnoid bleed; however, they usually are associated with
acute neurologic symptoms and focal abnormalities on neurologic
examination. It usually occurs in patients with uncontrolled hypertension.
Usually a noncontrast CT scan shows evidence of the bleed. If this is
negative, however, one should proceed with an MRI with gadolinium to
evaluate the pituitary gland to rule out pituitary apoplexy [13].
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 387

Internal carotid or vertebral dissections

The headache caused by internal carotid or vertebral dissections can be
gradual or thunderclap in quality. It is usually ipsilateral to the dissection
and can be frontal or occipital. Usually there is a delay of 3–4 days between
the onset of headaches and other neurologic symptoms. The most common
neurologic signs consist of Horner syndrome (ptosis, myosis, anhidrosis,
and flushing on the affected side of the face). There also may be symptoms
of a transient ischemic attack associated with transient monarticular
blindness and pulsatile tinnitus. Dissections can occur with patients on oral
contraceptives, central venous thrombosis, or with head trauma that can be
minimal. There have been case reports of dissection following chiropractic
manipulation or after unusual head positions. The diagnostic test of choice
is an MR angiogram of the neck [14].

Acute subdural hematoma

Acute subdural hematoma usually comes on after head trauma and is
seen commonly in alcoholic patients who have frequent falls. Often the
patient presents with headache associated with confusion, drowsiness, and
agitation. Usually there are focal neurologic signs, the most common one
being hemiparesis. Focal seizures also can occur. Less commonly seen are
epidural hematomas caused by head trauma causing laceration of the
middle meningeal artery by the undersurface of the temporal bone. There is
classically an initial period of lucidity followed by headache, agitation, and
decreased level of consciousness. Neurologic deterioration following
a significant closed head injury should merit immediate diagnostic
evaluation. Noncontrast CT scans usually suffice for diagnosis, and
a prompt neurosurgical consultation should be obtained once the diagnosis
is made [15].

Acute malignant hypertension

Usually blood pressures are in the 180/120–130 mm Hg range.
Hypertensive encephalopathy can manifest as headache associated with
focal neurologic findings and seizures, obtundation, and alterations in level
of consciousness. Prompt blood pressure lowering through pharmacologic
intervention is necessary. A very rare cause of headache associated with
severe hypertension is pheochromocytoma, which is a usually benign tumor
of the adrenal gland that secretes catecholamines that can cause periodic or
sustained hypertension associated with severe headache. There is usually
associated sweating, palpitations, and either flushing or pallor. A diagnosis
is made by obtaining a 24-hour urine for catecholamines, metanephrines,
norepinephrines, and VMA (vanillymandelic acid). A CT or MRI can be
diagnostic for an adrenal mass. Usually the hypertension and headaches
resolve after surgical removal of the tumor [16,17].
388 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

CSF hypotension
The headache seen in CSF hypotension is classically postural in that it
occurs or worsens within 15 minutes of going from a lying to an upright
position and disappears within 30 minutes of assuming a recumbent
position. The headache is usually bilateral frontal and is associated with
nausea, vomiting, dizziness, and tinnitus. One of the most common causes is
a persistent CSF leak post-lumbar puncture. MRI with gadolinium often
shows slit-shaped ventricles and diffuse meningeal enhancement. The
diagnosis is confirmed by a finding of a CSF pressure of less than 40 mm
Hg. Isotope cisternography can be done to locate the leak. Treatment can
consist of fluid replacement, bed rest, epidural blood patching, and caffeine
sodium infusion [18,19].

Obstructive hydrocephalus
Obstructive hydrocephalus can produce headache with gait change and
change in cognition. Usually the headache is worsened by neck movement
or bending over. Enlargement of the ventricular system is seen by CT scan
or MRI. Headaches also can be associated with Arnold-Chiari type I
malformations, which are caused by low-lying cerebellar tonsils that
intermittently obstruct CSF flow, causing episodic elevated intracranial
pressure. Classic symptoms consist of headache exacerbated by straining,
coughing, or bending over [18].

Acute closed angle glaucoma

Patients usually present with the sudden onset of eye pain and blurred
vision associated with halo reflections around lights. Pupils are often fixed in
mid-dilation. Acute closed angle glaucoma can be triggered by anticholin-
ergic medication. Tenonometry usually reveals intraocular pressures greater
than 40–80 mm Hg. Prompt ophthalmologic consultation is obtained once
glaucoma is diagnosed [20].

Headaches with a subacute presentation and rapid but not sudden buildup
Meningitis
Bacterial meningitis may present with either focal or diffuse severe
headache accompanied by the classic signs of neck stiffness, fever, and
altered level of consciousness. Rapid diagnosis is crucial and is based on
CSF evaluation by a lumbar puncture. In a study evaluating the accuracy of
bedside evaluation for meningitis by Thomas Ke et al, it was found that
Kernig sign, increased pain with flexion of the neck, and Brudzinski sign,
increased pain with extension of the flexed knee, had very low sensitivity for
detection of meningitis [21]. Nuchal rigidity had a sensitivity of only 30%.
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 389

Lumbar puncture therefore should be done in any patient who presents with
new onset of headache associated with fever. If there is a delay, a CT scan
should be done to rule out increased intracranial pressure before a lumbar
puncture is done. Rapid administration of antibiotics is lifesaving. A patient
also can present with a headache caused by viral meningitis. Usually these
patients are less severely ill than those with bacterial meningitis. The CSF
shows predominant lymphocytosis without evidence of bacteria. Patients
with encephalitis also can present with headache and fever. They usually
have an association with alteration in consciousness, seizures, or other focal
neurologic abnormalities.

Acute sinusitis
Acute sinusitis can present with a subacute onset headache. Patients
usually have purulent nasal discharge, pain localized over the involved
sinuses, and low grade fevers. Usually the diagnosis is made clinically;
however, the diagnostic test of choice is a coronal CT scan of the sinuses.
Patients who present with sinus symptoms, such as lacrimation, rhinorrhea,
and nasal congestion, usually have migraine, not sinusitis [22].

Cerebral vein thrombosis

Cerebral vein thrombosis should be considered in patients who have
seizures, focal neurologic deficits, and headache. It is seen more commonly
in patients who have hypercoagulable states, trauma, or rheumatologic
disorders. The sinuses most commonly involved are the superior sagittal and
medial sinuses. A magnetic resonance venogram is the diagnostic test of
choice. Once a diagnosis of CVST is made, treatment consists of prompt
anticoagulation [23].

Cerebral ischemia
A headache can be one of the symptoms of a cerebrovascular accident.
Usually a headache is a minor complaint when the cause is a cerebral
thrombosis or embolus. There are focal neurologic symptoms and signs that
lead one to this diagnosis. A noncontrast CT scan acutely followed by an MRI
at least 4 hours later are helpful tools in diagnosing cerebrovascular accidents.
There may be a mild headache associated with transient ischemic attacks that
usually present with neurologic symptoms lasting less than 1 hour [24,25].

Cerebral vasculitis
Patients with cerebral vasculitis often have other systemic diseases, such
as systemic lupus erythematosus. Patients often have evidence of fever and
seem clinically systemically ill. The MRI often shows many white matter
abnormalities. Rheumatologic consultation should be obtained once this
diagnosis is made [26].
390 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

Dental infections
Dental infections occasionally can cause chronic headaches. The most
common cause is pain related to dental caries causing a pulpitis. Dental
consultation should be obtained. Usually there is associated clenching,
bruxism, and TMJ tenderness. Patients may benefit from a TMJ splint [27].

Headaches presenting with insidious chronic buildup

Brain tumor
Rarely do patients present with headache caused by brain tumor as an
isolated complaint. The headache usually is preceded by neurologic
symptoms, such as seizure, hemiparesis, ataxia, and cognitive or speech
impairment. The headache can be intermittent or constant. Classically the
headache can disrupt sleep and is there upon awakening. It is also classically
associated with body positions, such as bending over or straining. There is
no correlation between tumor size and headache intensity. The progressive
symptoms of the headache usually are related to cerebral edema. An MRI
brain scan is the diagnostic test of choice. If metastatic disease is considered,
one should order an MRI with gadolinium [28].

Chronic subdural hematomas

Chronic subdural hematomas often manifest weeks to months after
injury, and associated symptoms include headache, apathy, confusion, and
inappropriate behavior. Often headache is worsened by sudden head
movements. Elderly patients who present with mental deterioration without
headache may have a hematoma. Patients often do not give a history of
trauma. There may be cranial percussion tenderness over the site of the
hematoma. Patients who present with mental deterioration and headache
should be evaluated for chronic subdural hematoma by obtaining an MRI
brain scan [13].

Brain abscess
Brain abscess usually presents with symptoms related to cerebral edema
causing increased intracranial pressure. Early symptoms include headache
associated with seizures, nausea, vomiting, and fever. MRI with contrast is
the diagnostic test of choice [29].

Arteriovenous (AV) malformations and cerebral aneurysms

Cerebral aneurysms are often present at birth, but symptoms do not
manifest until later in life. Bleeds from AVMs or aneurysms can present
acutely as subarachnoid hemorrhage. (See the previous discussion regarding
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 391

subarachnoid hemorrhage.) AVMs also can manifest as the new onset of

seizures and other focal neurologic deficits. If a patient complains of exertional
headaches or headaches associated with sexual orgasm, one should obtain an
MRA to rule out aneurysm or AVM. If an aneurysm or AV malformation is
found, one should proceed with cerebral arteriography and prompt
neurosurgical consultation [30].

Temporal arteritis
Temporal arteritis should be considered in patients older than age 50 years
who present with new onset of headache. Other associated symptoms include
jaw claudication, visual complaints, fatigue, or symptoms of polymyalgia
rheumatica, which includes pain in the hips or shoulders. The patient may
experience weight loss, fever, or night sweats. Often on physical examination
the patient has evidence of a tender, erythematous temporal artery with
a decreased pulse. The physician should obtain a STAT sedimentation rate
by Westergren method (ESR). The ESR is usually greater than 60 mm/hour.
A C-reactive protein also can be used as a confirmatory diagnostic test; it
may be more sensitive than the ESR. If one suspects temporal arteritis, one
should place the patient on 60 mg of prednisone and order a temporal artery
biopsy. Immediate treatment with prednisone is necessary to prevent
irreversible blindness [31].

Idiopathic intracranial hypertension (pseudotumor cerebri)

Idiopathic intracranial hypertension is associated with visual obscuration
and papilledema caused by intracerebral pressure. Usually the headache is
a generalized frontal headache, but it may be unilateral or bilateral. It is
often worsened by bending over or straining. There may be progressive
visual loss. This is seen most commonly in obese women of childbearing age.
The average age of onset is 30 years. CTs and MRIs are helpful to rule out
intracerebral masses. Often there are visual field defects. One should refer to
an ophthalmologist to confirm papilledema and to do a formal visual field
examination. The diagnosis is confirmed by a lumbar puncture showing
elevation of CSF pressure. Treatment consists of episodic lumbar punctures
to reduce intracerebral pressure, weight reduction, and pharmacotherapy
consisting of acetazolamide, diuretics, or steroids. In resistant cases,
ventricular shunts are effective [18].

Cervicogenic headache
This headache usually is characterized by continuous, unilateral pain
radiating from the occipital areas and spreading to the frontal area,
associated with neck pain. The pain can be exacerbated by neck movements.
Cervicogenic headache usually is caused by neck trauma. Diagnostic nerve
blocks can help determine which cervical discs are involved. Cervicogenic
392 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393

headache is best treated with physical therapy, use of NSAIDs, and

therapeutic nerve blocks [32].

References
[1] Dowson A, Tepper S, Dahloff C, Newman L. The landmark study. In press
[2] Linn FH, Wijdicks EF, van der Graaf Y, Weerdesteyn-van Vliet FA, Bartelds AI, van Gijn
J. Prospective study of sentinel headache in aneurysmal subarachnoid hemorrhage. Lancet
1994;344:590–3.
[3] Balmaceda C, Rossi J. Detecting potentially life-threatening headache syndromes. J Crit
Illn 2003;18:23–30.
[4] Saper J, Silberstein S, Gordon C, Hamel R, Swidan S. Diagnostic evaluation of the patient.
In: Handbook of headache management: a practical guide to diagnosis and treatment of
head, neck, and facial pain. 2nd ed. Baltimore (MD): Lippincott Williams and Wilkins;
1999. p. 15–6.
[5] Diamond S. Headaches due to organic causes. In: Diagnosing and managing headaches.
3rd ed. Chicago: Professional Communications, Inc.; 2001. p. 33–54.
[6] Evans R, Rozen T, Adelman J. Neuroimaging and other diagnostic testing in headache. In:
Silbersein S, Lipton R, Dalession D, editors. Wolff’s headache and other head pain. New
York: Oxford University Press; 2001. p. 27–49.
[7] Couch J. Complexities of presentation and pathogenesis of migraine headache. In: Cady R,
Fox A, editors. Treating the headache patient. New York: Marcel Dekker, Inc.; 1995.
p. 15–40.
[8] Standards of Care Committee. Headache diagnosis and treatment. Chicago: National
Headache Foundation; 1999.
[9] Kaniecki R. Migraine and tension-type headache: an assessment of challenges in diagnosis.
Neurology 2002;58(Suppl 6):S15–20.
[10] Silberstein S. Evaluation of the headache patient. In: Silberstein S, editor. Clinician’s
manual on migraine. 2nd ed. Philadelphia: Current Medicine; 2002. p. 9.
[11] U.S. Headache Consortium. Evidence-based guidelines for migraine headache: overview,
pharmacological management of acute attacks, pharmacological management for pre-
vention of migraine, neuroimaging in patients with nonacute headache, behavioral and
physical treatments. Neurology 2000;54:1553.
[12] Jakobsson K, Saveland H, Hillman J, Edner G, Zygmunt S, Brandt L, et al. Warning leak
and management outcome in aneurysmal subarachnoid hemorrhage. J Neurosurg 1996;85:
995–9.
[13] Melo T, Pinto A, Ferro J. Headache in intracerebral hematomas. Neurology 1996;47:
494–500.
[14] Silbert P, Mokri B, Schievink WI. Headache and neck pain in spontaneous internal carotid
and vertebral artery dissections. Neurology 1995;45:1517–22.
[15] Silberstein S, Lipton R, Dalessio D. Overview diagnosis and classification of headache. In:
Silberstein S, Lipton R, Dalessio D, editors. Wolff’s headache and other head pain. New
York: Oxford University Press; 2001. p. 6–26.
[16] Strandgaard S, Henry P. Arterial hypertension. In: Oleson J, Tfelt-Hansen P, Welch K,
editors. The headaches. New York: Raven Press; 1993. p. 675–8.
[17] Raskin N, Appenzeller O. Headache. Philadelphia: WB Saunders; 1980.
[18] Silberstein S, Marcelis J. Headache associated with changes in intracranial pressure.
Headache 1992;32:84–94.
[19] Pannullo S, Reich J, Krol G, Deck MD, Posner JB. MRI changes in intracranial
hypotension. Neurology 1993;43:919–26.
[20] Martin T, Corbett J. Disorders of the eye. In: Silberstein S, Lipton R, Dalessio D, editors.
Wolff’s headache and other head pain. New York: Oxford University Press; 2001.
p. 459–74.
 K.S. Peters / Prim Care Clin Office Pract 31 (2004) 381–393 393

[21] Ke T, et al. The diagnostic accuracy of Kernig’s sign, Brudzinski’s sign, and nuchal rigidity
in adults with suspected meningitis. Clin Infect Dis 2002;335:46–52.
[22] Schreiber C, Hutchinson S, Powers C, Webster C, Richardson M. Patient self-diagnosed
and physician-diagnosed ‘‘sinus’’ headache is predominately migraine and responds to
open-treatment with sumatriptan. Neurology 2003;60(Suppl 1):A493.
[23] Bousser M, Russell R. Cerebral venous thrombosis. In: Bousser M, Russell R, editors.
Major problems in neurology. London: WB Saunders; 1997. p. 175.
[24] Gorelick P. Ischemic stroke and intracranial hematoma. In: Olesen J, Tfelt-Hansen P,
Welch K, editors. The headaches. New York: Raven Press; 1993. p. 639–45.
[25] Ferro J, Melo T, Oliveira V, Salgado AV, Crespo M, Canhao P, et al. A multivariate study
of headache associated with ischemic stroke. Headache 1995;35:315–9.
[26] Bousser M, Good J, Kittner S, Silberstein S. Headache associated with vascular disorders.
In: Silberstein S, Lipton R, Dalessio D, et al, editors. Wolff’s headache and other head
pain. New York: Oxford University Press; 2001. p. 366–71.
[27] Graff-Radford S. Disorders of the mouth and teeth. In: Silberstein S, Lipton R, Dalessio
D, editors. Wolff’s headache and other head pain. New York: Oxford University Press;
2001. p. 475–93.
[28] Forsythe P, Posner J. Headache in patients with brain tumors: a study of 111 patients.
Neurology 1993;43:1678–83.
[29] Chun CH, Johnson JD, Hofstetter M, Raff MJ. Brain abscess: a study of 45 consecutive
cases. Medicine (Baltimore) 1986;65:415–31.
[30] Arteriovenous Malformation Study Group. Arteriovenous malformations of the brain in
adults. N Engl J Med 1999;340:1812–8.
[31] AbuRhama A, Thaxton L. Temporal arteritis: diagnostic and therapeutic considerations.
Am Surg 1996;62:449–51.
[32] Jansen J, Bardosi A, Hildebrandt J, Lucke A. Cervicogenic, hemicranial attacks associated
with vascular irritation or compression of the cervical nerve root C2: clinical
manifestations and morphological findings. Pain 1989;39:203–12.