Headache International headache society (HIS) classification of headache PowerPoint Presentation, PPT - DocSlides

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Headache

International headache society (HIS) classification of headache

Presentation by: Dr Kadivar Neurologist

at Hazrat -e- Ali Asghar Hospital

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Headache: Introduction

Headache is among the most common reasons patients seek medical attention.

Primary headaches

BenignRecurrentNo organic disease as their causeSecondary headachesUnderlying organic disease

Primary

headache often results in considerable disability and a decrease in the patient's quality of life.

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Common Causes of Headache

Primary Headache

Secondary Headache

Type

%

Type

%

Tension-type

69

Systemic infection63Migraine16Head injury4Idiopathic stabbing2Vascular disorders1Exertional1Subarachnoid hemorrhage<1Cluster0.1Brain tumor0.1

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Primary Headache Disorders

More common

Migraine, with or without auraTension typeCluster

Less common

Paroxysmal

hemicrania

SUNCT (short-lasting unilateral

neuralgiform

headache attacks with

conjunctival injection and tearing)Primary Stabbing HeadachePrimary Cough HeadacheCold-stimulusBenign coughBenign exertional

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Secondary Headache Disorders

Associated with non-vascular intracranial disorder

Benign intracranial hypertension

Intracranial infection

Low CSF pressure

Associated with

noncepalic

infection

Viral infection

Bacterial infectionAssociated with vascular disordersSubarachnoid hemorrhageAcute ischemic cerebrovascular disorderUnruptured vascular malformationArteritisCarotid or vertebral artery painVenous thrombosisArterial hypertension

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Secondary Headache Disorders

Associated with head trauma

Acute post-traumatic headache

Associated with substance use or withdrawalAcute use or exposureChronic use or exposure

Associated with metabolic disorders

Hypoxia

HypercapniaMixed hypoxia & hypercapnia

Dialysis

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Anatomy and Physiology of Headache

Relatively few cranial structures are pain-producing;

The scalp,Middle

meningeal artery, Dural sinuses, Falx cerebralProximal segments of the large pial arteries. The ventricular ependymal, choroid plexus, pial veins, and much of the brain parenchyma are not pain-producing.

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Clinical Evaluation of Acute, New-Onset Headache

In new-onset and severe headache, the probability of finding a potentially serious cause is considerably greater than in recurrent headache.

Patients with recent onset of pain require prompt evaluation and appropriate

treatmentIn most cases, CT or MRI study. In some circumstances, a lumbar puncture (LP) eyes by fundoscopy, intraocular pressure measurement, and refraction; cranial arteries by palpation is required

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Headache Symptoms that Suggest a Serious Underlying Disorder

"Worst" headache ever

First severe headache

Subacute worsening over days or weeks

Abnormal neurologic examination

Fever or unexplained systemic signs

Vomiting that precedes headache

Pain induced by bending, lifting, cough

Pain that disturbs sleep or presents immediately upon awakening

Known systemic illnessOnset after age 55Pain associated with local tenderness, e.g., region of temporal artery

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History in headache

Duration of headacheNature of headache Site

Severity of headacheContinuous / episodicDuration of episodes

Frequency of episodesAssociated featuresRelieving featuresDiurnal variations

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Intensity Throbbing pulsatile- migraine

Thunderclap – subarachnoid haemorrhage

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MIGRAINE

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CLUSTER HEADACHE

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TRIGEMINAL NEURALGIA

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Mode of onset, the variation of the pain over time,

and duration

subarachnoid haemorrhage (

caused by a ruptured aneurysm) occurs as an abrupt attack that attains its maximal severity in a matter of seconds or minutes;Thunder clap headacheMeningitisit may come on more gradually, over several hours or days.Migraine

Ophthalmodynia :

Brief

sharp pain, lasting a few seconds, in the eyeball or cranium

(“

ice-pick” pain

) and “ice-cream headache” caused by pharyngeal cooling is more common in migraines.

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Migraine of the classic typeonset in

the early morning hours or in the daytime, reaches

its peak of severity typically over several to 30 min, and

lasts, unless treated, for 4 to 24 h, occasionally for as long as 72 h or more. Often it is terminated by sleepCluster headache:unbearably severe unilateral orbit-temporal pain

Coming on

within an hour or two after falling asleep or at predictable times during the day

recurring nightly or daily for

a period of several weeks to months is typical of cluster headache;

usually

an individual attack of “cluster” dissipates in 30 to 45 min

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Intracranial tumour:may appear at any time of the day or night;

it will interrupt sleep, vary in intensity, last a few minutes

to hours; as the tumour

raises intracranial pressure. With posterior fossa masses, the headache tends to be worse in the morning, on awakening. premenstrual tension:occur regularly in the premenstrual periodare usually generalized and mild in degree catamenial

migraine:

attacks of migraine may also occur at this time

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Headaches of cervical spine disease

origin after a period of inactivity, such as a night’s sleep, movements of the neck are stiff and painful

.Sinusitis :often face ache,

with clock-like regularity, upon awakening or in midmorning is characteristically worsened by stoopingand changes in atmospheric pressure; there is associated midfrontal or maxillary tenderness

.

Eyestrain headaches,

follow prolonged use of the eyes, as after

long-sustained periods

of reading, peering into glaring headlights, or exposure to the glare of video displays.

alcohol, intense exercise (such as weight lifting), stooping, straining, coughing, and sexual intercourse are known to initiate a special type of bursting headache,

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MigraineMigraine is a neurovascular disease caused by neurogenic inflammation and characterized by severe, recurring headaches

It usually characterized by the severe pain on one side of the head

as compare to the pain in rest of the head second most common cause of headache, Women > men.

It is usually an episodic headache associated with certain features such as sensitivity to light, sound, or movement; nausea and vomiting often accompany the headache.

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Migraine cont.…Headache can be initiated or amplified by various triggers, including

glare, bright lights, sounds, or other afferent stimulation; hunger; excess stress; physical exertion; stormy weather or barometric pressure changes;

hormonal fluctuations during menses; lack of or excess sleep; and alcohol or other chemical stimulation.

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MIGRAINE

Migraine without aura

Migraine with aura

Childhood periodic syndromesRetinal migraineComplications of migraineProbable migraine

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Classification of Migraine headache

1)Migraine without Aura or common migraine

Does not give any warning signs before the onset of headache

. It occurs in about 70 to 80% of migraine patients2)Migraine with Aura

Give

some warning signs “ called aura” before the actual headache begins. Approximate, 20 to 30% migraine sufferers experience aura.

The most common aura is visual and may include both positive and negative (visual field defects) features.

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Negative

scotoma

. Loss of local awareness of local structure

Positive

Scotoma

. Additional structures

One

side loss of perception.Zigzag structure

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Classification of Migraine headache contd.

3)Retinal migraine-

It involves attacks of monocular scotoma or even blindness of one eye for less than an hour and associated with headache.

4)Childhood periodic syndromes that involve cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and

benign paroxysmal vertigo of childhood

(occasional attacks of vertigo). They may be precursors or associated with migraine.

5)

Complications

of migraine

describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion

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Simplified Diagnostic Criteria for Migraine

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 and phonophobia

Aggravation by movement

 Moderate or severe intensity 

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Symptoms Accompanying Severe Migraine

Symptom

Patients Affected, %

Nausea

87

Photophobia

82

Lightheadedness

72

Scalp tenderness65Vomiting56Visual disturbances36Paresthesias33Vertigo33Photopsia26Alteration of consciousness18Diarrhea16Fortification spectra10

Syncope

10

Seizure

4

Confusional state

4

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TREATMENT GOALS FOR MIGRANT SUFFERER

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MIGRAINE MANAGMENTNon pharmacological treatment

Identification of triggersMeditationRelax techniquesPsychotherapy

Pharmacological treatmentAbortive treatmentPreventive treatment

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MODE OF ACTIONERGOTAMINE

Structurally similar to amines serotonin dopamineCauses constriction of blood vesselsWide range of

effectTRIPTANSSerotonin is involved in migraine attack

Triptans mimic the action of serotoninTriptans act on receptors at smooth muscle cells of brain vesselsThey are an advance over ergots

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PREVENTIVE THERAPYBeta blockers – e.g.. Propranolol

Calcium channel blocker – e.g. verapamilTCA3 –

amitriptylineSSRI’s –fluoxetineanticonvulsant-

sodium valproate ,TopiramateAnti histaminic - cyproheptadineNEED FOR PROPHYLACTIC TREATMENTAbortive drugs should not be used for more than 2-3 times a weekLong term prophylaxis improves quality of life by reducing frequency and severity of attacks

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INDICATION OF PROPHYLAXISPatients who have very frequent headaches (more than 2-3/week)

Attack duration> 48hrsHeadache severity is extremeMigraine attacks are accompanied by severe auraContraindication to acute treatment

Unacceptable adverse effects occur with acute migraine treatmentPatients preference

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Neurohospitalist. 2012 Apr; 2(2): 51–59.

OpioidsThere are numerous disadvantages to the use of opioids in the treatment of migraine, and they typically should not be used as first-line

therapyIV therapyNotably

, many studies of acute migraine therapy required giving intravenous (IV) fluids as part of the treatment protocol prior to administration of the study drugcorticosteroids do not appear to be useful for the acute treatment of migraine

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There are 2 major subclasses of anti dopaminergic agents used in acute migraine therapy

: phenothiazine and butyrophenones. Metoclopramide

is in its own third class. The antiemetic properties of these medications make them quite useful in treating the nausea that frequently accompanies migraine

headache. American Academy of Neurology clinical practice guidelines recommend treating significant nausea with antiemetic in patients with migraine, even in the absence of vomiting

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Efficacy of chlorpromazine generally exceeds 80%. It appears to have comparable efficacy to injectable

sumatriptanTypical adult dosing is 10 mg given IV or IM. It can also be given as a 25 mg

suppository. Prochlorperazine appears to be superior to magnesium

, sodium valproate, ketorolac,  metoclopramide, octreotide, and perhaps subcutaneous sumatriptan.Metoclopramide is probably not as effective as prochlorperazine

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The dose is 6 mg by subcutaneous injection. When used for headaches whose duration has not exceeded 6 hours, the efficacy is as high as 91%Contraindications to triptan administration include cardiovascular disease, uncontrolled hypertension, and, in general, pregnancy. Concurrent use of a selective serotonin reuptake inhibitor (SSRI) or serotonin/norepinephrine reuptake inhibitor (SNRI) is not a contraindication to triptan administration, and this issue has been recently reviewed in an American Headache Society position paper

.

Triptan

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Ketorolac is the parenteral NSAID most frequently used in US emergency rooms for treatment of acute migraine, and there are prospective, randomized studies to support its use. Efficacy can be approximately 80% when using the higher dose of 60 mg IV. However, in some European countries the 60 mg dose was taken off the market because of an association with acute renal failure. Ketorolac 30 mg IV is inferior to prochlorperazine 10 mg IV

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For an acute migraine indication, sodium valproate is typically given as a single IV load, with the dosage used ranging from 300 to 1200 mgNaproxen :Dosages

used in these studies were 500 to 550 mg twice a day ([BID] 250 mg BID for the adolescent study) for 6 to 15 weeks

Oral sumatriptan and naproxen are well-proven therapies for headache recurrence and acute attacks alike, particularly when used in combination.

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Tension-Type Headache

The term tension-type headache (TTH) is commonly used to describe a chronic head-pain syndrome characterized by

bilateral tight, band like

discomfort. The pain typically builds slowly, fluctuates in severity, and may persist more or less continuously for many days. The headache may be episodic or chronic (present >15 days per month).

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Clinical Features

Completely

without accompanying features such as nausea, vomiting, photophobia, phonophobia, osmophobia, throbbing, and aggravation with movement

.In clinical practice, dichotomizing patients on the basis of the presence of associated features (migraine) and the absence of associated features (TTH) is highly recommended.

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Pathophysiology

Primary disorder of CNS pain modulation alone, unlike migraine, which involves a more generalized disturbance of sensory modulation.

. The name tension-type headache

implies that pain is a product of nervous tension, but there is no clear evidence for tension as an etiology. Muscle contraction has been considered to be a feature that distinguishes TTH from migraine, but there appear to be no differences in contraction between the two headache types.

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Treatment: Tension-Type Headache

The pain of TTH can generally be managed with simple analgesics such as acetaminophen, aspirin, or NSAIDs.

Behavioral approaches including relaxation can also be effective.

TRIPTANS in pure TTH are NOT HELPFUL, although triptans are effective in TTH when the patient also has migraine. For chronic TTH , AMITRIPTYLINE

is the only proven treatment

Other TCA, SSRI

and the benzodiazepines have not been shown to be effective.

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Cluster Headache Rare INCIDENCE only 0.1%.

THE PAIN IS

often excruciating in intensity,

no fluctuating, explosive in quality. periodic onset nocturnalrecurs at about the same hour The typical cluster headache patient has daily bouts of 1-2

attacks of

short-duration

unilateral pain for 8 to 10 weeks a year; usually followed by a pain-free interval little less than

1 year.

Patients tend

to move about during attacks, WHILE PATIENTS WITH MIGRAINE REMAIN SILENT

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Cluster Headache

Gender Pain

M >

F 3:1

  Type

Stabbing, boring

  Severity

Excruciating

  Site

Orbit, templeAttack frequency1/alternate day–8/dDuration of attack15–180 minAutonomic featuresYesMigrainous featuresYes ; Nausea, photophobia, or phonophobia; photophobia and phonophobia are typically unilateral on the side of the painAlcohol triggerYesCutaneous triggersNo

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Treatment: Cluster Headache

The most satisfactory treatment is the administration of drugs to prevent cluster attacks until the bout is

overACUTE ATTACK TREATMENT

Many patients respond very well to oxygen inhalation. This should be given as 100% oxygen at 10–12 L/min for 15–20 min. Sumatriptan 6 mg SC is rapid in onset and will usually

shorten

an attack to 10–15 min; there is no evidence of

tachyphylaxis.

Sumatriptan

(20 mg) and zolmitriptan (5 mg) nasal

sprays are both effective ORAL SUMATRIPTAN IS NOT EFFECTIVE

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Preventive Management of Cluster Headache

Short-Term Prevention

Long-Term Prevention

Episodic Cluster Headache

Episodic Cluster Headache & Prolonged Chronic Cluster Headache

Prednisone 1 mg/kg up to 60 mg

Qd,

tapering over 21 days

Verapamil 160–960 mg/d

 Lithium 400–800 mg/dMethysergide 3–12 mg/dVerapamil 160–960 mg/dTopiramatea 100–400 mg/dGreater occipital nerve injectionGabapentina 1200–3600 mg/d Melatonina 9–12 mg/d

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Cases

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Case #1

A 65 y/o gentleman presents to his PCP with headache and transient “funny vision” in the R eye. Headache was in the right-sided, intermittent, pressure pain, started 2 weeks ago, progressively worse. He never had similar headache in the past. Also felt fatigue recently and had a low grade fever. Two days ago, he had an episode of right temporal vision loss for about 10 mins. Today, he had another similar episode for about 15 mins.

What is your diagnosis?

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Dx: temporal arteritis

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Case #2

55 yo man presents to the ER 36 hours after sudden onset severe headache. He initially rated the pain 10/10; now 8/10. He endorses neck pain, nausea/vomiting, and photophobia. His BP is 170/100, P 120. Exam is normal except for meningismus. A noncontrast head CT is normal. LP is performed. CSF has 3 WBC, 1200 RBCs/mm3 in tube 1 and 1220 RBCs/mm3 in tube 4. Protein is 85 mg/dL and glucose 32 mg/dL.

What is your diagnosis?

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Dx: subarachnoid hemorrhage

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Case #3

A 48y/o F with h/o migraine presents with severe persistent headache for 1 week. The headache was similar to her previous migraine, but much more severe. Throbbing, left frontal temporal area, nausea, photophobia and

phono phobia, worse with movement. No focal weakness, loss of consciousness, jerky movements, gait instability or other complaints. She tried Maxalt, but the pain only went away for two hours. She tried Topamax, Lyrica, Nortriptyline, Propranolol and Zonegran. None of these medications helped her headache very much. She used Tylenol,

Ibuprofen and Vicodin almost every day.What is your diagnosis?

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Dx: Migraine, with rebound

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Case

4

44 year old business man

3 week history of intermittent severe right eye painLasts about 1 hour, eye goes red, paces about. No sickness.

Occurs

2-3 times a day.

What is the diagnosis?

What do you do?

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case4Cluster headache

Triptan….lithium…….verapamil……valproate….

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Case

5

A 34 year old man presents in surgery.

4 days before, while walking, he had a sudden severe headache that had stopped him in his tracks. He still had a mild headache.He occasionally got migraine with aura – but this was quite different. Examination normal.

What is the diagnosis?

What do you do?

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Case 5Subarachnoid hemorrhage

Ct scan…..LP….Brain MRI &MRA

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Case

6

78 year old lady

Always fit and well4 weeks history of thick headache. Feels out of sorts.Never really had headaches.

No signs on examination

What is the diagnosis?

What do you do?

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Case 6GCA

Prednisolone……ESR……Temporal artery biopsy

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Case

7

48 year old housewife with mild asthma

Generalised headache over the last 5 months, present all the time. Present morning on waking. Examination normal. Retinal venous pulsation present.

What is the diagnosis?

What do you do?

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Case 7Tension type headache

Amitriptyline…….Relaxation exercise….

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Case

8

45 year old woman – normally fit and well – long history of infrequent migraine

New type of headaches over last 10 months – occipital – last 3-6 hours with nausea – occur once every 2-3 weeks.Examination is normal

What is the diagnosis?

What do you do?

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Case 8Migraine HA

Avoid triggering…..diet…..triptans…..topiramate…..valproate……

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Case

9

21 year old woman – normally fit and well.

Headache – bifrontotemporal, ‘blurry’ vision, ‘noise in ears’

Examination – Obese, constricted visual fields &

papilloedema

What is the diagnosis?

What do you do?

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Case

9

IIH

Ophthalmoscopy….papilledema

Brain MRI

LP

Acetazolamide

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PART II- SECONDARY HEADACHE

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SECONDARY HEADACHE

Post traumatic Headache Vascular Headache of

cranial or cervical originNon vascular headache intracranial origin

Post infective headacheHeadache due to substance abuse/withdrawalHeadache due to disorder of homoeostasisHeadache due to non cranial causesHeadache

attributed to psychiatric

disorders

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1. POST TRAUMATIC HEADACHE

Acute post-traumatic headacheChronic post-traumatic headacheAcute

whiplash headacheChronic whiplash headacheTraumatic

intracranial hematomaOther head and/or neck traumaPost-craniotomy headache

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2. Vascular headache of cranial or cervical origin

No traumatic

intracranial haemorrhageIschemic stroke or TIA

Un-ruptured vascular malformationArteritisCarotid or vertebral artery painCerebral venous thrombosisOther intracranial vascular disorder

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3. Nonvascular headache of intracranial origin

High CSF pressure (

intracranial hypertension)Low CSF pressure (intracranial hypotension

)Non-infectious inflammatory diseaseIntracranial neoplasmIntrathecal injectionEpileptic seizureChiari malformation type ITransient headache and neurological deficits with CSF lymphocytosis

Other

nonvascular

intracranial disorder

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4. Headache due to a substance abuse/ withdrawal

Acute substance use or exposureMedication-overuse headache (MOH)

Adverse effect of chronic medicationSubstance withdrawal

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5. Headache attributed to infection

Intracranial infectionSystemic infection

HIV/AIDSChronic post-infection headache

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6. Headache due to to disorder ofhomoeostasis

Hypoxia and/or hypercapnia

FastingArterial hypertensionDialysis headacheCardiac cephalalgia

HypothyroidismOther disorder of homoeostasis

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7. Headache or facial pain due to extra cranial causes

Disorder of cranial bone

Disorder of neckDisorder of eyesDisorder of earsRhino sinusitis

Disorder of teeth, jaws, or related structuresDisorder of temporo-mandibular joint(TMJ)Other disorder of cranial, facial, or cervical structures

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PART IIICranial neuralgias and central causes

of facial pain and other headaches

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Trigeminal neuralgia Glossopharyngeal neuralgiaNasociliary

neuralgia Superior laryngeal neuralgiaSupraorbital neuralgia

Occipital neuralgiaOther terminal branch neuralgias Neck−tongue syndrome

Nervus intermedius neuralgia External compression headache Cold-stimulus headache Optic neuritisupper cervical roots lesions Herpes zosterOcular diabetic neuropathy Tolosa-Hunt syndromeOphthalmoplegic “migraine” Central causes of facial pain

Constant pain caused by compression irritation, or distortion of cranial N

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Pain-Sensitive Cranial Structures

(1) skin, subcutaneous tissue, muscles, extracranial

arteries, and periosteum of the skull;

(2) delicate structures of the eye, ear, nasal cavities, and paranasal sinuses; (3) intracranial venous sinuses and their large tributaries, especially pericavernous structures; (4) parts of the dura

at the base of the brain and

the arteries

within the dura, particularly the proximal parts of the anterior and middle cerebral arteries and the

intracranial segment

of the internal carotid artery;

(5) the middle meningeal and superficial temporal arteries; and (6) the optic, oculomotor, trigeminal, glossopharyngeal, vagus, and first three cervical nerves.

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Pain insensitive structure

Much of the pia-arachnoid

and dura over the convexity of the brain, parenchyma

of the brain,ependyma Choroid plexuses lack sensitivity.

Slide84

Pain pathway in headache

V1 and V2

division Fore head Orbit Anterior & middle cranial fossa

upto superior surface of tentorium :sphenopalatine branches of the facial nerve impulses from the nasoorbital regionNinth and tenth cranial nerves and the first three cervical nerves

impulses from the inferior

surface of the tentorium and

All of the posterior fossa.

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Sympathetic fibers from the three cervical ganglia and parasympathetic fibers

from the sphenopalatine and otic ganglia are mixed with the trigeminal and other sensory

fibers.The tentorium roughly demarcates

the trigeminal from the cervical–vagal–glossopharyngeal innervation zones. To summarize, pain from supratentorial structures is referred to the anterior two-thirds of the head, i.e., to the territory of sensory supply of the first and second

divisions of

the trigeminal nerve;

pain from infratentorial structures

is

referred to the vertex and back of the head and neck

by 9th 10th and the upper cervical roots.

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Referred pain

Trigeminal and cervical sensory inputs converge on the second order neurons at the

C2 level. Permitting pain from the neck and occipital regions to be

referred to the forehead, and vice versaThe 7,9,10th cranial nerves refer pain to the nasoorbital region, ear, and throat. There may be local tenderness of the scalp at the site of the referred

pain

With the

exception of the cervical portion of the internal carotid artery,

from which

pain is referred to the

eyebrow and supraorbital regionthe upper cervical spine, from which pain may be referred to the occiput, pain because of disease in extracranial parts of the body is not referred to the head.

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Mechanisms of Cranial Pain

Intracranial mass lesionscause headache only if they deform, displace,

or exert traction on vessels and dural structures

at the base of the brain, and this may happen long before intracranial pressure rises.High intracranial pressurebioccipital and bifrontal

headaches

that

fluctuate in severity, probably because of traction on

vessels or

dura

.

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Dilatation of intracranial or extracranial arteries

follow seizures, infusion of histamine, ingestion of alcohol

Nitroglycerin.headache that accompanies febrile illnesses

rises in blood pressure as occurs with pheochromocytoma, malignant hypertension, sexual activity, cough and exertional headaches

Slide89

Cerebrovascular diseases causing head pain

extracranial

temporal and occipital arteries,when involved in giant cell arteritis (cranial or “temporal” arteritis), give rise to severe, persistent headache,

at first localized on the scalp and then more diffuseVertebral artery, occlusion or dissection produce pain in the upper neck or postauricular area; Basilar artery thrombosis

causes

pain to be projected to the

occiput and sometimes to the forehead

Slide90

carotid artery Occlusion/dissection may produce

ipsilateral eye and brow and the forehead also produced by

occlusion of the stem of the middle cerebral arteries.

PCA/ DISTAL ICA:Aneurysm /dilatation produce pain projected to the eye

Slide91

Sinusitis :frontal and ethmoidal

sinusitis, the pain tends to be

worse on awakening gradually subsides when the patient

is upright; Maxillary and sphenoidal sinusitisthe opposite happenspain is ascribed to filling of the sinuses and its relief to their emptying, induced

by

the dependent

position of the ostia. Bending over intensifies the

pain by causing changes in pressure, as does

blowing the

nose and air travel, especially on descent,

Slide92

Headache of ocular origin,

Site :orbit, forehead, or temple, is of the steady,

aching type

follow prolonged use of the eyes in close work.Hypermetropia and astigmatism (rarely myopia), which result in sustained contraction of extraocular as well as frontal, temporal, and even

occipital muscles

.

Correction of the refractive error abolishes the headache.Iridocyclitis

and

in acute angle closure glaucoma,

in which raised intraocular pressure causes steady, aching pain in the region of the eye, radiating to the forehead

Slide93

Headache of upper cervical spine

Headaches that accompany disease of ligaments, muscles,and

apophysial joints in the upper part of the cervical spineare referred to the occiput and nape of the neck on

the same side and sometimes to the temple and forehead.Degenerative changes in the cervical spineArthritic Pain on first movements after prolonged rest for some hours are

stiff

and painful.

Pain of fibromyalgia: a controversial entity, is

putatively characterized

by tender areas

near the cranial insertion of cervical and other muscles.

Slide94

Headache of meningeal irritation

(infection

or hemorrhage) is acute in onset, usually severe, generalized, deep seated, constant,

associated with stiffness of the neck, particularly on forward bending.dilatation and inflammation of meningeal vessels chemical irritation of pain receptors in the large vessels and meninges by

endogenous chemical agents, particularly

serotonin and

plasma kinins, are probably more important factors

in the

production of pain and spasm of the neck extensors.

Slide95

Spontaneous/post LP low CSF pressure headache,

steady occipitonuchal

and frontal pain coming on within a few minutes after arising from a recumbent position

is relieved within a minute or two by lying downthis type of headache is increased by compression of the jugular veins but is unaffected by digital obliteration of the carotid artery.Headache caused by caudal displacement of the brain, with traction on

dural

attachments

and dural sinuses

Slide96

Exertional headaches are usually benign but sometimes related to

pheochromocytoma, arteriovenous

malformation, or other intracranial lesions, in addition to

the aforementioned subarachnoid hemorrhage from ruptured aneurysm

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Thanks for your attention

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