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Diagnosing and Managing Headaches - Chaper 3

Seymour Diamond, MD

Chapter 3: Headaches Due to Organic Causes

3.1 - Introduction
3.2 - Tumor
3.3 - Hematomas
3.4 - Subarachnoid Hemorrhage
3.5 - Brain Abscess
3.6 - Arteriovenous Malformations
3.7 - Infections
3.8 - Low Cerebrospinal Fluid Pressure Headache
3.9 - Chronic or Marked Increases in
Intracranial Pressure
3.10 - Cranial Arteritis
3.11 - Major Neuralgias
3.12 - Temporomandibular Joint Disorder
References 


3.1 Introduction

The classification of organic headache includes headache due to:

Space occupying lesion 
Infection 
Low cerebrospinal fluid (CSF) pressure 
Cranial arteritis 
Major neuralgias. 

As with other types of headache, diagnosis is based on:

History 
Physical examination 
Laboratory results 
Radiologic examinations. 

All patients must undergo careful and thorough examinations to rule out these possibly morbid causes. Selection of therapy is totally dependent on the cause of the headaches.

Physicians should always be alert to recent onset of headaches starting in a patient age 40 or older. They should also be vigilant in evaluating the patient who has experienced a recent change in a headache pattern that had been consistent for many years. The physician should also be wary of the presentation of recent onset of headache in a patient with a prior history of cancer.

A headache produced by an intracranial lesion is usually attributed to:

Inflammation 
Traction 
Displacement of the pain-sensitive structures of the head, most often the
blood vessels. 

The term "traction headache" is based on the displacement of these structures as a result of traction.

The following pattern is demonstrated in headaches resulting from intracranial
lesions:

A steady, non-throbbing, deep, dull ache 
The headache can awaken the patient from a sound sleep 
The headache is intermittent, although it can be continuous in some patients 
The headache is rarely as intense as the headache associated with fever 
Exertion can trigger or exacerbate the headache 
The frequency and duration will progressively increase. 

Headache is always a cardinal sign of rapidly increasing intracranial pressure. However, a slow growing tumor may cause a dull, transitory headache that is relieved by simple analgesics. Some generalizations can be made about headache due to brain tumor:

In about one third of patients with headache due to brain tumor, the pain
overlies the tumor. However, in the remaining patients, the headache may be
referred from a distant intracranial source.  A tumor below the tentorium will frequently cause occipital pain and cervical muscle spasm.  A tumor above the tentorium will often manifest as a headache at the vertex or in the frontal regions.  If the tumor is at the midline, exertion such as coughing, straining or sudden head movement can exacerbate the headache.  A tumor that is chiasmal at the sella may cause the pain to be referred to the vertex.  A posterior fossa tumor usually manifests as a headache.  If the tumor is hemispheric, the headache is usually felt on the ipsilateral side.  A lesion in the pituitary fossa often causes a frontal and bitemporal headache, which is bursting in character. Pain is often present behind the ear in a cerebellopontine angle lesion. 

Headache rarely occurs as an initial symptom with several lesions, such as craniopharyngiomas and hypophysial adenomas. However, it can be an initial manifestation with other tumors, such as:

Meningiomas 
Gliomas. 

Meningiomas (which compress the brain from the outside) will cause seizures, focal symptoms, and/or progressive impairment of intellectual function before they will produce a headache. The slow growth and bone invasions of these lesions probably counter the effects of their proximity to pain-sensitive structures.

Gliomas and large infiltrating tumors can advance throughout one hemisphere
without causing headache because the position of the large vessels is not disturbed. These lesions may cause headache early due to their rapid growth and possible occlusion of the lateral, third and fourth ventricle.

The headache associated with hematomas is similar to that described previously in this chapter. There are no characteristic symptoms that will help the physician differentiate an acute subdural hematoma from a cerebral contusion or laceration. Chronic subdural hematomas may occur after trivial or closed-head trauma. Although headache is a prominent symptom of subdural hematoma, the diagnosis will be difficult to establish if the patient presents in a confused state. Other symptoms of acute subdural hematoma are:

Drowsiness 
Confusion 
Slowness in thinking 
Occasional agitation. 

These symptoms will progressively intensify. Focal and lateralizing signs occur late
and are less prominent than the disturbance in consciousness. In both the subacute
and chronic types of subdural hematomas, the clinical picture resembles the
presentation of progressive supratentorial mass. Its characteristics include:

Hemiparesis 
Focal seizures 
Choked discs. 

In distinguishing the types of subdural hematomas, the following should be
considered:

Acute subdural hematomas usually become clinically significant within 48
hours of injury. 
Subacute subdural hematomas will become clinically significant within 2 to 14
days after injury. 
Chronic subdural hematomas will become clinically significant 14 or more
days after injury. 

Headache is not an important clinical sign in acute subdural hematoma since the
patient is often unconscious upon admission after severe head injury. Headache may
or may not be present in patients with subacute subdural hematomas. Surgical
intervention is usually indicated in these patients as these hematomas rarely absorb
spontaneously.

Headache is the most common complaint of patients with the chronic form. The
injury experienced by these patients is usually mild to moderate, and a history of
injury may be absent. If the headache is not treated, progressive signs of brain
compression may occur and are often nonlocalizing and nonspecific. These
symptoms include:

Apathy 
Inappropriate behavior 
Confusion. 

Sudden head movements or jolts can exacerbate the headache. Head tapping can
be used as a clinical sign. In the elderly, chronic subdural hematoma may present as
mental deterioration without headache.

Epidural hematoma most often presents in the patient after injury to the middle
meningeal artery on the under surface of the temporal bone. As the injured patient
progresses from a complaint of headache to restlessness, the physician should be
concerned about the possibility of expanding intracranial mass. As the lesion
increases in size and produces brain compression and decreasing levels of
consciousness, the patient may be combative, restless and not necessarily complain
of headache.


3.4 Subarachnoid Hemorrhage
After head injury, bleeding into the subarachnoid space may occur. It is the most
common cause of intracranial hemorrhage or may be secondary to intracerebral
hemorrhage. The bleeding may also occur spontaneously from:

Preexisting aneurysms 
Vascular malformations 

Rarely:

Blood dyscrasia 
Intracranial tumor 
Some form of arteritis. 

The clinical presentation for all subarachnoid hemorrhage is:

Acute onset of severe headache 
Frontal or diffuse pain radiating to the neck, back and even the lower
extremities 
The patient will describe the pain as "the worst headache ever" 
Within minutes, a variable degree of mental confusion may occur. 

Blood in the subarachnoid space causes a chemical meningitis. The "meningeal signs"
include:

Stiff neck 
Kernig's sign (inability to extend the leg with the thigh flexed) 
Mildly elevated temperature, pulse and blood pressure. 

Signs and symptoms following a subarachnoid hemorrhage are largely due to
vascular spasm resulting in brain ischemia, infarct and cerebral edema. The cause of
a subarachnoid hemorrhage may be suggested by:

A history of progressive neurological deficits 
A history of seizure disorder 
Auscultating a cranial bruit. 

These signs would suggest an intracranial vascular malformation. Aneurysms may be
symptomatic before hemorrhage and cause varied degrees of headache or
extraocular paresis by compression of the third cranial nerve. Easy bruising or
prolonged bleeding from lumbar or venipuncture sites may indicate blood dyscrasia.

Generally, an unruptured aneurysm does not require surgical intervention. The
performance of invasive diagnostic procedures should be minimized with unruptured
aneurysms.


3.5 Brain Abscess

The signs and symptoms of brain abscess are comparable to those with an
intracranial expanding lesion. Cerebral edema is significant in the pathophysiology.
Early symptoms include:

Headache 
Nausea 
Vomiting 
Seizures. 

Brain abscess may be due to:

Active or acute bacterial infections involving extracranial sites 
Extracranial fungal and parasitic infections. 

Early diagnosis can expedite treatment measures and be established by specific
procedures, including:

Chest x-ray to rule out lung abscess 
EEG to rule out characteristic focal high- voltage waves 
Complete blood count 
Computed tomography (CT) scan or magnetic resonance imaging (MRI). 

Parenchymal abscess is often associated with disease of adjacent nasal and aural
structures, and the patient may experience headache from the latter source before
brain tissue is actually involved. A headache will not occur until the abscess is of
adequate size to cause traction and displacement, usually 2 months after the
parenchymal breakdown has started. The abscess will then be of maximal size,
walled off, and have become a cystic tumor that gradually developed in size from
accumulation of fluid. The headache of brain abscess is usually associated with:

Leukocytosis 
Fever 
Pleocytosis. 

Brain abscess from ear infections may occur either above or below the tentorium.
Evidence of brain stem embarrassment occurs early in the illness and includes:

Hiccoughing 
Vomiting 
Occipital headache. 

Epidural abscess is often present in headache associated with sinus disease and
osteomyelitis of the adjacent bony wall, and which persists after drainage of the
sinus. These epidural abscesses occur in the frontal region adjacent to the diseased
sinus, which may be:

Frontal sinus 
Ethmoid sinus 
Sphenoid sinus. 

Also, the abscess may occur after osteomyelitis of the mastoid bone in the
postauricular occipital region.


3.6 Arteriovenous Malformations

Arteriovenous malformations (AVMs) vary in size from a mass of tortuous vessels
occupying most of one cerebral hemisphere to barely visible blemishes involving any
part of the brain. Although an AVM may be present at birth, the symptoms may not
manifest until adolescence or in early adulthood. Occasionally, the symptoms may
never occur. The AVMs attain clinical significance depending on the major
neurological complications associated with or caused by the malformation, including:

Subarachnoid hemorrhage 
Seizure disorder 
Progressive neurological deficits. 

The presence of AVMs can be established by CT scanning or MRI.


3.7 Infections

Headache associated with fever and stiff neck should always alert the physician to
the possibility of meningitis. Meningitis may be caused by a variety of sources:

Viral infection 
Bacterial infection 
Fungal infection 
Blood disorder 
Metastatic disease to the meninges, such as lymphoma. 

The symptoms of meningitis are determined by:

Type of structure involved 
Degree of inflammation 
Location of the inflammatory process. 

The headache associated with meningitis is:

Severe and global 
Throbbing in nature 
Associated with: 
Nausea 
Vomiting 
Photophobia 
Stiff neck 
An alteration in the level of consciousness (occasionally) 
Occasional occurrence of a rash. 

It may be due to the extreme reflex spasm of the cervical musculature. In the early
stages, with mild to moderate headache and minimal neck stiffness, the cause may
be attributed to influenza. Lumbar puncture will establish the diagnosis. A morbid
outcome of this disorder may be prevented with:

Early diagnosis 
Aggressive antibiotic therapy. 

Four other conditions may be mistaken for meningitis. The common element in these
disorders is severe headache and/or the presence of resistance to anterior flexion of
the neck. These conditions include:

Retropharyngeal abscess, particularly in children 
Superior longitudinal sinus thrombosis 
Subarachnoid hemorrhage 
Meningismus that may accompany certain infections, such as typhoid fever. 


continued... 
3.8 Low Cerebrospinal Fluid Pressure Headache

The most common form of low CSF pressure headache is the post-puncture
headache. This headache may be mild or severe and occur within a few hours to
several days after lumbar puncture. The headache duration varies from a few days
to several weeks. One in four patients undergoing lumbar puncture will experience
these headaches. The pain of these headaches is described as:

A dull, deep ache or throbbing 
Bifrontal or suboccipital 
May be associated with moderate neck stiffness. 

The most recognized characteristic of these headaches is the occurrence when the
patient is erect and its disappearance when the patient is horizontal. Pain may be
exacerbated with shaking the head. This headache is usually resistant to all forms of
treatment except bed rest in the horizontal position and the passage of time. Its
cause is attributed to the loss of CSF secondary to leakage through the dural hole.

Other causes of low CSF pressure headache have been identified:

Primary intracranial hypotension 
CSF rhinorrhea 
Inappropriate ventricular shunt. 

The appropriate therapy for these disorders is correction of the cause.


continued...3.9 Chronic or Marked Increases in Intracranial Pressure

Two disorders are identified as causing these headaches:

Acute hydrocephalus 
Benign intracranial hypertension. 

Acute hydrocephalus occurs in patients with ventricular obstruction or with shunt
malfunction in a treated hydrocephalic patient. The severe headache is followed by
visual disturbances. Emergency ventricular drainage must be completed rapidly to
prevent permanent neurological deficit or death.

No specific cause can be established for benign intracranial hypertension (BIH)
although there is evidence of increased intracranial pressure. Because this disorder
can stop spontaneously, it is described as benign. However, permanent visual loss
may occur. Etiological factors which may be involved include:

Menstrual dysfunction 
Adrenal deficiency 
Corticosteroid therapy 
Hypoparathyroidism 
Vitamin A intoxication 
Tetracycline administration in infants 
Poisons 
Insecticides. 

The one finding common to all these cases of BIH is papilledema. Other symptoms
include:

Generalized headache 
Giddiness 
Vomiting 
Blurred vision in some cases 
Rarely, seizures 
Patient's feeling and appearance of well-being are striking. 

Pseudotumor is one of the syndromes associated with BIH. The symptoms include:

Nonspecific, intermittent headache 
Present for several weeks or months before seeking medical advice. 

There is a high incidence of this disorder in young, obese females. The resting spinal
pressures vary from 220 mg to 600 mm of water. The spinal fluid is always:

Clear 
Colorless 
Exhibiting no abnormality of cellular or chemical constituents 
Protein count of the CSF is unusually low. 

Most patients respond well to acetazolamide. Some patients will require shunt
placement.


3.10 Cranial Arteritis

Headaches due to cranial arteritis are related to inflammatory processes of
undetermined cause, which are limited to the cranial arteries. In the process, the
elasticity of the arterial walls seems to fade as the tissues appear frayed or
fragmented. Giant cells within the vessel walls are most numerous in the region of the
deranged internal elastic lamina. The pain is evoked by inflammatory responses that
include those of the pain-sensitive structures of the head. The headaches occur
coincidentally with the inflammatory process and once the disease is managed, the
headaches do not recur.

Giant cell arteritis is also referred to as temporal arteritis. The classification
committee of the International Headache Society requires one of the following
criteria to establish the diagnosis of giant cell arteritis:

Swollen and tender scalp artery (usually superficial temporal artery) 
Elevated RBC sedimentation rate 
Disappearance of headache within 48 hours of the initiation of steroid
therapy. 

Diagnosis is confirmed with a temporal artery biopsy that will demonstrate giant cell
arteritis.

The physician should be alert to this disorder in patients over age 50 experiencing
recent onset of headache. The physician should obtain a sedimentation rate by
Westergren's method on all patients over age 50. In patients with giant cell arteritis,
the sedimentation rate is usually above 60 mm/hr, although some patients may
present with normal sedimentation rates. Early diagnosis and treatment are essential
to prevent the irreversible blindness associated with this disorder.

The headache is probably the most prominent presenting complaint. Patients will
describe it as:

Very severe intensity 
Often unilateral, localized over one temple; however, the pain may be bilateral
Throbbing or boring 
Occasionally, a stabbing sensation across the temporal area 
Often having a burning component. 

The headache is often worse when the patient lies flat in bed and decreases in
severity when the patient is sitting upright. Applying pressure to the common carotid
artery may diminish the pain, and stooping may exacerbate the pain.

Many patients will present a history similar to rheumatoid arthritis and giant cell
arteritis is often associated with polymyalgia rheumatica. Other symptoms include:

Night sweating 
Aching of the joints 
Fever 
Weight loss. 

The patient may experience pain or discomfort on opening the mouth as well as pain
and stiffness in the area of the temporomandibular joint. Intermittent claudication of
the jaw may be triggered by excessive chewing, thus resulting in weight loss. Facial
swelling and red nodules may be observed over the temporal region. The visual
symptoms may develop 5 or more months after the symptoms manifest. These
symptoms are believed to be caused by a decrease in the blood supply to the optic
nerve, and include:

Ophthalmoplegia 
Diplopia 
Ptosis 
Other symptoms of ocular motor paralysis. 

Resultant ischemia of the optic nerve occurs in about 50% of untreated patients.
Many patients with untreated giant cell arteritis may experience transient visual
blurring before the onset of the irreversible blindness.

Because imminent treatment is essential to prevent the blindness, therapy with
corticosteroids should be initiated before receiving the results of the biopsy. The
usual starting dose is prednisone 40 mg to 60 mg daily. Maintenance dose is 10 mg
to 20 mg per day, with the sedimentation rate used as a guide in administering the
drug. The disease process usually disappears 6 to 8 months after initiation of
therapy.

Before the major manifestation of giant cell arteritis, pain may occur in other areas
including:

Teeth 
Jaw 
Ear 
Zygoma 
Nuchal area 
Occiput. 

These symptoms indicate involvement of other branches of the external carotid
artery, particularly the external and internal maxillary arteries. Other arteries may be
involved including:

Major vessels of the aorta 
Coronary arteries 
Arteries of the limbs. 

The large and medium size arteries are the principal sites of the inflammatory
process.


continued... 
3.11 Major Neuralgias

Major neuralgias include trigeminal neuralgia and glossopharyngeal neuralgia.
Trigeminal neuralgia is also known as tic douloureux. Characteristically, trigeminal
neuralgia consists of:

Episodic, recurrent pain 
Unilateral location, more common on the right side of the face 
Rarely begins before age 50 
Female to male ratio is 2:1. 

This disorder rarely occurs before age 30 unless the patient has concomitant multiple
sclerosis.

The pain is of high intensity and particularly affects trigger zones that are increased
areas of sensitivity on the face, especially above the nares and mouth. When
stimulated, these areas will trigger the attacks, often by trivial stimulation. Because of
these trigger zones, the patient will demonstrate the "avoidance mechanism." This
mechanism is a major diagnostic clue. The patient with trigeminal neuralgia will
typically avoid washing the face, shaving, chewing or any other action that will
stimulate a trigger zone. Because many trigger zones are located in or near the oral
cavity, patients with trigeminal neuralgia will lose a great deal of weight.

The distribution of trigeminal neuralgia affects the second or third divisions of the fifth
cranial nerve and will radiate to the first division late in the disease. Patients have
described the pain as:

Short, sharp, momentary bursts, like electric shock or a rapid repeating rifle 
Excruciating and severe enough to cause the patient to cry out or twitch 
Periods of remission are interrupted by attacks caused by stimulation of the
trigger zones 
High intensity jabs last less than 20 to 30 seconds with short-term remission
periods lasting a few seconds, followed by another jab of pain. 

Treatment of choice for trigeminal neuralgia is anticonvulsant therapy. These drugs
will reduce the sensitivity of the trigger zones as well as relieve the pain, often
dramatically, within hours after initiation of therapy. Table 3.1 reviews the agents
used for trigeminal neuralgia. Initial therapy is carbamazepine 100 mg to 200 mg 2
or 3 times per day. If this dose is well tolerated and if the pain is quickly relieved,
the drug may be continued for an indefinite period, depending on the course of the
disease. Severity of the pain will determine the titration of the drug. Maintenance
dose is usually 200 mg per day.

If the symptoms persist, phenytoin may be added to the regimen in doses up to 400
mg per day. Chlorphenesin should be considered if the patient is refractory to the
first two agents. This drug is prescribed in doses of 400 mg 3 to 4 times daily.
Surgical intervention may be considered if the patient has reached a three-drug
treatment level. Baclofen has been used successfully in refractory trigeminal neuralgia
at doses of 60 mg to 80 mg per day.

The final stage in therapy may be surgical intervention (Table 3.2). Surgical
procedures should only be considered after other methods have failed and include:

Glycerol injections 
Radiofrequency rhizotomy 
Microsurgical decompression of the trigeminal root. 

Because the decompression of the trigeminal root requires a formal craniotomy,
resulting in extended hospitalizations and convalescence, glycerol injections are
preferred. These injections are accomplished rapidly.

Glossopharyngeal neuralgia is similar to trigeminal neuralgia except that the
symptoms manifest from the anatomical base of the glossopharyngeal nerve. This
pain is usually located in the: 

Pharynx 
Tonsils 
Ear. 

It can be triggered by swallowing, yawning or eating. Treatment is similar to that of
trigeminal neuralgia.

Certain atypical neuralgias may present which cannot be categorized according to
the symptomatology and are not associated with trigger zones. The pain does not
occur as jabs but rather as continuous pain. Atypical facial pain can be described as:

Steady diffuse aching, not neuritic 
Continuous for hours, days, months 
No trigger zones 
Often localized tenderness 
May have a vascular component 
May radiate to other regions of the face, neck, cranium. 

Autonomic symptoms may also occur and include:

Cutaneous pallor 
Sweating 
Flushing 
Rhinitis. 

To alter the responses to autonomic stimuli, the patient may respond to
beta-blockers, including propranolol. Due to the chronic nature of atypical facial
pain, the patient has the potential to develop depression or habituation problems. A
multidisciplinary approach to this patient, possibly in an inpatient facility, may be
indicated. Psychological testing and counseling may be required in patients with
atypical facial pain. Treatment measures include:

Non-habituating analgesics 
Antidepressants 
Nerve blocks 
Transcutaneous electrical stimulation 
Biofeedback 
Psychological counseling. 

Some patients will experience postinfectious neuralgia, particularly as a complication
of herpes zoster of the face and head. This neuralgia most often affects the elderly.
Most of these affected patients will demonstrate pain with involvement of the
gasserian ganglion. In some patients, the ophthalmic division of the nerve is infected,
or present with a herpetic rash in the external auditory canal with facial palsy
(Ramsay Hunt syndrome). Unfortunately, the pain of postherpetic neuralgia will
dominate the remaining years of these patients. The pain of postherpetic neuralgia
has been described as:

Steady and sustained 
Almost always unilateral 
Burning and aching 
Frequently interrupts sleep. 

Diagnosis is usually obvious as the scars of the herpetic eruption are apparent, and
trophic changes to the skin may result from this disorder. The pain of herpes zoster
usually abates within 2 to 3 weeks although the neuralgia may persist for months or
years.

These patients also tend to develop depression and dependency problems. The
tricyclic antidepressants may be beneficial although the dose increases should be
undertaken cautiously in elderly patients. The addition of a phenothiazine may be
considered. These patients require reassurance and patience, and may need
psychological counseling. Surgical intervention is not indicated for these patients.

3.12 - Temporomandibular Joint Disorder

Temporomandibular joint (TMJ) disorder is one of the most overly publicized and
overly diagnosed disorders. Symptoms of TMJ disorder include:

Localized facial pain 
Limitation of motion of the jaw 
Muscle tenderness 
Joint crepitus. 

The pain of TMJ disorder is usually localized in front of and behind the ear on the
affected side. This pain may radiate over the cheek and face. X-rays of the jaw are
usually normal. Due to the localized pain, the patient will always use the opposite
side of the mouth for chewing, thus splinting the painful side. There is no evidence
that hearing loss, damage to the cranial nerves, disturbances of equilibrium,
development of Ménière's syndrome, or difficulty with the eustachian tubes are
associated with TMJ disorder.

Pain relief of TMJ disorder should be directed toward abating muscle spasm. Mouth
reconstructions are usually not indicated and extensive oral surgery should not be
undertaken unless other measures have failed. Simple analgesics and muscle relaxant agents, such as chlorphenesin, may be beneficial. Non-drug methods, such as heat, hot packs and massage, may be beneficial. Dental splints and similar procedures may prove helpful.

References for:
Chapter 3: Headaches Due to Organic Causes

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Dr. Seymour Diamond, is Director of the Diamond Headache Clinic and the Inpatient Headache Unit, Columbus Hospital, Chicago, Illinois. He is adjunct Professor of Pharmacology and Molecular Biology, The Chicago Medical School, North Chicago, Illinois. He serves the National Headache Foundation as Executive Director.