Re: a few things

a_weisman_at_yahoo.com
Date: 02/23/05

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Date: 22 Feb 2005 17:17:07 -0800

a_weisman@yahoo.com wrote:

<snip my own stuff LOl

> I do think we should be much more careful though in using "herxes" to
> corroborate treatment. The term is in my opinion very overused by
> doctors and patients and is applied to such a wide range of
phenomenon
> as to be less helpful than it might be. Every worsening of symptoms
is
> not necessarily a herx--it might indicate treatment failure and
> progression of an illness; it might indicate an illness that has
> cylcical symptoms without any relation to treatment etc. Sometimes it
> is side effects of the meds. I think that "llmds" need to more
narrowly
> define herx and use it corroboratively more sparingly even if this
> means being underinclusive in definining it--so a TRUE herx in my
> opinion and lacking better understanding of it, would be a clear and
> limited exacerbation of existing symptoms and or appearance of new
ones
> in response to initiation of treatment or a new treatment
particularly
> when not typical common side effects of a medication. That might be
> underinclusive yes. But a herx in syphillis is like that. A herx like
> response in Lyme is probably similar. What patients and too many
> "llmds" call herxes I think are actually either side effects or
> cyclical symptoms or other things going on such as other diseases or
> sequelae of Lyme. Either way, calling everything bad that happens
> during treatment a "herx" is not helpful diagnostically and is often
> dangerous (a bad headache might be a brain tumor or could be a side
> effect of the medicine rather than a "herx" and better to rule out
the
> more serious thing than assume it is a "herx"--at some point I'd
rather
> see herx more rigorously applied even if it means not counting some
> things that MIGHT be herxes).
>
> A rationale for limiting herxes to "true herxes" is obvious. And
> ultimately whether a herx or not if the patient is having NO positive
> response to antibiotics, why are they still being prescribed? So a
few
> weeks of treatment later if the patient is just getting worse and
> worse, I don't think one can call that a herx. At some point a
positive
> response, amelioration and or elimination of symptoms or some
symptoms
> is the goal of treatment and if that isn't happening I find it
> difficult to attribute constant and ongoing worsening with no
> improvement to a herx and even if it were, are we going to continue a
> treatment that does nothing but continuosly make a patient worse with
> no improvement seen?

Regarding headaches as "herxes" here is an interesting article. Did you
know that doxycycline can cause severe intracranial hypertension? That
can be threatening to sight?

Lesson of the week: Doxycycline induced intracranial hypertension --
Lochhead and Elston 326 (7390): 641 -- BMJ
http://bmj.bmjjournals.com/cgi/content/full/326/7390/641

BMJ 2003;326:641-642 ( 22 March )

Clinical review
Lesson of the week

Doxycycline induced intracranial hypertension
Doxycycline prescribed for malaria prophylaxis may cause intracranial
hypertension that threatens sight
J Lochhead, specialist registrar, J S Elston, consultant.

Department of Ophthalmology, Oxford Eye Hospital, Radcliffe Infirmary,
Oxford OX2 6HE

Correspondence to: J S Elston mary.spearman@orh.nhs.uk

Preventing malaria in travellers is difficult because of the widespread
emergence of drug resistance and the increasing popularity of travel to
endemic locations. Mefloquine is the most effective recommended
antimalarial, but doxycycline (a tetracycline derivative) is being
increasingly used in areas where there is resistance to mefloquine or
in patients who have side effects to this drug.1

Intracranial hypertension is a well recognised side effect of
tetracyclines and has been associated with the medium to long term use
of minocycline for acne vulgaris.2-6 We report on two patients with
acute onset of severe intracranial hypertension associated with
doxycycline, in one instance causing permanent loss of most vision.

Case reports
Top
Case reports
Discussion
References

Case 1A 21 year old Afro-Caribbean woman who had been on holiday in
Uganda for three weeks complained of headaches and blurred vision. She
had been taking doxycycline 100 mg once daily for malaria prophylaxis
throughout this period. Her vision was 6/9 in the right eye and 6/5 in
the left. She had severe papilloedema with associated haemorrhages and
cotton wool spots, more so in the right eye. A magnetic resonance
imaging scan of the brain was normal. A lumbar puncture had an opening
pressure of 52.5 cm H2O. All other investigations were normal.
Intracranial hypertension was diagnosed and the doxycycline stopped.
Oral acetazolamide 250 mg four times daily was started. Her visual
fields were normal. Symptoms gradually improved, and the lumbar
puncture was repeated after three weeks. The opening pressure was still
high at 40 cm H2O. Cerebrospinal fluid was drained. Her vision was
recorded as 6/5 in both eyes. The papilloedema subsequently resolved.
The acetazolamide was continued for a further two months, after which
it was gradually reduced. During this period and after cessation of the
acetazolamide she remained asymptomatic and had normal optic discs.

Case 2A 19 year old white woman who had been teaching in West Africa
for four months began vomiting spontaneously. She had had mild and
transient headaches the week before. The vomiting continued for three
weeks, and then she developed blurred vision in both eyes. She had been
taking doxycycline 100 mg once daily for malaria prophylaxis throughout
her stay. A computed tomogram of the head was normal. She returned to
the United Kingdom where her vision was recorded as 6/5 in the right
eye and 6/12 in the left. She had reduced colour vision in both eyes
(zero score with Ishihara plates). Examination of her fundi showed
bilateral gross papilloedema with associated haemorrhages and cotton
wool spots (fig 1). Both visual fields were severely constricted, more
so on the left. A magnetic resonance imaging scan of the brain was
normal. Lumbar puncture showed an increased cerebrospinal fluid
pressure of >40 cm H2O with normal cerebrospinal fluid composition. All
other investigations were normal. Intracranial hypertension was
diagnosed and oral acetazolamide 250 mg four times daily started. The
doxycycline was stopped. Over the next two weeks the vomiting became
less frequent but her vision continued to deteriorate to 6/24 in the
right eye and 6/36 in the left. Two further lumbar punctures were
performed over this period, with opening pressures of 18 cm H2O and 36
cm H2O. Her symptoms stabilised, and over the next few days her vision
improved to 6/12 in the right eye and 6/18 in the left. A repeat lumbar
puncture showed a normal opening pressure of 9 cm H2O. The
acetazolamide was tailed off over one month. The disc swelling resolved
rapidly, but consecutive optic atrophy developed (fig 2). Despite
reasonable recovery of central acuity her colour vision and visual
fields remained poor, with an estimated 70% loss of vision.

Fig 1. Swelling of left optic disc

Fig 2. Left consecutive atrophy of optic disc

Discussion

Top
Case reports
Discussion
References
Primary idiopathic intracranial hypertension occurs predominantly in
obese women in their 30s and 40s. It has been referred to as benign
intracranial hypertension. The diagnostic criteria consist of symptoms
and signs of raised intracranial pressure, no other neurological signs,
measured increase in intracranial pressure, normal cerebrospinal fluid
composition, and normal imaging studies.7 Typically, primary idiopathic
intracranial hypertension is a chronic disease with a major long term
risk to vision requiring regular monitoring. 8 9 Treatment includes
weight loss, carbonic anhydrase inhibitors, and occasionally surgery to
lower the intracranial pressure and to protect the optic nerve.
Intracranial hypertension may also occur secondary to several drugs,
including tetracyclines, steroids, nalidixic acid, and amiodarone.3
Several other drug associations have been reported. The mechanism of
these reactions is unknown.5 Stopping the culprit drug leads to
resolution of the intracranial hypertension usually over 2-4 weeks. The
disorder presents in a similar way in both the primary and the
secondary cases, with symptoms and signs of increased cerebrospinal
fluid pressure including headaches, visual obscurations, and occasional
double vision due to paresis of the sixth nerve.

Although the patients described here were slightly overweight neither
was morbidly obese, having a body mass index below 30 kg/m2. In
idiopathic intracranial hypertension associated with poor visual
outcome, the body mass index is usually over 40 kg/m2.10 Investigation
in both cases did not reveal an underlying disorder associated with the
hypertension. The symptoms of raised intracranial pressure began one
and three months after starting doxycycline. The cerebrospinal fluid
pressure was substantially increased and with appropriate treatment and
withdrawal of the drug fell to normal. The evidence that doxycycline
was responsible is therefore compelling.

The unusual feature in the first case was the extent of the increased
intracranial pressure (52.5 cm H2O). The mean intracranial pressure in
acute idiopathic intracranial hyerptension is around 34 (SD 8) cm
H2O.11 Severe acute papilloedema was present with signs of axonal
compromise (haemorrhages and cotton wool spots) not typically seen in
idiopathic intracranial hypertension. Overall vision was, however,
maintained and the patient remained asymptomatic after stopping
treatment at six months.

In the second case, the intracranial pressure was increased to the
extent usually measured in idiopathic intracranial hypertension, but
symptoms had been present for six weeks before the first lumbar
puncture was undertaken and while doxycycline treatment continued. When
the patient was first examined at our institute her vision was severely
reduced, with optic nerve signs indicative of major axonal compromise
(see fig 1). Intracranial pressure returned to normal within three
weeks of starting treatment, but despite some improvement in vision,
the optic discs became atrophic. The resulting visual field defects
make this patient eligible for partial sight registration and leave her
outside the minimum driving requirement.

Intracranial hypertension as a side effect of doxycycline has not been
previously reported. As trends change in the prescribing of
antimalarials, and doxycycline is more widely used, it is important
that prescribers make patients aware of the symptoms associated with
intracranial hypertensionheadaches, visual obscurations, blurred
vision, diplopia, back and neck pain, although occasionally these can
be less specific, as in case 2. If symptoms occur, medical advice
should be sought. Visual acuities should be measured and the optic
discs examined. The successful management of this condition follows
cessation of the drug. Individuals who have had this idiosyncratic
response to doxycycline should probably avoid all tetracyclines.

Doxycycline should be prescribed with caution to women of childbearing
age who are overweight or have a history of idiopathic intracranial
hypertension. Awareness of this side effect is essential among
travellers. Prompt cessation of the drug along with appropriate medical
therapy can curtail an attack of secondary intracranial hypertension,
hence any permanent threat to vision.

Acknowledgments

Contributors: JL and JSE conceived the idea for the paper. Both authors
drafted and revised the article and approved the final version. JSE
will act as guarantor for the paper.

Footnotes

Editorial by Digre

Funding: None.

Competing interests: None declared.
References
Top
Case reports
Discussion
References

1. Juckett G. Malaria prevention in travelers. Am Fam Phys 1999; 59:
2523-2530[ISI][Medline], 2535-6.
2. Goulden V, Glass D, Cunliffe WJ. Safety of long term high-dose
minocycline in the treatment of acne. Br J Dermatol 1996; 134:
693-695[ISI][Medline].
3. Lander CM. Minocycline induced BIH. Clin Exp Neurol 1989; 26:
161-167[Medline].
4. Monaco F, Agnetti V, Mutani R. Benign intracranial hypertension
after minocycline therapy. Eur Neurol 1978; 17: 48-49[ISI][Medline].
5. Stuart BH, Litt IF. Benign intracranial hypertension with
tetracycline therapy. J Paediatr 1978; 93: 901[ISI][Medline].
6. Nagarajan L, Lam GC. Tetracycline-induced benign intracranial
hypertension. J Paediatr Child Health 2000; 36:
82-83[CrossRef][ISI][Medline].
7. Johnston I, Paterson A. Benign intracranial hypertension II. CSF
pressure and circulation. Brain 1974; 97: 301-312[ISI][Medline].
8. Corbett JJ, Savino PJ, Thompson S, Kansu T, Schatz NJ, Orr LS, et
al. Visual loss in pseudotumour verebri. Arch Neurol 1982; 39:
461-474[Abstract].
9. Orcutt JC, Page NG. Factors affecting visual loss in BIH.
Ophthalmology 1984; 91: 1303-1312[ISI][Medline].
10. Rowe FJ, Sarkies NJ. The relationship between obesity and
idiopathic intracranial hypertension. Int J Obes Relat Metab Disord
1999; 23: 54-59[CrossRef].
11. Corbett JJ. Problems in the diagnosis and treatment of
pseudotumour cerebri. Can J Neurol Sci 1983; 10: 221[ISI][Medline].

(Accepted 25 November 2002)

--------------------------------------------------------------------------------

� 2003 BMJ Publishing Group Ltd

Not so benign intracranial hypertension
Kathleen B Digre
BMJ 2003 326: 613-614. [Extract] [Full Text]

This article has been cited by other articles:

K. B Digre
Not so benign intracranial hypertension
BMJ, March 22, 2003; 326(7390): 613 - 614.
[Full Text] [PDF]

--------------------------------------------------------------------------------

Rapid Responses:
Read all Rapid Responses

Nalidixic acid major culprit in children in eastern India
Dhiraj Ahlawat
bmj.com, 24 Mar 2003 [Full text]
Doxycycline, dentists and adverse effects
Trevor LP Watts
bmj.com, 13 Jun 2003 [Full text]

*****************************************************************************

SEE ALSO:
Evaluation of Acute Headaches in Adults - February 15, 2001 - American
Family Physician
http://www.aafp.org/afp/20010215/685.html
Evaluation of Acute Headaches in Adults
C. RANDALL CLINCH, D.O.,
Uniformed Services University of the Health Sciences, F. Edward H�bert
School of Medicine, Bethesda, Maryland
Classifying headaches as primary (migraine, tension-type or cluster) or
secondary can facilitate evaluation and management. A detailed headache
history helps to distinguish among the primary headache disorders. "Red
flags" for secondary disorders include sudden onset of headache, onset
of headache after 50 years of age, increased frequency or severity of
headache, new onset of headache with an underlying medical condition,
headache with concomitant systemic illness, focal neurologic signs or
symptoms, papilledema and headache subsequent to head trauma. A
thorough neurologic examination should be performed, with abnormal
findings warranting neuroimaging to rule out intracranial pathology.
The preferred imaging modality to rule out hemorrhage is noncontrast
computed tomographic (CT) scanning followed by lumbar puncture if the
CT scan is normal. Magnetic resonance imaging (MRI) is more expensive
than CT scanning and less widely available; however, MRI reveals more
detail and is necessary for imaging the posterior fossa. Cerebrospinal
fluid (CSF) analysis can help to confirm or rule out hemorrhage,
infection, tumor and disorders related to CSF hypertension or
hypotension. Referral is appropriate for patients with headaches that
are difficult to diagnose, or that worsen or fail to respond to
management. (Am Fam Physician 2001;63:685-92.)
A PDF version of this document is available. Download PDF now (8
page(s) / 188 KB). More information on using PDF files.

Headache, or cephalalgia, is defined as diffuse pain in various parts
of the head, with the pain not confined to the area of distribution of
a nerve. Headache is among the most common pain problems encountered in
family practice. One epidemiologic study1 found that 95 percent of
young women and 91 percent of young men experienced headache during a
12-month period; 18 percent of these women and 15 percent of these men
consulted a physician because of their headache.

TABLE 1
Acute Primary Headache Disorders
--------------------------------------------------------------------------------

More common
Migraine with or without aura
Tension-type headache
Cluster headache
Less common
Paroxysmal hemicrania
Idiopathic stabbing headache
Cold-stimulus headache
Benign cough headache
Benign exertional headache
Headache associated with sexual activity

--------------------------------------------------------------------------------

Adapted with permission from Classification and diagnostic criteria for
headache disorders, cranial neuralgias and facial pain. Headache
Classification Committee of the International Headache Society.
Cephalalgia 1988;8(suppl 7):1-96.

The direct and indirect costs of migraine have been estimated at
approximately $17 billion per year. Missed workdays and medical
benefits associated with headache cost American industry approximately
$50 billion annually.2

In 1988, the International Headache Society published a classification
system for headache disorders.3 This extensive system is not convenient
to apply in the clinical setting. However, it is diagnostically and
therapeutically useful to consider headaches as being divided into two
categories: primary and secondary. Primary headaches, which include
migraine, tension-type headache and cluster headache, are benign; these
headaches are usually recurrent and have no organic disease as their
cause4 (Table 1).3 Secondary headaches are caused by underlying organic
diseases ranging from sinusitis to subarachnoid hemorrhage (Table 2).3

The primary task of the family physician is to determine whether a
patient has an organic, potentially life-threatening cause of headache.
In most instances, the physician can accurately diagnose a patient's
headache and determine whether additional laboratory testing or
neuroimaging is indicated by considering the various headache types in
each category (primary or secondary), obtaining a thorough headache
history and performing a focused clinical examination.

Headache History

Because most patients with headache have normal neurologic and general
physical examinations, a thorough history is crucial to determining the
etiology of a headache. The approach to the headache history given in
Table 3 and discussed in the following sections facilitates the
generation of a differential diagnosis and preliminary classification
of the headache type based on the criteria established by the
International Headache Society.3 This level of detail is also necessary
to identify "red flags" that suggest an underlying organic disorder as
the cause of headache.5

First or Worst Headache
The question "Is this your first or worst headache?" addresses the
issue of new-onset headache and the age at which it becomes a concern.
Of the two headache classes, primary disorders are more common. These
disorders can occur at any age but most often begin during childhood or
between 20 and 50 years of age.6 Onset of headache after 50 years of
age is a red flag for consideration of a secondary headache disorder
such as temporal arteritis or a mass lesion (Table 4).6

Careful attention to and thoughtful consideration of neuroimaging
and/or cerebrospinal fluid (CSF) analysis are mandatory when a patient
of any age complains of a first or worst headache.7-9 If the patient
routinely has headaches, it is important to determine whether the
current episode is typical.

Primary headache disorders (migraine, tension-type and cluster) are
usually recurrent and have no organic disease as their cause.

Symptoms
The patient should be asked to describe current symptoms as well as
symptoms experienced before and during the headache. This information
can help the physician identify a primary headache disorder such as
cluster headache (ipsilateral lacrimation and/or nasal congestion) or
migraine with aura (e.g., scintillating scotomata, photophobia,
phonophobia, nausea). It is important to note that most patients with
migraine do not have an associated aura.

A potentially life-threatening secondary headache disorder may also be
identified based on the patient's description of symptoms (diplopia,
dimming of vision in a single eye, stiff neck, disorientation, rash,
fever, eye pain, unilateral paresthesias, unilateral weakness, balance
change, etc.). Symptoms suggesting a secondary headache disorder
require further investigation.

Onset
Questions should be asked about the time and nature of headache onset
(e.g., gradual, sudden, subacute). Secondary headache disorders that
may have a sudden, severe onset include subarachnoid hemorrhage,
vascular malformations (ruptured or unruptured), acute ischemic
cerebrovascular disorder or posterior fossa mass lesions.

TABLE 2
Acute Secondary Headache Disorders
--------------------------------------------------------------------------------

Headache associated with head trauma
Acute post-traumatic headache
Headache associated with vascular disorders
Subarachnoid hemorrhage
Acute ischemic cerebrovascular disorder
Unruptured vascular malformation
Arteritis (e.g., temporal arteritis)
Carotid or vertebral artery pain
Venous thrombosis
Arterial hypertension
Headache associated with nonvascular intracranial disorder
Benign intracranial hypertension (pseudotumor cerebri)
Intracranial infection
Low cerebrospinal fluid pressure (e.g., headache subsequent to lumbar
puncture)
Headache associated with substance use or withdrawal
Acute use or exposure
Chronic use or exposure Headache associated with noncephalic infection

Viral infection
Bacterial infection
Headache associated with metabolic disorder
Hypoxia
Hypercapnia
Mixed hypoxia and hypercapnia
Hypoglycemia
Dialysis
Other metabolic abnormality
Headache or facial pain associated with disorder of cranium, neck,
eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial
structures
Cranial neuralgias, nerve trunk pain and deafferentation pain

Location and Radiation of Pain
It is important to determine the location of a patient's pain and
whether the pain radiates to another area. Cluster headaches are
strictly unilateral (Table 5),3 whereas tension-type headaches are
usually band-like and bilateral (Table 6).3 Migraines generally begin
unilaterally but may progress to involve the entire head (Table 7).3

Pain along the distribution of the temporal artery may suggest temporal
arteritis, and pain along the distribution of the trigeminal nerve may
be a sign of trigeminal neuralgia (tic douloureux). Eye pain may
suggest acute glaucoma.

Quality of Pain
A patient's pain may be throbbing, stabbing, dull, pressure-like or
other. Based on the patient's description of pain quality, the
physician may be able to further classify the headache as migraine,
tension-type or cluster (Tables 5, 6 and 7).3

TABLE 3
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 (1 means not too bad, and 10 means very bad)? Do you have
headaches on a regular basis? Is this headache like the ones you
usually have?

What symptoms do you have before the headache starts? What symptoms do
you have during the headache? What symptoms do you have right now?

When did this headache begin? How did it start (gradually, suddenly,
other)?

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)?

Do you have other medical problems? If so, what?

Do you take any medicines? If so, what?

Have you recently hurt your head or had a medical or dental procedure?

Concurrent Medical Conditions
An organic cause of headache is more likely in patients with human
immunodeficiency virus infection, cancer or another chronic medical
condition (e.g., hypertension with a diastolic pressure higher than 110
mm Hg).10 Organic causes might include meningitis (chronic or
carcinomatous), central nervous system (CNS) lymphoma, toxoplasmosis,
metastases or intracranial vascular disorder. The patient who has an
acute viral syndrome or an acute bacterial infection (e.g., sinusitis)
often presents with acute headache in addition to disease-specific
complaints.

Medications
Prescription and over-the-counter medications (especially
caffeine-containing analgesics) have been implicated as triggers for
drug-rebound and nonspecific headaches.2 Thus, it is important to
review any medication that a patient is taking for its potential to
cause headache. A search of the online Physicians' Desk Reference, 54th
ed.,11 yielded more than 1,000 references to medications with headache
as a side effect.

TABLE 4
Red Flags in the Evaluation of Acute Headaches in Adults
--------------------------------------------------------------------------------

Red flag Differential diagnosis Possible work-up
Headache beginning after 50 years of age Temporal arteritis, mass
lesion Erythrocyte sedimentation rate, neuroimaging
Sudden onset of headache Subarachnoid hemorrhage, pituitary apoplexy,
hemorrhage into a mass lesion or vascular malformation, mass lesion
(especially posterior fossa mass) Neuroimaging; lumbar puncture if
neuroimaging is negative*
Headaches increasing in frequency and severity Mass lesion, subdural
hematoma, medication overuse Neuroimaging, drug screen
New-onset headache in a patient with risk factors for HIV infection or
cancer Meningitis (chronic or carcinomatous), brain abscess
(including toxoplasmosis), metastasis Neuroimaging; lumbar puncture
if neuroimaging is negative*
Headache with signs of systemic illness (fever, stiff neck, rash)
Meningitis, encephalitis, Lyme disease, systemic infection, collagen
vascular disease Neuroimaging, lumbar puncture,� serology
Focal neurologic signs or symptoms of disease (other than typical aura)
Mass lesion, vascular malformation, stroke, collagen vascular disease
Neuroimaging, collagen vascular evaluation (including
antiphospholipid antibodies)
Papilledema Mass lesion, pseudotumor cerebri, meningitis
Neuroimaging, lumbar puncture�
Headache subsequent to head trauma Intracranial hemorrhage, subdural
hematoma, epidural hematoma, post-traumatic headache Neuroimaging of
brain, skull and, possibly, cervical spine

HIV = human immunodeficiency virus.
*--Lumbar puncture may follow a negative neuroimaging procedure if
suspicion of hemorrhage, infection or malignancy remains high.
�--Suspicion of specific central nervous system infections (Lyme
disease, syphilis, etc.) or intracranial hypertension (pseudotumor
cerebri) warrants lumbar puncture with cerebrospinal fluid analysis and
pressure measurement.

Adapted with permission from Newman LC, Lipton RB. Emergency department
evaluation of headache. Neurol Clin 1998;16:285-303.

Drug-related intracranial hypertension can occur with use of
antibiotics (e.g., tetracycline, minocycline [Minocin],
trimethoprim-sulfamethoxazole [Bactrim, Septra], nalidixic acid
[NegGram]), corticosteroids and other drugs (e.g., isotretinoin
[Accutane], tamoxifen [Nolvadex], cimetidine [Tagamet]).12

Recent Trauma or Procedures
Headache subsequent to trauma may signify a postconcussive disorder,
although intracranial hemorrhage should always be suspected. Migraine
and cluster headaches may be triggered by head trauma.6 Headache has
also been associated with common medical procedures (e.g., lumbar
puncture, rhinoscopy) and dental procedures (e.g., tooth extraction).

Physical Examination

The primary purpose of the physical examination is to identify causes
of secondary headaches. The examination should target areas identified
as abnormal during the headache history. The general physical
examination should include vital signs, funduscopic and cardiovascular
assessment, and palpation of the head and face.

TABLE 5
Diagnostic Criteria for Cluster Headache
--------------------------------------------------------------------------------

At least five attacks fulfilling criteria B through D
Severe unilateral orbital, supraorbital and/or temporal pain lasting 15
to 180 minutes (untreated)
Headache associated with at least one of the following signs on the
pain side:
Conjunctival injection
Lacrimation
Nasal congestion
Rhinorrhea
Forehead and facial sweating
Miosis
Ptosis
Eyelid edema
Frequency of attacks: one attack every other day to eight attacks per
day

--------------------------------------------------------------------------------

TABLE 6
Diagnostic Criteria for Episodic Tension-Type Headache
--------------------------------------------------------------------------------

At least 10 previous headache episodes fulfilling criteria B through D;

number of days with such headaches: less than 180 days per year
Headache lasting from 30 minutes to 7 days
At least two of the following pain characteristics:
Pressing or tightening (nonpulsating) quality
Mild or moderate intensity
Bilateral location
No aggravation by walking stairs or similar routine physical activity
Both of the following:
No nausea or vomiting (anorexia may occur)
Photophobia and phonophobia are absent, or one but not the other is
present.

--------------------------------------------------------------------------------

A complete neurologic examination is essential, and the findings must
be documented. The examination should include mental status, level of
consciousness, cranial nerve testing, pupillary responses, motor
strength testing, deep tendon reflexes, sensation, pathologic reflexes
(e.g. Babinski's sign), cerebellar function and gait testing, and signs
of meningeal irritation (Kernig's and Brudzinski's signs). Particular
attention should be given to detecting problems related to the optic,
oculomotor, trochlear and abducens nerves (cranial nerves II, III, IV
and VI, respectively).

TABLE 7
Diagnostic Criteria for Migraine
--------------------------------------------------------------------------------

Migraine without aura

At least five attacks fulfilling criteria B through D
Headache lasting 4 to 72 hours (untreated or unsuccessfully treated)
At least two of the following pain characteristics:
Unilateral location
Pulsating quality
Moderate or severe intensity
Aggravation by walking stairs or similar physical activity
During headache, at least one of the following:
Nausea and/or vomiting
Photophobia and phonophobia
Migraine with aura

At least two attacks fulfilling criterion B
At least three of the following characteristics:
One or more fully reversible aura symptoms indicating focal cerebral
cortical and/or brain-stem dysfunction
At least one aura symptom develops gradually over more than 4 minutes,
or two or more symptoms occur in succession.
No aura symptom lasts more than 60 minutes; if more than one aura
symptom is present, accepted duration is proportionally increased.
Headache follows aura, with a free interval of less than 60 minutes
(headache may also begin before or simultaneously with aura).

--------------------------------------------------------------------------------

Red Flags

Only a minority of headaches are secondary, but this category contains
the most life-threatening diagnoses (Table 2).3 Although prospective
studies are lacking, several publications have commented on historical
and physical findings that are considered red flags for serious
problems based on clinical experience2,5,6,9,10,13-15 (Table 4).6
Currently, these findings offer the best means of identifying a
secondary headache disorder.

Focal neurologic findings should prompt additional evaluation. Among
others, these findings include unilateral loss of sensation, unilateral
weakness, unilateral hyperreflexia and papilledema.

Possible work-ups for various red flags are listed in Table 4.6 Limited
laboratory testing might include a complete blood count when systemic
or intracranial infection is suspected or an erythrocyte sedimentation
rate (ESR) when temporal arteritis is a possibility. In temporal
arteritis, the ESR is usually elevated to above 50 mm per hour; this
disorder should be considered in all patients older than 50 years. CSF
analysis is warranted in patients with red flags who have normal
neuroimaging.

Cluster headaches are strictly unilateral, whereas tension-type
headaches are usually band-like and bilateral. Migraines generally
begin unilaterally but may progress to involve the entire head.

Random use of laboratory testing in the evaluation of acute headache is
not warranted. In certain situations, referral to a headache
subspecialist may be appropriate (Table 8).2

Neuroimaging

To provide quality yet cost-effective care, the physician needs to know
when to order computed tomographic (CT) scanning or magnetic resonance
imaging (MRI) in the evaluation of an adult patient with acute headache
disorder. The Ambulatory Sentinel Practice Network,16 a group of
community primary care practices in the United States and Canada,
conducted a collaborative clinical research study to examine the
reasons that physicians ordered CT scanning during the evaluation of
headaches.

The study16 found that CT scans were ordered for approximately 3
percent of patients with headache. In most instances, CT scanning was
ordered because a tumor (49 percent) or subarachnoid hemorrhage (9
percent) was suspected. Patient expectations and medicolegal concerns
were the reasons for 17 percent of CT scans. Although almost one half
of CT scans were ordered to search for a brain tumor, the evidence does
not support this level of concern. Data from a prospective study17
revealed that isolated headache was the first and only clinical symptom
in just 8.2 percent of patients with intracranial tumor.

TABLE 8
Diagnostic Criteria for Episodic Tension-Type Headache
--------------------------------------------------------------------------------

Physician has inadequate level of comfort in diagnosing or treating
patient's headache.
Patient requests a referral.
Patient does not respond to treatment.
Patient's condition or disability continues or worsens.
Physician is unable to classify patient's headache according to
diagnostic criteria for primary or secondary headache disorders.

Habituation or rebound headaches limit outpatient management.

Patient has intractable or daily headaches.

--------------------------------------------------------------------------------

Information from Solomon GD, Cady RK, Klapper JA, Ryan RE. Standards of
care for treating headache in primary care practice. National Headache
Foundation. Cleve Clin J Med 1997;64:373-83.

Factors to consider in deciding whether to order CT or MRI studies
include the need to identify acute hemorrhage (CT scanning is
preferred), the need to evaluate the posterior fossa (MRI studies are
preferred), general availability (CT scanning is more available) and
cost and reimbursement issues (CT scanning is less expensive). Barring
these factors, MRI is more sensitive than CT scanning in identifying
pathologic intracranial changes. However, it is uncertain whether the
identification of additional pathology on MRI studies would improve
outcomes, because the percentage of abnormalities noted on CT scans
that potentially benefit from neurosurgical intervention is already
extremely small (as low as 0.01 percent).9

The U.S. Headache Consortium18 recently developed evidence-based
guidelines for the use of neuroimaging in patients with nonacute
headache (i.e., headache occurring at least four weeks during a
patient's lifetime). Grade A recommendations are based on multiple,
well-designed, randomized clinical trials and a consistent relevant
pattern of findings. Grade B recommendations are supported by some
evidence from clinical trials, but supportive evidence is not optimal.
Grade C recommendations are based on consensus in the absence of
sufficient data from controlled trials.

According to the consortium's guidelines, neuroimaging should be
considered in patients with nonacute headache and an unexplained
abnormal finding on the neurologic examination (grade B
recommendation). Neuroimaging is not usually warranted in patients with
migraine and a normal neurologic examination (grade B recommendation).
Because insufficient evidence was available, the consortium panel made
no recommendations for neuroimaging in patients with or without
neurologic symptoms, such as headache causing awakening from sleep
(grade C recommendation).

Lumbar Puncture and Electroencephalography

CT scanning without contrast medium, followed by lumbar puncture if the
scan is negative, is preferred to rule out subarachnoid hemorrhage
within the first 48 hours. A negative CT scan and a negative lumbar
puncture do not completely rule out subarachnoid hemorrhage because it
may take hours for blood to enter the CSF after hemorrhage. If a
relatively recent hemorrhage is suspected, the CSF should be evaluated
for xanthochromia, which is a yellow discoloration detectable on
spectrophotometry. Xanthochromia may be present for at least a week
after a subarachnoid hemorrhage.19

Focal neurologic findings detected on the physical examination should
be considered "red flags" and warrant additional evaluation.

Lumbar puncture is useful for assessing the CSF for blood, infection
and cellular abnormalities. It is also important for documenting
abnormalities of CSF pressure that might be related to headache.
Headaches are associated with low CSF pressure (less than 90 mm of
water as measured by a manometer) and elevated CSF pressure (greater
than 200 to 250 mm of water).19 Headaches related to CSF hypotension
include those caused by post-traumatic leakage of CSF (i.e., after
lumbar puncture or CNS trauma). Headaches related to CSF hypertension
include those associated with idiopathic intracranial hypertension and
CNS space-occupying lesions (i.e., tumor, infectious mass, hemorrhage).

The National Headache Foundation reports that electroencephalography
(EEG) has "not been shown to effectively identify headache subtypes or
headaches caused by structural defects."2(p375) Hence, routine use of
EEG in the evaluation of headaches is not warranted.

The opinions expressed herein are the private views of the author and
are not to be construed as official or as reflecting the views of the
Uniformed Services University, U.S. Air Force or U.S. Department of
Defense.

The author thanks Jeannette E. South-Paul, COL, MC, USA, Thomas Miller,
CAPT, MC, USN, Francis G. O'Connor, LTC, MC, USA, and Joanne Clinch,
M.D., for their gracious and expert assistance with the review of the
manuscript.

Members of various family practice departments develop articles for
"Problem-Oriented Diagnosis." This article is one in a series
coordinated by the Department of Family Medicine at the Uniformed
Services University of the Health Sciences, Bethesda, Md. Guest editors
of the series are Francis G. O'Connor, LTC, MC, USA, and Jeannette E.
South-Paul, COL, MC, USA.

--------------------------------------------------------------------------------

The Author

C. RANDAL CLINCH, D.O.,
is currently assistant professor and associate director of clinical
operations in the Department of Family and Community Medicine at Wake
Forest University School of Medicine, Bowman Gray Campus,
Winston-Salem, N.C. Previously he was director of the predoctoral
programs division in the Department of Family Medicine at the Uniformed
Services University of the Health Sciences, F. Edward H�bert School of
Medicine, Bethesda, Md. Dr. Clinch received a doctor of osteopathy
degree from the University of Medicine and Dentistry of New Jersey
School of Osteopathic Medicine, Stratford, N.J., and completed a family
medicine residency at Somerset Medical Center, Somerville, N.J. He has
also completed the National Institutes of Health's core course in
clinical research.

Address correspondence to C. Randall Clinch, D.O., Department of Family
and Community Medicine, Wake Forest University School of Medicine,
Bowman Gray Campus, Medical Center Blvd., Winston-Salem, NC 27157-1084
(e-mail: crclinch@wfubmc.edu). Reprints are not available from the
author.

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Copyright � 2001 by the American Academy of Family Physicians.
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