Headache / dental implant courses by Indian dental academy

HEADACHE

INDIAN DENTAL ACADEMYLeader in continuing Dental

Education

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INTRODUCTION

Headache is one of the most common reasons for a patient to see adoctor. While most patients have a benign headache type, theheadache can be the initial presentation of a serious underlyingillness.It is important, to understand the possible etiologies ofheadache,as well as the clinical features suggestive of a Seriousunderlying cause for headache. Estimates of headache prevalencevary, but most surveys report that as many as 90% of all individualsexperience at least one headache annually, with severe, disablingmigraine headache affecting over 35% of the population. Headachesare relatively rare in children but increase with age.


International classification of headache disorders

• Primary• Secondary• Neuralgias and other headaches


Primary 1. Migraine, including: 1.1 Migraine without aura 1.2 Migraine with aura

2. Tension-type headache, including: 2.1 Infrequent episodic tension-type headache 2.2 Frequent episodic tension-type headache 2.3 Chronic tension-type headache

3. Cluster headache and other trigeminal autonomic cephalalgias, including:

3.1 Cluster headache

4. Other primary headaches


Secondary 5. Headache attributed to head and/or neck trauma, including: 5.2 Chronic post-traumatic headache 6. Headache attributed to cranial or cervical vascular disorder,

including: 6.2.2 Headache attributed to subarachnoid haemorrhage 6.4.1 Headache attributed to giant cell arteritis

7. Headache attributed to non-vascular intracranial disorder, including:

7.1.1 Headache attributed to idiopathic intracranial hypertension 7.4 Headache attributed to intracranial neoplasm


8. Headache attributed to a substance or its withdrawal, including:

8.1.3 Carbon monoxide-induced headache 8.1.4 Alcohol-induced headache 8.2 Medication-overuse headache 8.2.1 Ergotamine-overuse headache 8.2.2 Triptan-overuse headache 8.2.3 Analgesic-overuse headache 9. Headache attributed to infection, including: 9.1 Headache attributed to intracranial infection


10. Headache attributed to disorder of homoeostasis

11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures, including:

11.2.1 Cervicogenic headache 11.3.1 Headache attributed to acute glaucoma

12. Headache attributed to psychiatric disorder


Neuralgias and other headaches

13. Cranial neuralgias, central and primary facial pain and other headaches, including:

13.1 Trigeminal neuralgia

14. Other headache, cranial neuralgia, central or primary facial pain


Blue and red flag headaches

• Blue and red flag headaches are those in which some feature of the history or examination suggests that the headache is due to a secondary cause.

• Blue flag features indicate secondary headaches that do not require urgent investigation.

• Red flag features require urgent attention


Blue flag headaches

• Headache that is mainly occipital but sometimes radiates to the temple, exacerbated by examination of neck mobility (cervicogenic headache or cervical spondylosis)

• Headache temporally linked to whiplash injury of the neck

• Headache related to reading (eye strain)

• Headache clearly temporally linked to the ingestion of medications (eg. vasodilators)

• Headaches associated with systemic viral illness (eg. influenza)


Red flag headaches• New onset, specific setting. New headache in the setting of cancer (metastases), HIV

infection (opportunistic infection), postmanipulation or trauma of the neck, or associated with mild head trauma in the elderly (subdural haematoma)

• New headache that is persistent

• Focal signs or symptoms (other than the typical visual or sensory aura of migraine.

• Headache with focal neurological signs that precede or outlast the headache (the rare exception is hemiplegic migraine)

• Headache that is progressive (may suggest a mass lesion)

• Headache of sudden onset (may indicate a bleed either into the subarachnoid space or the cerebral parenchyma)

• Headache with rash (may indicate meningococcal meningitis or lyme disease.


• Persistent unilateral temple headache in adult life (may indicate cranial arteritis)

• Headache with a raised erythrocyte sedimentation rate (ESR) (may be an indication of cranial arteritis, collagen disease or systemic infection)

• Headache with papilloedema (raises the suspicion of raised intracranial pressure due to a mass lesion or benign intracranial hypertension)

• Nonmigraine headaches in pregnancy or postpartum (cerebral vein thrombosis can occur during or just after pregnancy)

• Headache triggered by cough or straining (may be an indication of either a mass lesion or a subarachnoid bleed)

• Headache clearly triggered by changes in posture (may indicate low cerebrospinal fluid [CSF] pressure, for instance due to spontaneous CSF leak)

• Headache associated with pressing visual disturbances (may indicate conditions such as glaucoma or optic neuritis)

• Headaches that have primary characteristics, but with unusual featureswww.indiandentalacademy.com

MIGRAINE

They are often classified by whether auras accompanythem or not:

• Common migraines are without auras. About 75% of migraines are the common type.

• Classic migraines are those with auras.


Diagnostic Criteria For MigraineWithout Aura

The patient must have had at least five attacks meeting theDiagnostic criteria below:

• For headaches that are untreated or unsuccessfully treated, headache duration should be between four and 72 hours.

• The headache should have at least two of the following characteristics:

- Unilateral location; - Pulsating quality; - Moderate or severe intensity; and - Aggravation by walking stairs or similar physical activity.


• During headache there should be at least one of the following:

- Nausea and/or vomiting; and - Photophobia and phonophobia.

• History, physical and neurologic examinations do not suggest another cause for the patient’s headache.

Modified from Headache Classification Committee of the InternationalHeadache Society: Classification and diagnostic criteria for headachedisorders, cranial neuralgias, and facial pain.Cephalalgia 1988; 8(Suppl. 7):1-96.


Pathophysiology Of Migraine


Vascular Theory

• In the 1940s and 1950s, the vascular theory was proposed to explain the pathophysiology of migraine headache.

• Wolff et al believed that intracranial vasoconstriction is responsible for the aura of migraine and that the subsequent rebound vasodilatation and activation of perivascular nociceptive nerves resulted in headache.

• This theory was based on the observations that (1) extracranial vessels become distended and pulsatile during a migraine attack; (2) stimulation of intracranial vessels in an awake person induces headache; and (3) vasoconstrictors (eg, ergots) improve the headache, whereas vasodilators (eg, nitroglycerin) provoke an attack.


Neurovascular Theory Cortical spreading depression

• In 1944, Leao proposed the theory of CSD to explain the mechanism of migraine with aura. A migraine aura is due to a well-defined wave of neuronal excitation in the cortical gray matter that spreads from its site of origin at the rate of 2-6 mm/min. This spread is followed by a wave of neuronal suppression in the same manner. The blood vessels in this area simultaneously dilate and then constrict. Therefore, migrainous aura is a cortical event with a definite and well-defined neuroelectrical basis.

• The neurochemical basis of the CSD is the release of potassium or the excitatory amino acid glutamate from neural tissue. This release depolarizes the adjacent tissue, which, in turn, releases more neurotransmitters, propagating the spreading depression.


• Positron emission tomography (PET) scanning demonstrates that blood flow is moderately reduced during a migrainous aura, but the spreading oligemia does not correspond to vascular territories. The oligemia itself is insufficient to impair function. Instead, the flow is reduced because the spreading depression reduces metabolism.

• The reason why these neurons are more excitable at a cellular level in certain patients is not entirely clear. Specific groups of patients with migraine have a genetic defect leading to a lowered threshold for CSD, and this is called familial hemiplegic migraine (FHM). However, for the vast majority of patients, a clear metabolic or genetic defect that easily explains this neuronal excitability cannot be determined.


Brainstem activation

• PET scanning in patients having an acute migraine headache demonstrates activation of the contralateral pons, even after medications abort the pain. It has been proposed that brainstem activation may be the initiating factor of migraine.

• Once the CSD occurs on the surface of the brain, H+ and K+ ions diffuse to the pia mater and activate C-fiber meningeal nociceptors, which releases proinflammatory neurochemicals (eg, calcitonin gene–related peptide) and plasma extravasation occurs. Therefore, a sterile, neurogenic inflammation of the trigeminovascular complex is present. Once the trigeminal system is activated, it stimulates the cranial vessels to dilate. The final common pathway to the throbbing headache is the dilatation of blood vessels.


Cutaneous allodynia

• Burstein et al 1998 described the phenomenon of cutaneous allodynia, in which secondary pain pathways of the trigeminothalamic system become sensitized during a migrainous episode.This observation further demonstrates that sensitization of central pathways in the brain mediates the pain of migraine, in addition to the previously described neurovascular events.


Dopamine Pathway

• Some authors have proposed a dopaminergic basis for migraine.In 1977, Sicuteri postulated that a state of dopaminergic hypersensitivity is present in patients with migraine. Interest in this theory has recently been renewed.

• A variety of prodromal symptoms (eg, yawning, irritability, nausea, vomiting) can be attributed to relative dopaminergic stimulation. Dopamine antagonists, such as prochlorperazine, completely relieve almost 75% of acute migraine attacks.


Magnesium Deficiency

• Another theory proposes that deficiency of magnesium in the brain triggers a chain of events, starting with platelet aggregation and glutamate release and finally resulting in the release of 5-hydroxytryptamine, which is a vasoconstrictor.


Migraine triggers can include the following:

• Alcohol, especially beer and red wine • Certain foods, such as aged cheeses, chocolate, nuts, peanut

butter, some fruits (like avocado, banana, and citrus), foods with monosodium glutamate (MSG), onions, dairy products, meats containing nitrates (bacon, hot dogs, salami, cured meats) fermented or pickled foods

• Skipping meals • Fluctuations in hormones (for example, during pregnancy, before

and during period, and menopause) • Certain odors, such as perfume or smoke • Bright lights • Loud noises • Stress, physical or emotional (often, the headache occurs during a

period of relaxation after a particularly stressful time) • Sleeping too little or too much • Caffeine • Smoking or exposure to tobacco smoke


In general, there are four symptom phases to aMigraine (although they may not all occur in everypatient):

• The prodrome• Auras• Migaine attack • The postdrome phase.


Prodrome

The prodrome phase is a group of vague symptomsthat may precede a migraine attack by several hours, oreven a day or two. Such prodrome symptoms can includethe following:

• Sensitivity to light or sound.• Changes in appetite.• Fatigue and yawning.• Malaise.• Mood changes.• Food Cravings


AurasAuras are sensory disturbances that occur before the migraine attack inbetween 20% and 25% of patients. There is occurrence of transient focal neurologic symptoms(the aura),10 to 30 minutes prior to the onset of headache pain.

Visually, auras are referred to as being positive or negative:

• Positive auras include bright or shimmering light or shapes at the edge of their field of vision called scintillating scotoma. They can enlarge and fill the line of vision.

Other positive aura experiences are zigzag lines or stars.

• Negative auras are dark holes, blind spots, or tunnel vision (inability to see to the side).

• Patients may have mixed positive and negative auras. This is a visual experience that is sometimes described as a fortress with sharp angles around a dark center.


Other neurologic symptoms may occur at the same time asthe aura, although they are less common.

They include the following:

• Speech disturbances.• Tingling, numbness, or weakness in an arm or leg.• Perceptual disturbances such as space or size

distortions.• Confusion.


Migraine AttackIf untreated, attacks usually last from four to 72 hours. A typicalmigraine attack produces the following symptoms:

• Throbbing pain on one side of the head. The word migraine, in fact, is derived from the Greek word hemikrania, meaning "half of the head" because the pain of migraine often occurs on one side. Pain also sometimes spreads to affect the entire head.

• Pain worsened by physical activity.• Nausea, sometimes with vomiting.• Photophobia• Phonophobia• Osmophobia

Less common symptoms include -tearing and redness in one eye, swelling of the eyelid, andnasal congestion, including runny nose.


Postdrome

After a migraine attack, there is usually a postdrome phase,in which patients may feel exhausted and mentally foggyfor a while.


Drugs for Prevention

• Preventive medications if two or more migraines attacks per month, use pain relievers more than twice a week, or if the symptoms are especially debilitating. Depending on the condition taking the medication daily or when a known trigger is about to occur.

• Beta-blockers -- also used to treat heart disease; researchers aren't sure why they also work for migraines, although they may help keep blood vessels in the brain from constricting and dilating. Beta-blockers include – Atenolol – Metoprolol – Propranolol

• Calcium-channel blockers -- another type of cardiovascular drug that can help prevent migraines, including – Verapamil – Diltiazem www.indiandentalacademy.com

• Anti-depressants -- Tricyclic antidepressants are helpful in preventing all kinds of headaches, including migraines. Tricyclic antidepressants include: – Amitriptyline – Nortriptyline – Doxepin – Imipramine

• Anticonvulsants -- Some anti-seizure drugs help prevent migraines, although researchers aren't sure why: – Divalproex sodium – Topiramate


Drugs for Treatment

• To be effective, these medications should be taken as soon as it is felt a migraine coming on.

• Triptans -- This class of medications tends to be the front-line treatment for severe migraines and relieve pain, nausea, and sensitivity to light and sound. They work by constricting the blood vessels in the brain. Triptans include –

– Almotriptan – Eletriptan – Frovatriptan – Naratriptan – Rizatriptan – Sumatriptan – Zolmitriptan


• Ergots -- Ergots also work by constricting blood vessels, but tend to have more side effects than triptans. Ergots include – Ergotamine – Dihydroergotamine

• Isometheptene, dichloralphenazone, and acetaminophen (Midrin) -- Midrin combines a pain reliever (acetaminophen) and sedative (dichloralphenazone) with a medication that constricts blood vessels (isometheptene) to prevent migraines.

Other medications used to treat the headache pain or associatedsymptoms:

• Anti-nausea drugs • Acetaminophen for pain • Ibuprofen or other nonsteroidal anti-inflammatory drugs (NSAIDs) • Narcotics, such as codeine, are sometimes used for people who

can't take triptans or ergots; however, they can cause dependency and rebound headaches.


Tension-type headache (TTH)

• In its classification of headache disorders, the International Headache Society defines tension-type headache as a headache lasting 30 minutes to 7 days.

• The pain is usually reported as pressure or a tight sensation of mild to moderate intensity, typically on both sides of the head or around the head in a “band-like” distribution.

• There tend to be no other symptoms associated with the headache, and there is no exacerbation of pain with physical activity.

• Tension-type headaches occurring at a frequency of less than 15 episodes or days per month are classified as episodic, whereas those occurring at a frequency of 15 episodes (days) or more per month are classified as chronic.


• The mechanism of TTH is poorly understood, although it has long been regarded as a headache with muscular origins.

• It may be stress-related or associated with musculoskeletal problems in the neck.

• Headache in either case is usually mild or moderate and

generalized, though it can be one-sided. It is described as pressure or tightness, like a band around the head, with pounding characteristic sometimes spreading into or from the neck. It lacks the specific features and associated symptoms of migraine.


• TTH often begins during the teenage years, affecting three women to every two men, and reaches peak levels in the 30s.

• Episodic TTH is the most common headache disorder, reported by over 70% of some populations. Its prevalence varies greatly.

• Chronic TTH affects 1-3% of adults.


Treatment

• Treatment of TTH includes psychological, physiologic, and pharmacologic therapies.

• Psychological management includes simple counseling and hypnosis.

• Whereas relaxation and biofeedback measures, including acupuncture, are helpful physiologic treatments.

• TTH is most often effectively treated with analgesics, including NSAIDS, acetaminophen or aspirin, and tricyclic antidepressants


Cluster headache (CH)• CH is one of a group of primary headache disorders

(trigeminal autonomic cephalalgias) of uncertain mechanism that are characterized by frequently recurring, short-lasting but extremely severe headache.

• CH also has episodic and chronic forms.

• Episodic CH occurs in bouts (clusters), typically of 6-12 weeks’ duration once a year or two years and at the same time of year.

• Strictly one-sided intense pain develops around the eye once or more daily, mostly at night, until the pain diminishes after 30-60 minutes. The eye is red and waters, the nose runs or is blocked on the affected side and the eyelid may droop.


• In addition, 10 to 20% of patients report superimposed paroxysms of stabbing, ice pick-like pains in the periorbital region that last for a few seconds and may occur once or several times in rapid succession;

• This paroxysmal pain usually heralds the end of an attack. The symptoms often resolve in 1 to 2 minutes. The pain usually begins in, around, or above the eye or the temple; occasionally, the face, neck, ear, or hemicranium may be affected, and the pain can be confused with pain of odontogenic origin.


• In the less common chronic CH there are no remissions between clusters. The episodic form can become chronic, and vice versa, but once CH has struck it may recur over 30 years or more.

• Though relatively uncommon (affecting fewer than 1 in 1000 adults), CH is clearly highly recognizable. It is unusual among primary headache disorders in affecting six men to each woman. Most people developing CH are in their 20s or older.


Management of cluster headache

• Management of cluster headache includes use of medications to prevent cluster attacks until the bout is over as well as abortive therapies.

• Individual headaches are difficult to treat because they are short-lived. Abortive medications, including the use of 100% oxygen at the outset of an episode, are often useful in confirming a diagnosis of cluster.

• Oxygen inhalation (9 L/min) results in rapid resolution of symptoms in over 70% of cases. Intranasal sprayed lidocaine 4% is also effective in nearly half of cases.


• Triptan therapy can be effective, although, typically, parenteral forms are required due to their more rapid absorption. Most cluster headaches occur repeatedly and require more than just abortive therapy.

• Short courses of oral glucocorticoids are typically effective in aborting repeated clusters of headaches. For more chronic cluster, effective prophylactic medications include lithium, methysergide, ergotamine, sodium valproate, and verapamil.

• Since cluster occurs as a series of episodes with a period of remission, preventive measures should be discontinued to see if remission has occurred.


Chronic paroxysmal hemicrania (CPH) Chronic paroxysmal hemicrania (CPH), as the name implies, is typically anunremitting, unilateral headache disorder, although episodic versions havebeen identified.

Chronic paroxysmal hemicrania is characterized by short-lasting (2 to 45minutes), frequently occurring attacks of pain (five per day for more than half ofThe time) .

The quality of pain is throbbing or pounding, with an intensity that parallels thatof cluster headaches, the patient often choosing to pace the floor during anattack.

Pain location is predominantly oculotemporal and frontal, always on the sameside, and can spread to involve the entire side of the head and the neck,shoulder, and arm..Cases involving CPH presenting as intermittent toothachehave been reported.


• Turning or bending the head forward may precipitate an attack in some cases.

• Associated symptoms include unilateral lacrimation, nasal stuffiness, and conjunctival injection.

• Nausea and vomiting are usually absent, as are visual or somatosensory auras.

• In contrast to cluster headache, CPH is seen predominantly in women. Age at onset appears to be 20 years, although a variable pre-CPH period may exist.


Treatment

• Chronic Paroxysmal Hemicrania. Indomethacin is the medication of choice for CPH.

• If the pain does not resolve with this medication, it is unlikely to be CPH.

• Aspirin and naproxen have a partial effect, but the relief is not as dramatic as with indomethacin.


Hemicrania continua

• Hemicrania continua is a rare, strictly unilateral headache sometimes evolving from an intermittent pattern, and sometimes arising de novo, that has the features of cluster headache.

• The severity of the pain is usually moderate, but there can be severe pain during exacerbations.

• The autonomic features are not as pronounced as in cluster headache.

• It is dramatically responsive to indomethacin. Rarely, bilateral features and side shift have been documented.


Short-lasting Unilateral Neuralgiform Headaches

• Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) is distinguished by the short duration of attack (5 to 240 seconds) and the frequency of occurrence (3 to 200 times per day).

• Short-lasting unilateral neuralgiform headache with cranial autonomic symptoms (SUNA) has been proposed as a broader category of pain, lasting 2 seconds to 10 minutes, occurring in the unilateral orbital, supraorbital or temporal area and having a stabbing or pulsating quality.

• SUNA is accompanied by one of the following: conjunctival injection or lacrimation, nasal congestion or rhinorrhea, or eyelid edema. There is currently no effective treatment for SUNCT or SUNA.


Temporal (or giant cell) arteritis

• Temporal (or giant cell) arteritis is a systemic inflammatory disorder that often involves the extracranial carotid circulation.

• This is commonly a disorder of elderly individuals, with an annual incidence of 77:100,000 individuals, usually over age 50.

• The average age at onset is 70 years, and women account for 65% of cases.

• This is a rare form of chronic daily headache with clinical importance because it is treatable. Failure to treat giant cell arteritis may lead to serious ischemic complications, including blindness, stroke, and myocardial infarction.www.indiandentalacademy.com

• Inflammation of the temporal artery on biopsy is seen in over half of cases and can spread to arteries other than the temporal artery and extracranial vessels.

• The inflammatory process appears to be similar to both an acute immune-mediated vasculitis and chronic noncaseating granulomatous inflammation similar to that seen in sarcoid.

• Blindness occurs when the posterior ciliary artery is affected, which supplies the optic disk, leading to ischemic papillopathy and atrophy.


Clinical Features

• Symptoms include diffuse unilateral headache, polymyalgia rheumatica, chest pain, jaw pain and claudication, fever, and weight loss.

• Symptoms initially are low grade; progress in severity and duration, increasing in the evening when the patient reclines; and are reported as a bitemporal constant dull ache.

• Most patients are able to recognize that their pain is superficial and extracranial and associated with scalp tenderness that interferes with hair brushing or resting the head on a pillow. www.indiandentalacademy.com

• Pain in the temporal and masseter muscles on chewing is virtually pathognomonic of temporal arteritis, making it easily confused with other causes of facial pain (eg, myofascial pain and TMDs) in a clinical setting.

• Erythrocyte sedimentation rate and C-reactive protein are frequently, although not always, elevated, and patients may be anemic. A temporal artery biopsy should be performed to confirm the diagnosis.


Management

• Approximately half of patients with untreated temporal arteritis develop blindness due to involvement of the ophthalmic artery.

• This significant complication can be prevented by immediate initiation of glucocorticoid therapy (75 mg daily), underscoring the importance of prompt recognition.

• Steroid doses are reduced by 5 mg per week to a maintenance dose of 10 mg daily and then continued for 3 months.


Cervicogenic Headache• The term ‘cervicogenic’ means ‘relating to the cervical spine’.

Headaches arising from the cervical spine are attributed to the upper three cervical joints (nearest the base of the skull).

• The trigeminal nerve (which supplies the head) has a close relationship with the upper three cervical joints.

• This means that there is a two way relationship: headaches can refer pain to the upper neck and neck pain can refer pain into the head.

• The history of a cervicogenic headache may relate to a previous neck injury, such as whiplash.

• However the onset may be insidious and related to normal degenerative changes in the joints and muscles of the neck.


Signs and Symptoms

• The pain is usually unilateral and associated with the side of neck pain.

• The frequency of the headaches is more variable than with other forms of headaches.

• The headaches may be associated with prolonged postures, movements of the head or any physical activity which may increase the load and stress placed on the joints.

• There may be restriction in the range of movement in the neck• There is usually pain with palpation of the joints and muscles of the

affected area.

• There maybe shoulder or arm pain.

• The pain usually starts in the neck and there is a relationship with the onset of neck pain and onset of headaches.

• The intensity of headaches is moderate to severewww.indiandentalacademy.com

Treatment

• Careful assessment by a physiotherapist can help identify if there is a cervicogenic component to the headache.

• Assessment of range of movement, joint mobility, posture, muscle imbalances and strength will help guide the therapist to an appropriate treatment plan.

• Joint mobilizations and manipulations will be used to improve any restrictions in range of movement.

• Posture will be assessed and corrected with appropriate advice given on ways to reduce the stresses placed on the neck throughout the day.

• Certain strength exercises for particular muscle groups in the neck and shoulder may be prescribed to improve postural control of these areas and strengthen muscles which may be weak due to previous

trauma. www.indiandentalacademy.com

Medication Overuse (Rebound) Headache

About a third of persistent headaches−−whether chronic migraine ortension−type−−are medication−overuse headaches (MOHs).

These are the result of a rebound effect caused by theregular overuse of headache medications.

Nearly any headache medication can produce this effect. In one studyof headache sufferers, MOH developed after an average of 1.7 yearsof regular use of triptans (18 doses a month), after 2.7 years of ergotuse (37 doses a month), and after 4.8 years using pain killers (114doses a month).

It should be noted that regular use of pain killers for any chronicproblem (such as arthritis) poses a 2% risk for medication−overuseheadache, with risk being highest in people who already have primaryheadaches, especially migraines. www.indiandentalacademy.com

Strategies for Medication Overuse Withdrawal

• Reduce total daily dosage 20% every 4 to 7 days

• Rapid taper or immediate elimination of the agent if done should be under medical supervision switching to a long-acting agent and tapering medication being overused

• Inpatient detoxification with or without behavioral support

• Behavioral therapywww.indiandentalacademy.com

HEMORRHAGE• Most vascular disorders associated with headache require

immediate medical or surgical intervention.

• Severe, acute headaches associated with a stiff neck in the absence of fever are highly suggestive of subarachnoid hemorrhage (SAH).

• Sudden onset of the "worst headache of life" is a medical emergency, and aneurysmal SAH must be excluded by a CT scan, which is approximately 90% sensitive for SAH, and a lumbar puncture if the CT scan is negative.

• Other causes of headache can include ruptured aneurysm, arteriovenous malformation, or intraparenchymal hemorrhage, but these often present as headache alone without nausea, vomiting, and mental and emotional changes.


• Headache following lumbar puncture usually begins 48 hours to 2 weeks following the procedure.

• It is relatively common, with an incidence of 10 to 30%, and is associated with head pain that worsens with positional changes.

• Nausea, stiff neck, vertigo, photophobia, tinnitus, and blurred vision are frequent complaints.

• Loss of cerebrospinal fluid (CSF) decreases the brain's supportive cushion, resulting in dilation and tension on pain-sensitive dural structures when patients are upright.


• Intracranial hypotension often occurs, but severe lumbar puncture headache can be present in patients with normal CSF pressure.

• Spontaneous CSF leaks can also occur due to exertion or following surgical procedures near the dura and are also characterized by positional modulation.


Raised intracranial pressure

• Headache resembling that of brain tumor is a common presenting symptom of raised intracranial pressure, usually resulting from impaired CSF absorption by arachnoid villi.

• This disorder, called pseudotumor cerebri, is most commonly seen in young, obese adult females and is associated with morning headaches that worsen with coughing or straining.

• The pain is usually retro-ocular and worsened by eye movements, which are often restricted by sixth cranial nerve dysfunction.


• Patients may have a history of exposure to precipitating agents such as tetracycline, vitamin A, or glucocorticoids.

• Intracranial hypertension is diagnosed by lumbar puncture, which can also provide temporary relief.

• Chronic management includes diuretics or surgical implantation of a shunt.

• Ophthalmologic evaluation for visual field testing is required in patients with intracranial hypertension as it can enlarge the blind spot due to pressure transduced along the optic nerve. Patients with enlarging blind spots can be treated surgically with an optic nerve sheath fenestration.


Trauma• Many patients following relatively trivial head injuries, such as

extension-flexion injuries (ie, whiplash), report symptoms such as headache, dizziness, vertigo, and impaired memory.

• Symptoms may resolve after a few weeks or can persist months to years after injury. In nearly all cases, clinical neurologic examination and radiographic and imaging studies are normal.

• Although the etiology of this headache is poorly understood, it does not appear to be entirely psychogenic.

• These headaches may be part of a TMD also related to direct or indirect trauma to the temporomandibular complex.


Headache associated with intracranial masses

• Headache associated with intracranial masses is usually nondescript.

• Approximately 30% of patients with brain tumors consider headache to be their chief complaint or first presenting symptom.

• Intermittent deep, dull, and aching pain of moderate intensity that worsens with physical exertion or position change and is associated with nausea and vomiting is the symptom most commonly described in migraine but is also seen in brain tumor headaches.

• Sleep disturbances occur in 10% of patients, and vomiting preceding headaches by weeks is highly characteristic of tumors of the posterior cranial fossa.

• Tumors should be suspected in patients with progressively severe new "migraine" headaches that are unilateral.www.indiandentalacademy.com

Primary angle closure glaucoma: It is rare before middle age,and may present dramatically with acute

ocular hypertension, a painful red eye with the pupil dilated and fixed and, essentially, impaired vision, and nausea and vomiting. In other cases, headache or eye pain is episodic and mild. The diagnosis is suggested if patient reports coloured halos around lights.

Subacute carbon monoxide poisoning: uncommon but potentially fatal. Symptoms include headaches, nausea, vomiting, giddiness, muscular weakness, dimness of vision, and double vision.

Meningitis: usually accompanied by fever and neck stiffness in an obviously ill patient.


Hypnic Headache• Hypnic headache is a rare headache occurring in both men and

women after age 60 years.

• The headaches are generally characterized by bilateral, throbbing pain and occur 2 to 4 hours after onset of sleep.

• The pain is usually short-lived, lasting 15 minutes to 3 hours. There tends to be an absence of autonomic features.

• The similarities to cluster headache have suggested a relationship between the 2 types, but thus far none has been proven.

• The nocturnal association and possible disturbances in the biological clock have implicated serotonin in this particular headache as well in other headache types.

• The pain often resolves with lithium, caffeine or indomethacin


Ice Pick/Ice cream Headache Type

• Typically the patient is young to middle aged and patients describe a short piercing pain like a flash of lightening lasting from seconds to minutes and may occur several times a day.

• Ice Pick/Ice cream Headache usually involves one eye. Some patients find cold foods trigger the pain. Sometimes the patient has multiple attacks per day on a daily basis.


Facial Headache Types

SINUSITIS

• It is caused by infection of one or more of the sinuses. • Acute sinusitis lasts for days up to three weeks.

• The International Headache Society's criterion of purulent discharge and acute febrile illness is indicative of acute sinusitis (sinus headache).

• The site of the pain varies according to the location of the infection.

• Maxillary sinusitis pain is mostly in the cheek, gums, teeth and upper jaw.

• When pain is presented between and around the eyes this is referred to as ethmoidal sinusitis.

• Frontal sinusitis pain is seen in the forehead and sphenoidal sinusitis presents with pain at the crown of the head. The pain often has a a dull aching quality which is worsened by bending. Very rarely complications can occur such as meningitis or abscesses.www.indiandentalacademy.com

TRIGEMINAL NEURALGIA

• It is considered to be the most common neurological syndrome in the elderly.

• Women are three times more likely to get it than men.

• Over 95% of cases are unilateral.

• The pain is often described as an electric shock or spasm or burning sensation in one or more of the three divisions of the trigeminal nerve.

• The pain lasts from 2-120 seconds.

• The condition has been called 'tic douloureux' because the facial muscles may twitch. •

• The trigger can be cold air, washing the face or cleaning the teeth. The pain can be excruciating. The most common cause is thought to be vascular compression resulting from abnormal arterial roots near the nerve root.

• MRI scans can confirm this. Other possible causes include malignancy, multiple sclerosis, intracranial aneurysms and cranial arteritis.www.indiandentalacademy.com

POST HERPETIC NEURALGIA

• Shingles (herpes zoster virus) can cause pain resulting from various cranial nerves.

• The pain may start during an acute rash of herpes but the main problem is pain that persists after the herpes rash has gone.

• Common symptoms include a constant deep pain, with repeated stabs, or needle pricking pain.

• Even light touch can trigger these symptoms which may be accompanied by itching.


Temporomandibular Joint Disorder • Temporomandibular Joint Disorder (TMJ, also called TMD).

• Muscle contractions that cause headaches may be a result of temporomandibular joint dysfunction, which is caused by clenching the jaws or grinding the teeth (usually during sleep), or by abnormalities in the jaw joints themselves.

• The diagnosis is easy if chewing produces pain or if jaw motion is restricted or noisy.

• TMJ pain can occur in the ear, cheek, temples, neck, or shoulders. This condition often coexists with chronic tension headache.


CONCLUSION

Patients with headache may present a diagnostic dilemma.It is important that the physician have a good workingknowledge of the common benign headache syndromes,and that he or she know when to suspect a seriousunderlying cause for the patient’s headache. Headache diagnosis is indeed challenging, both to thefamily physician and specialist alike.

A better understanding and appreciation of headaches canlead to improved outcomes and better overall management.


REFERENCES• Scott S.DeRossi,John A.Detre.Headache.In: Burket’s,Oral

Medicine.11th edition, Chapter 11. BC decker Inc, 2008:289-297.

• Ingle and Bakland . Nonodontogenic toothache and chronic head and neck pains. In: Endodontics.5th ed, Chapter 8. PMPH-USA; 2002 :287-356.

• International classification of headache disorders.World Health Organization. Fact sheet N°277,March 2004.

[email protected]

• Jean Schoenen,Differential diagnosis of facial pain. Acta neurol. belg. 2001;101: 6-9


• Sujay A. Mehta et al. Recognition and Management of Headache. J Can Dent Assoc. 2006; 72(9):835–9

• Jacques Joubert. Diagnosing headache. Australian Family Physician . 2005 August ; 34 ( 8):621-625

• Werner J. Becker. Is this just a Headache? The Canadian Journal of CME. 2003 February : 45-52

• Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia 1988; 8(Suppl. 7):1-96.

• Soma Sahai Srivastava, David Y Ko . Pathophysiology and Treatment of Migraine and Related Headache. emedicine.medscape.com/article/1144656-overview


Differential Diagnosis of Headaches


A systematic case history should include the following in patients presenting with the complaint

of headache:

• Age at onset• Presence or absence of aura and prodrome• Frequency, intensity, and duration of attack• Time and mode of onset• Quality, site, and radiation of pain• Associated symptoms and abnormalities• Family history of migraine• Precipitating and relieving factors• Effect of activity on pain


• Relationship with food/alcohol• Response to any previous treatment• Association with recent trauma• Any recent changes in sleep, exercise, or diet• State of general health• Change in work or lifestyle• Possible association with environmental factors• Effects of menstrual cycle (women)


• The patient presenting with a history of headaches is a diagnostic challenge.

• The patient presenting with the complaint of acute onset headache without any prior history of headache should be checked for nuchal rigidity to rule out meningitis and subarachnoid headache. Severe, acute headaches associated with a stiff neck in the absence of fever are highly suggestive of subarachnoid hemorrhage (SAH).

• A careful neurologic examination should be done to rule out a brain tumor or other space-occupying lesion. These steps are particularly important if a patient is experiencing his or her first serious headache. If there is nuchal rigidity or focal neurologic signs, it is wise to immediately refer the patient to a neurologist or neurosurgeon for further workup and possible hospitalization.


• The specialist will probably order a CT scan of the brain and follow that with a spinal tap if a subarachnoid hemorrhage or meningitis is suspected.

• It is clear that a CT scan should be done prior to a spinal tap if there are focal neurologic signs or papilledema.

• One other condition that must be considered in acute headache particularly in the elderly is temporal arteritis. A sedimentation rate will usually be positive but a neurology consult is axiomatic so that steroids can be started immediately .


• In the patient with chronic or recurring headaches and no neurologic findings, it is wise to see the patient during the attack.

• Migraine headaches can be diagnosed by the response to sumatriptan by mouth or injection. It is suggested that during migraine attacks there might be a rise in the urinary excretion of 5-hydroxyindoles ( metabolite of serotonin )whereas platelet 5-HT decreases during migraine attacks.

• If the headaches are due to chronic allergic or infectious rhinitis, relief can be had by spraying the turbinates with phenylephrine.

• Muscle traction headaches will often be relieved by occipital nerve blocks supporting the diagnosis.

• Compression of the superficial temporal artery will often relieve migraine temporarily supporting that diagnosis.

• Compression of the jugular veins will often give relief to post spinal tap headaches.


• If the patient is seen between headaches, certain prophylactic measures may help establish the diagnosis.

• For migraine, β-blockers may be prescribed and if the headaches are prevented, there is good support for the diagnosis.

• A course of corticosteroids may be initiated in patients with histamine (cluster) headaches to help establish the diagnosis.

• Muscle relaxants and/or tricyclic drugs may be given to help diagnose muscle contraction headaches. www.indiandentalacademy.com

• Temporomandibular Joint Disorder (TMJ, also called TMD). The diagnosis is easy if chewing produces pain or if jaw motion is restricted or noisy. TMJ pain can occur in the ear, cheek, temples, neck, or shoulders. This condition often coexists with chronic tension headache.

• Dental related conditions should also be ruled out as a possible cause of referring pain to the temporal region leading to headache. Thus caries or periodontal infections leading to periapical and periodontal abscesses should be detected.

• Trigeminal neuralgia- can be diagnosed by it’s characteristic clinical presentation of sharp, lancinating ,electric shock like pain which has trigger points along any one of the trigeminal nerve branch.

• Chronic nasal stuffiness or chronic respiratory infection suggests a diagnosis of sinusitis, although patients with migraine may also have nasal symptoms.



• Impaired vision or seeing ‘haloes’ around light suggests the presence of glaucoma.

• Visual field defects suggest the presence of a compressed optic pathway, e.g., due to a pituitary mass.

• Blurring of vision on forward bending of the head, headaches upon waking early in the morning that improve with sitting-up, and double vision, or loss of coordination and balance, should raise the suspicion of raised intracranial pressure. This disorder should

also be considered in patients with chronic, daily, progressively worsening headaches associated with

chronic nausea.


• The presence of nausea, vomiting, worsening ofheadache with changes in body position (particularly bending over), an abnormal neurologic examination,and/or a significant change in prior headache patternsuggest that the headache is caused by a tumour.

• Intermittent headache with high blood pressure issuggestive of phaeochromocytoma





Physical Examination• Record blood pressure and pulse

• Listen for bruit at neck, eyes, and head for clinical signs of arteriovenous malformation

• Palpate the head, neck, and shoulder regions

• Check temporal and neck arteries

• Examine the spine and neck muscles

• A functional neurological examination including patient getting up from a seated position without any support, walking on tiptoes and heels, cranial nerve examination, fundoscopy and otoscopy, tandem gait and Romberg test, and symmetry on motor, sensory, reflex and cerebellar (coordination) tests.


Neuroimaging should be considered in the following conditions-

• Recent significant change in the pattern, frequency, or severity of headache

• Progressive worsening of headache despite appropriate therapy• Focal neurologic signs or symptoms• Onset of headache with exertion, cough.• Orbital bruit• Onset of headache after 40 years of age.

The data are insufficient to recommend CT or MRI whenneuroimaging is deemed necessary. A head CT scan(without and with contrast) is likely to be sufficient in mostpatients. An MRI along with MRA is indicated whenposterior fossa or vascular lesions are suspected.


• The diagnostic workup of chronic headaches might include a CT scan of the brain, x-rays of the sinuses, x-rays of the cervical spine and routine blood work. Certainly if headache persists after careful follow up, these need to be done.


Other Useful Tests

• Sedimentation rate (temporal arteritis) • X-ray of the teeth (dental abscess) • MRI of the brain (brain tumor) • Spinal fluid analysis (meningitis, subarachnoid

hemorrhage) • 24-hour blood pressure monitoring (pheochromocytoma) • 24-hour urine catecholamines (pheochromocytoma) • Tonometry (glaucoma) • Allergy skin tests (allergic rhinitis) • Temporal artery biopsy (temporal arteritis)


InvestigationsFor Subarchanoid Haemorrhage

CTscan* The scan shows blood in the subarachnoid space (if done in the first

few days) and presence of intracerebral haematoma, hydrocephalus, associated brain ischaemia and occasionally location of aneurysm itself.

Lumbar puncture* It should be done if clinical suspicion is high but CT scan fails to

show subarachnoid blood, and there is no mass effect.CSF will be uniformly blood stained in the initial hours and becomes xanthochromic in later days (first appears after 4-6 hours of the bleed).

Angiography* It is needed to locate the site of aneurysm which has bled, and other

details that neurosurgeon needs to know in order to ligate the aneurysm adequately.

MRI angiography* It has replaced conventional angiography in most centres and should

be performed in all patients fit for surgery (age <65 years, not in coma). www.indiandentalacademy.com

Investigations for intracranial space occupying lesions

Skull radiography:It shows features of raised ICP at sella with shift of calcified pineal gland.

Calcification within tumours may be seen.

CTscan: It allows localisation of the tumour, its size, characters, etc., allowing

identification of nature of underlying pathology in most of the cases.

Magnetic resonance imaging (MRI): Detects early gliomas and posterior fossa tumours by eliminating bone

artefacts (a disadvantage with CT scan).

Angiography: Occasionally required to study the vascularity of the tumour or to rule out giant

aneurysms which mimic or act as space occupying lesions.

Technetium brain scan: Rarely done nowadays. May demonstrate destruction of skull vault or skull

base. www.indiandentalacademy.com

MeningitisMeningitis is an inflammation of the meninges, the tissues whichenvelop the brain and the spinal cord. The classic presentation ofbacterial meningitis is a relatively sudden onset of headache, fever, stiffneck, sensitivity to light, and an altered level of consciousness.

Physical examination may demonstrate

• Neck stiffness (neck rigidity)—The examiner is unable to put the patient's chin on the chest by passive flexion of the neck (due to neck muscle spasm).

• Kernig's sign— If the patient's thigh is flexed to 90° from the abdomen, it is then impossible to straighten the knee passively owing to spasm of hamstrings. This manoeuvre stretches roots of the sciatic nerve which are inflamed at their exits from the spinal theca.

• Brudzinski's neck sign— On passively flexing the neck, both the legs flex at hip and knee automatically.

• Brudzinski's leg sign— On passively flexing one lower limb, the other leg gets flexed automatically. www.indiandentalacademy.com

• Viral causes tend not to follow these classic patterns and are sometimes harder to diagnose. In general, the viral infections have a more indolent and unpredictable clinical path, and are often preceded by a mild viral syndrome.

• In the previously healthy adult, the most common bacterial causes of meningitis are: Strep. Pneumonia (previously termed pueumococcal), Neisseria Meningitis (meningococcus) and H. Influenzae.

• In the neonate, child, older adult and persons with previous head surgery or head trauma, there are other bacteria to consider.

• Of the many other probable viral causes, the more common causes are: adenovirus, arbovirus and influenza.


Investigations for meningitis

• Total leucocytes increased, polymorphonuclear leucocytosis and raised ESR.

• Cerebrospinal fluid studies.

• Hyponatraemia due to SIADH.

• Blood urea is elevated due to dehydration.

• Blood culture may be positive for H. influenzae, meningococci or pneumococci.

• Culture of pus from middle ear or sinuses.

• Biopsy of skin lesions (if present) to demonstrate meningococci.


• Radiography:

-Radiograph of chest for pneumonia and lung abscess. -Radiograph of skull for chronic osteomyelitis and fracture. -Radiograph of paranasal sinuses for sinusitis. -Radiograph of mastoids for mastoiditis.

• CT scan

CT scan may detect evidences of cerebritis, vascular occlusion, encephalomalacia, hydrocephalus, brain abscess or subdural empyema. Commonest CT finding is increased contrast enhancement of meninges.


CSF findings in pyogenic meningitis

• Appearance is turbid.

• Pressure is elevated above 180 mmH2O.

• Cell count is raised, ranging from 5000 to 20,000/mL, neutrophil leucocytes predominate.

• Protein level is elevated (more than 45 mg/dL).

• Sugar level is decreased (less than 40 mg/dL or less than 40% of blood sugar).

• Gram stain of the sediment of CSF may show meningococci as Gram-negative, kidney-shaped, intracellular diplococci (inside neutrophils).

• Culture of CSF grows the pathogen in 70-80% of cases.

• Measurement of bacterial antigen in the CSF (Latex agglutination test).

• Limulus amoebocyte lysate assay detects Gram-negative endotoxin in CSF and is highly sensitive. www.indiandentalacademy.com

CSF in viral meningitis

• Cerebrospinal fluid: Clear.• Increased pressure.• Protein levels are mildly elevated (70-700 mg/dL; values

>800 mg/dL rarely seen). • Sugar is normal or mildly reduced.• Cell count is increased (usually 5-500/mm3) and is

lymphocytic.• Antibodies to specific virus in increasing titres are seen if

serial examinations are done. It is useless for immediate diagnosis.


Encephalitis• Encephalitis is an inflammation of the brain tissue itself.

• In Encephalitis, the CSF findings may not be as clear or dramatic, but will show presence of white blood cells and non-specific changes in cerebro spinal fluid glucose and protein levels. Viral and bacterial cultures are usually helpful for final diagnosis.

• PCR of CSF is the diagnostic method of choice for viral encephalitis including Herpes simplex encephalitis and therapy should be instituted pending the results of PCR.

• CT scan is usually normal in encephalitis. In herpes simplex encephalitis, it may show low attenuating areas particularly in the temporal lobes with surrounding oedema.

• EEG and MRI of brain are important in patients with suspected herpes encephalitis. T2-weighted images show increased signal over the thalamic region in most patients. Haemorrhagic lesions are found in 70% of patients: similar lesions are less commonly found over the cortex, midbrain, cerebellum and spinal cord.

• Brain biopsy in select patients.www.indiandentalacademy.com

Thus the appropriate evaluation of headache should be as per the following:

• Rule-out serious underlying pathology, and look for other secondary causes of headache.

• Determine the type of primary headache using the patient’s history as the primary diagnostic tool. There may be overlap in symptoms, particularly between migraine and tension-type headache, and between migraine and some secondary causes of headache (such as sinus disease).

• Patients with any of the danger signs noted need urgent brain

imaging.

• The diagnostic workup of chronic headaches might include a CT scan of the brain, x-rays of the sinuses, x-rays of the cervical spine and routine blood work. Certainly if headache persists after careful follow up, these need to be done.



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