Headache and facial pain

HEADACHE AND FACIAL PAIN

Headache is among the most common reasons that patients seek medical attention.
It is seldom associated with significant neurological disease unless accompanied by other symptoms or neurological signs.

Headaches are classified into primary and secondary type.

Primary headaches are those in which headache and its associated features are the disorder in itself, whereas secondary headaches are those caused by exogenous disorders.

Pathophysiology

The brain parenchyma, pial arteries over the convexities, and the cerebral ventricles and choroid plexus are known to be insensitive to pain.

The dura (including the dural sinuses and falx cerebri) and the proximal parts of the large pial blood vessels are the main structures sensitive to pain.

The pain-sensitive intracranial structures are mostly innervated by branches of the trigeminal nerve and some by branches of the upper cervical nerves.

DIAGNOSTIC APPROACH TO THE PATIENT WITH HEADACHE

Unless the history is suggestive of structural disease, patients with headache who are normal on neurological examination are unlikely to have a serious disorder.

Headache Symptoms that Suggest a Serious Underlying Disorder (red flags):

1-"Worst" headache ever
2-First severe headache
3-Subacute worsening over days or weeks
4-Abnormal neurologic examination
5-Fever or unexplained systemic signs
6-Vomiting on awakening
7-Pain induced by bending, lifting, cough
8-Pain that disturbs sleep or presents immediately upon awakening
9-Known systemic illness
10-Onset after age 55
11-Pain associated with local tenderness, e.g., region of temporal artery

A general evaluation of acute headache might include the investigation of cardiovascular and renal status; blood pressure monitoring; eyes by fundoscopy, intraocular pressure measurement, and refraction; cranial arteries by palpation; and cervical spine by the effect of passive movement of the head and by imaging.

Secondary Headaches

Meningitis
Intracranial Hemorrhage
Brain Tumor
Temporal Arteritis
Glaucoma
Features of raised intracranial pressure headache
Worse in morning, improves through the day
Associated with morning vomiting
Worse bending forward
Worse with cough and straining
Relieved by analgesia


Primary headaches

TENSION-TYPE HEADACHE

This is the most common type of headache and is experienced at some time by the majority of the population in some form.
The pain is usually constant and generalised but often radiates forward from the occipital region.
It is described as 'dull', a band round the head or pressure at the vertex.

In contrast to migraine, the pain may continue for weeks or months without interruption, no associated vomiting or photophobia.

The patient can usually continue normal activities, and the pain may be less noticeable when the patient is occupied. The pain is characteristically less severe in the early part of the day and becomes more troublesome as the day goes on.

The cause of tension-type headaches is obscure.

Emotional strain or anxiety is a common precipitant to tension-type headache and there is sometimes an associated depressive illness.

Management:

Discussion of likely precipitants.
Explanation of the fact that the symptoms are not due to any sinister underlying pathology.
Excessive use of analgesics, particularly of codeine, may actually worsen the headache (analgesic headache).
Physiotherapy (with muscle relaxation and stress management).
Low-dose amitriptyline (10 mg nocte increased gradually to 30-50 mg) may be necessary.


MIGRAINE
Migraine is a benign and recurring syndrome of headache associated with other symptoms of neurologic dysfunction.
Aetiology and pathogenesis:
The aetiology of migraine is largely unknown.
Genetic factors: Many patients report a history of migraine in their relatives, particularly on the maternal side.
Hormonal factors: There is a great female preponderance and the tendency for some women to have migraine attacks at certain points in their menstrual cycle.
The 'aura' probably represents a spreading front of electrical excitation followed by depression of activity of cortical cells (especially serotoninergic transmission).
Number of biochemical processes in peripheral blood vessels, modulated by the trigeminovascular reflex, is another contributing factor.

Clinical features:

Simplified diagnostic criteria for migraine headache:

Repeated attacks of headache lasting 4–72 h in patients with a normal physical examination, no other reasonable cause for the headache, and:

At least 2 of the following features:

Plus at least 1 of the following features:
Unilateral pain
Nausea/vomiting
Throbbing pain
Photophobia / phonophobia
Aggravation by movement


Moderate or severe intensity

Typically, a classical migraine attack starts with a non-specific prodrome of malaise and irritability followed by the 'aura' of a focal neurological event, and then a severe, throbbing, hemicranial headache with photophobia and vomiting.
Over 90% of migraine sufferers will have their first attack before 40 years old.
In common migraine, aura is not present and headache may be generalised.

Visual aura (the commonest type) often takes the form of 'fortification spectra': shimmering, silvery zigzag lines which march across the visual fields over 20 minutes, sometimes leaving a trail of temporary visual field loss.
Other types of aura: sensory march, aphasia, weakness.
During the headache phase, patients prefer to be in a quiet, darkened room and to sleep. The headache may persist for several days.
In some patients there are identifiable dietary precipitants such as cheese, chocolate or red wine.
Other triggers: OCP, psychological stress, and physical strain.

Management

-Nonpharmacologic
Identification and avoidance of precipitants or exacerbating factors (such as the contraceptive pill)
A regulated lifestyle is helpful, including a healthy diet, regular exercise, regular sleep patterns, avoidance of excess caffeine and alcohol.
-Pharmacologic
Acute Attack Therapies for Migraine

Mild migraine attacks can usually be managed by oral agents. Severe migraine attacks may require parenteral therapy.
Three major pharmacologic classes are effective in acute migraine:


NSAIDs (e.g. naproxen, Ibuprofen, aspirin)
5-HT1 Agonists include ergotamine and triptans (e.g. Sumatriptan, Zolmitriptan). They are available as oral, nasal, or parenteral preparation.
Dopamine Antagonists like Metoclopramide or Prochlorperazine.

Long-term use of codeine-containing analgesic preparations should be avoided.

Preventive Treatments for Migraine
Patients with an increasing frequency of migraine attacks, or with attacks that are either unresponsive or poorly responsive to abortive treatments, are good candidates for preventive agents.

1-Pizotifen

2-Beta blocker (Propranolol)
3-Tricyclics antidepressant (Amitriptyline)
4-Anticonvulsants (Valproate, Topiramate)
5- Methysergide (old drug, may lead to retroperitoneal fibrosis)
6-calcium channel bocker (verapamil)

Women should be warned that the small risk of ischemic stroke attributable to taking oral contraception is increased if they have migraine, especially if they also smoke.

CLUSTER HEADACHE (MIGRAINOUS NEURALGIA)

Less common than migraine.
There is a 5:1 predominance of males and onset is usually in the third decade.
Periodic, unilateral periorbital pain accompanied by unilateral lacrimation, nasal congestion and conjunctival injection, often with the other features of Horner's syndrome.
The pain, whilst being very severe, is characteristically brief (30-90 minutes).
Typically, the patient develops these symptoms at a particular time of day (often in the early hours of the morning).
Patients are usually heavy smokers with a higher than average alcohol consumption.
Acute attacks are usually halted by subcutaneous injections of sumatriptan or by inhalation of 100% oxygen.
Attacks can be prevented by verapamil (80-120 mg 8-hourly), Methysergide, or short courses of corticosteroids or lithium therapy.


TRIGEMINAL NEURALGIA
Middle-aged and elderly persons are affected primarily, and ~60% of cases occur in women.
lancinating pains in the second and third divisions of the trigeminal nerve territory
The pain is severe and very brief but repetitive, causing the patient to flinch ('tic douloureux').
The pain may be precipitated by touching trigger zones within the trigeminal territory or by eating, speaking, chewing, or smiling.
The current aetiological hypothesis suggests that the neuralgia is most commonly caused by compression of the trigeminal nerve rootlets at their entry to the brain stem by aberrant loops of the cerebellar arteries.
The pain usually responds to carbamazepine, in doses of up to 1200 mg daily.
In patients who cannot tolerate carbamazepine, gabapentin or phenytoin may be effective.
Various surgical treatments are available,: injection of alcohol or phenol into a peripheral branch of the nerve, percutaneous placing of a radiofrequency lesion in the nerve near the Gasserian ganglion, release of vascular compression of the trigeminal nerve.