![Clinical manifestation of carotid or vertebral artery dissection Head, face, orbital, or neck pain Cerebral ischemic symptoms SAH [intracranial artery dissection] Incomplete ipsilateral Horner’s syndrome [extracranial ICA dissection] Subjective or objective bruits](https://image.slidesharecdn.com/headachelectureforstudent2-100509220008-phpapp01/85/Headache-lecture-for-student2-33-320.jpg)
![Clinical manifestation of Pseudotumor cerebri Headache Pulsatile, daily, continuous Unilateral, bilateral, frontal, occipital [ bifrontotemporal is the most common ] Nausea/vomiting Orbital pain Papilledema Visual symptoms : transient visual obscuration, diplopia, visual loss, cranial nerve VI palsy](https://image.slidesharecdn.com/headachelectureforstudent2-100509220008-phpapp01/85/Headache-lecture-for-student2-50-320.jpg)
Headache lecture for student2
- 1. Headache and increased intracranial pressure
- 2. Causes of Headaches 1. Traction, tension, or displacement of pain-sensitive structures 2. Distention or dilation of intracranial arteries 3. Inflammation of pain-sensitive structures 4. Obstruction of CSF pathways with consequent increased intraventricular pressure 5. Primary central pain: involvement of pain-modulating systems
- 6. The Fifth cranial nerve Trigeminal nerve V1 (Ophthalmic) sensation V2 (Maxillary) sensation V3 (Mandibular) sensation
- 7. Trigeminal neuralgia Intense momentary spasms of pain make the patient wince Pain occur in the face, usually radiating from the corner of the mouth or from the gums towards the cheek and ear Sudden electric-shock-like quality Pain triggered by touching, shaving, cold winds, eating Usually occur in elderly. If occurs in young adults, multiple sclerosis should be suspected.
- 8. Headache classification Pain sensitive meninges vascular nerves Headache Primary Secondary Migraine Tension Cluster Miscellaneous Extracranial Intracranial
- 9. Secondary headache Intracranial Extracranial
- 10. What should be asked when you see a patient with headache ??
- 11. History Temporal profile Age of onset Time to maximum intensity Frequency Time of the day Duration Headache feature Location Quality of pain Severity of pain
- 12. Associated symptoms and signs Before, during, and after headache Aggravating or precipitating factors Trauma Medical conditions; pregnancy, obese women, pheochromocytoma, HIV-cryptococcal meningitis, metastatic disease Triggers : menstruation, loud noise, heat, alcohol, stress Activity and postures Pharmacologic : drug-abused headache, oral contraceptive pills
- 13. Relieving factors Nonpharmacologic Pharmacologic Evaluation and treatment history Psychosocial history Substance use Occupational and personal life Psychologic history Sleep history Impact of headache Family history
- 14. Headache Primary headache Secondary headache
- 15. DIAGNOSIS AND TESTING Red flag Primary headache? Secondary headache Diagnostic testing Detailed history and physical examination Atypical features No Yes
- 16. Red flags in the diagnosis of headache(1) Sudden onset headache Subarachnoid hemorrhage Worsening pattern headache Mass lesion, subdural hematoma Medication overuse Headache with systemic illness Meningitis, encephalitis Systemic infection Collagen vascular disease, arteritis
- 17. Red flags in the diagnosis of headache(2) Focal neurological signs or symptoms Mass lesion AVM Triggered by cough, exertion, or Valsalva SAH Mass lesion New headache type in a patient with cancer : metastasis With HIV : opportunistic infection, tumor
- 18. Causes of Secondary headache Intracranial Paracranial Extracranial Head trauma Vascular disorders Nonvascular disorder Disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, other facial or cranial structures Substances or their withdrawal Noncephalic infection Metabolic disorder
- 19. Sinusitis Pain is localized to the cheek : maxillary sinusitis To the forehead : frontal sinusitis Midline behind the nose : ethmoid and sphenoid sinusitis * the pain is throbbing and tenderness of overlying skin
- 20. Posttraumatic headaches Mild head injury and postconcussion syndrome Mild head injury >= 75% of all brain injuries Mild closed head injury 50% of patient with mild Head injury will develop postconcussion syndrome
- 21. Postconcussion syndrome Headache : within 14 days or 3 months Cranial nerve signs and symptoms Psychologic and somatic complaint Cognitive impairment Rare sequelae Subdural and epidural hematoma, cerebral venous thrombosis, seizure
- 23. Subarachnoid hemorrhage (SAH) Abrupt onset : subarachnoid hemorrhage(SAH) Headache on awakening after lying down or occur everyday : suspect raised intracranial pressure Focal neurological deficit : brain tumor, stroke, abscess, encephalitis
- 24. Subarachnoid hemorrhage (SAH) Headache occurs in about 90% of SAH patient Classic : acute, severe, continuous, and generalized and is often associated with nausea, vomiting, meningismus, focal neurologic symptoms, and loss of consciousness “ worst headache of my life”
- 25. Investigation in suspected SAH CT brain First 24 hrs ---- detect SAH ~95%
- 26. Investigation in suspected SAH Lumbar puncture in suspected SAH with normal CT or MRI brain Differentiate traumatic tap from SAH by xanthochromia (colored supernatant)
- 27. Further investigation for SAH 4 vessel cerebral arteriogram MRA (magnetic resonance angiography) Spiral (helical) CT angiography
- 28. Stroke Headaches may be due to electrochemical or mechanical stimulation of trigeminovascular afferent system Headache occurred in infarcts, parenchymal hemorrhage, TIA, lacunar infarcts Quality, onset, duration of headache varied widely
- 29. Clinical manifestations of headache in stroke Unilateral and focal headache Mild to moderate severity Abrupt or gradual in onset throbbing or nonthrobbing More often ipsilateral than contralateral to side of cerebral ischemia Associated symptoms : nausea, vomiting, light and noise sensitivity
- 30. Unruptured AVM and migraine Migraine-like headaches with and without visual symptoms Typical migraine-like due to an AVM Unusual associated signs (papilledema, field cut, bruit) Short duration of headache attacks Brief scintillating scotoma Absent family history Atypical sequence of aura, headache and vomiting seizure
- 31. MRI T1 and Angiogram of AVM
- 32. Carotid and vertebral artery dissections Dissections occur due to penetration of circulating blood through an intimal tear into subintimal, medial, and, less commonly adventitial layers of vascular wall
- 33. Clinical manifestation of carotid or vertebral artery dissection Head, face, orbital, or neck pain Cerebral ischemic symptoms SAH [intracranial artery dissection] Incomplete ipsilateral Horner’s syndrome [extracranial ICA dissection] Subjective or objective bruits
- 34. Character of headache in artery dissection Onset : gradual 75%, thunderclap headache 10-20%, Constant, steady aching or steady sharp pain or less commonly as throbbing
- 35. Headache in CVT Usually due to raised intracranial pressure Diffuse, progressive and constant Almost always associated with Papilledema Focal deficits Partial/ generalized seizures
- 36. Diagnostic evaluation in CVT CT brain Exclude cerebral infarction and hemorrhage ‘ Empty delta sign’ ; nonenhancing clot within the sinus is present in only 35% MRI and MRV Best way to detect CVT Lumbar puncture ---should be avoided if there is a large cerebral infarction or hemorrhage Document elevated intracranial pressure and help exclude infectious or leptomeningeal malignancy
- 37. MRV of Superior sagittal, transverse sinus thrombosis
- 38. Temporal arteritis (Giant cell arteritis) Systemic panarteritis that selectively involves arterial walls with significant amount of elastin 50% of patient with temporal arteritis have polymyalgia rheumatica 15% of patient with polymyalgia rheumatica have temporal arteritis Mean age of onset ~70 years
- 39. Temporal arteritis (giant cell arteritis)
- 40. Temporal arteritis (Giant cell arteritis) Headache 60-90% Often throbbing Intermittent or continuous Severe Location : temporofrontal, temple, not involve temple, generalized 50% tenderness or decreased pulsation of superficial temporal artery
- 41. Temporal arteritis (cont) Intermittent jaw claudication 38% Neurologic manifestation are common Ophthalmologic findings ; visual loss, ophthalmoparesis Mononeuropathies and peripheral neuropathies TIA or stroke others
- 42. Diagnosis of temporal arteritis Based on clinical suspicion that is usually confirmed by laboratory testing 3 best test : westergren ESR, C-reactive protein(CRP), temporal artery biopsy
- 43. Headache due to severe HT Usually bioccipital throbbing Can be generalized or frontal throbbing Often present in the morning on awakening Diastolic BP usually elevated to 120 mmHg or higher
- 44. Headaches and neoplasms Brain tumors are an uncommon cause of headache 8% of patient with headaches and brain tumors have a normal neurological examination Papilledema is present in 40% Headache related to size of tumor and amount of midline shift
- 45. Headaches and neoplasms (cont) Most common location of headaches is bifrontal Most of headache are intermittent with moderate to severe intensity ‘ classic’ brain tumor headache---severe, worse in the morning, associated N/V---occurs in a minority of patients
- 46. Headache and intracranial pressure
- 48. Pseudotumor cerebri (idiopathic intracranial hypertension) Neurological examination is normal except papilledema, visual loss, cranial nerve VI palsy CSF pressure is increased (>20 cm H2O in nonobese and >25 cmH2O in obese patient) CSF analysis is normal except decreased protein No hydrocephalus or mass lesion There are no other identifiable causes
- 49. Pseudotumor cerebri >90% of patients are young obese women Usually Primary or idiopathic Secondary causes and associations Intracranial mass Obstruction of ventricular system Cerebral venous thrombosis Meningitis/ encephalitis Medications : Vitamin A, Minocycline, Anabolic steroids, Corticosteroid withdrawal
- 50. Clinical manifestation of Pseudotumor cerebri Headache Pulsatile, daily, continuous Unilateral, bilateral, frontal, occipital [ bifrontotemporal is the most common ] Nausea/vomiting Orbital pain Papilledema Visual symptoms : transient visual obscuration, diplopia, visual loss, cranial nerve VI palsy
- 51. Diagnostic evaluation of Pseudotumor cerebri CT or MRI brain Exclude tumor or hydrocephalus Lumbar puncture If the scans show no other explanation for papilledema Measure opening pressure CSF analysis should be normal except low protein level in some cases Ophthalmologist consultation Evaluate fundus, visual acuity, visual field
- 52. Management of Pseudotumor cerebri Treat causes Treatment of idiopathic Pseudotumor cerebri Lose weight for obese patients Repeated LP to reduce pressure to 12-17.5 cm H2O Medication for persistent headache drug for migraine headache Diuretics Acetazolamide Surgical treatments for papilledema and headache Optic nerve sheath fenestration Lumboperitoneal shunt
- 53. Low CSF pressure headache Most often due to Post LP Spontaneous occurrence CSF shunt overdrainage
- 54. Diagnostic evaluation of low CSF pressure headache Repeat LP : opening pressure 0-7cmH2O or in normal range CSF analysis: normal or moderate, primarily lymphocytic pleocytosis, RBC, elevate protein MRI brain : diffuse meningeal enhancement with gadolinium or subdural fluid collection
- 56. Post-Lumbar puncture headache Most common complication of lumbar puncture Risk factors Female Age 18-30 years Lesser body mass index Prior chronic or recurrent headache Prior PLPH Larger-diameter needle, perpendicular orientation of bevel, not reinsert the stylet
- 57. Clinical manifestation of PLPH Bilateral, frontal, occipital, generalized pressure or throbbing occurring in upright position and decreasing or resolving when supine Worse with headache movement, coughing, straining, sneezing, jugular venous compression Begins within 48 hrs or 72 hrs Additional symptoms : neck stiffness, nausea, vomiting
- 58. Headaches caused by Vasoactive substances Dilation of intracranial vessels Throbbing in nature and made worse by sudden head movement Examples Alcohol Marijuana Cocaine Monosodium glutamate “Chinese restaurant syndrome” Nitrite and Nitrates Histamine headache Rebound headache : nicotine and caffeine
- 59. Headache due to infection and inflammation HIV and headache Cryptococcal meningitis, neurosyphilis, tuberculous meningitis, toxoplasmosis, CMV encephalitis, tumors, sinusitis, medications, primary headache Brain abscess Meningitis and encephalitis Drug-induced aseptic meningitis : NSAIDs, ATBs, vaccines, others,…
- 60. Metabolic disorders and headache Fever Hypoxia Hypercapnia Hypoglycemia Dialysis High altitude Decompression sickness Hyperventilation syndrome
- 61. Primary Headache Migraine Tension-type headache Cluster
- 62. Headache type Migraines Tension-type Cluster Age at onset 10-40 20-50 15-40 Location Hemicranial Bilateral Unilateral peri/retro-orbital duration Several hours to 3 days 30 min to 7days+ 30-120 min Frequency/timing Variable Variable 1-8/day, nocturnal attacks severity Moderate to severe Dull ache may wax/wane Excruciating quality Throbbing, steady ache Band-like pressure Boring, piercing Associated features N/V, photo/phono/osmophobia, scotoma, neurologic deficits Generally none Ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, miosis, facial sweating
- 64. Age- And Gender-specific Prevalence Of Migraine Lipton RB, Stewart WF. Neurology . 1993. Migraine Prevalence (5)
- 66. Migraine without aura A . At least 5 attacks fulfilling criteria B - D B . Headache attacks lasting 4-72 hours ( untreated or unsuccessfully treated ) C . Headache has at least 2 of the following characteristics : - Unilateral location - Pulsating quality - Moderate or severe pain intensity - Aggravation by or causing avoidance of routine physical activity ( eg, walking or climbing stairs ) D . During headache at least 1 of the following : - Nausea and / or vomiting - Photophobia and phonophobia E . Not attributed to another disorder
- 68. Typical aura with Migraine headache(1) A . At least 2 attacks fulfilling criteria B - D B . Aura consisting of at least 1 of the following, but no motor weakness : - Fully reversible visual symptoms including positive features ( eg, flickering lights, spots or lines ) and / or negative features ( ie, loss of vision ) - Fully reversible sensory symptoms including positive features ( ie, pins and needles ) and / or negative features ( ie, numbness ) - Fully reversible dysphasic speech disturbance
- 69. Typical aura with Migraine headache(2) C . At least two of the following : - Homonymous visual symptoms and / or unilateral sensory symptoms - At least one aura symptom develops gradually over > /= 5 minutes and / or different aura symptoms occur in succession over > /= 5 minutes - Each symptom lasts > /= 5 and < /= 60 minutes D . Headache fulfilling criteria B - D for “Migraine without aura” begins during the aura or follows aura within 60 minutes E . Not attributed to another disorder
- 70. Visual Aura
- 71. Aura-Numbness
- 72. 1. Prodrome 2. Aura Phases of Migraine Attack 3. Headache 4. Postdrome
- 73. Migraine Treatment Reassure and educate patient Identify and remove triggers Start a wellness program : exercise, balanced meals, adequate sleep, smoking cessation pharmacotherapy physical therapy psychological therapy
- 74. Migraine Triggers Stress and emotion Hormonal changes Diet Environmental factors Too much or too little sleep Physical factors
- 75. Acute vs Preventive Therapy Acute (Abortive) : Taken after attack has begun to relieve pain and disability and stop progression Preventive Therapy : Taken daily to reduce attack frequency, severity, and duration
- 76. Acute Migraine Medications Non-specific NSAIDs : naproxen, ibuprofen Combination analgesics : acetaminophen/aspirin/caffeine Neuroleptics/antiemetics : metoclopramide, prochlorperazine Specific Ergotamine/DHE Triptans : sumatriptan, zolmitriptan CGRP antagonist :olcegepant, MK-0974
- 77. Migraine Prevention Classes of preventive drugs: Antiepileptics : topiramate, valproate, gabapentin Tricyclic antidepressant : amitryptyline, nortriptyline SNRI : venlafaxine, duloxetine Beta-blockers : propanolol Calcium channel blockers : flunarizine Other treatment : magnesium, riboflavin, co-enzyme Q10, feverfew, butterbur root, botulinum toxin No efficacy : nimodipine, clonidine, fluoxetine
- 79. Tension - type headache ( TTH ) - Headache lasting from 30 minutes to 7 days - Headache has at least 2 of the following characteristics : - Bilateral location - Pressing / tightening ( non - pulsating ) quality - Mild or moderate intensity - Not aggravated by routine physical activity such as walking or climbing stairs - Both of the following : - No nausea or vomiting ( anorexia may occur ) - No more than one of photophobia or phonophobia - Not attributed to another disorder
- 80. TTH management Simple analgesic : acetaminophen, aspirin, NSAIDs Behavioral approach : relaxation Triptans in pure TTH are not helpful For chronic TTH : amitryptyline
- 81. Cluster Headache Severe unilateral pain Associated with lacrimation, sweating, ptosis, conjunctival injection, and eyelid edema May be precipitated by alcohol, histamine, or nitroglycerine
- 82. Cluster Headache A . At least 5 attacks fulfilling criteria B - D B . Severe or very severe unilateral orbital, supraorbital and / or temporal pain lasting 15-180 minutes if untreated C . Headache is accompanied by at least 1 of the following : - Ipsilateral conjunctival injection and / or lacrimation - Ipsilateral nasal congestion and / or rhinorrhea - Ipsilateral eyelid edema - Ipsilateral forehead and facial sweating - Ipsilateral miosis and / or ptosis A sense of restlessness or agitation D . Attacks have a frequency from 1 every other day to 8 / day E . Not attributed to another disorder
- 83. Treatment of Cluster Headache Acute treatment 100% Oxygen inhalation Rapid acting DHE Sumatriptan subcutaneously
- 84. Cluster Headache Preventive Treatment Short-term Prednisolone 1 mg/kg/d tapering over 21 days Verapamil Greater occipital nerve injection Long-term verapamil Lithium Topiramate Gabapentin melatonin
- 85. Thank you for your attention
Editor's Notes
- #16: The cause or type of most headaches can be determined by a careful history and physical examination. The clinical imperative is to recognize the warning signals, which should raise red flags and prompt further diagnostic testing. In the absence of worrisome features in the history or examination, the task is then to diagnose the primary syndrome based upon the clinical features. If there are atypical features or a lack of response to conventional therapy, the diagnosis should be questioned and the possibility of a secondary headache disorder revisited. Since migraine and TTH account for over 90% of the primary headache disorders in clinical practice, this discussion will focus on their clinical features, the warning signals of serious secondary headaches, and the role of diagnostic testing in the evaluation of headache.
- #65: In both males and females, the prevalence distribution of migraine is an inverted U-shape curve. Prevalence rises through early adult life and then falls after middle life. The second important point to emphasize on this slide is that, at all post-pubertal ages, migraine is substantially more common in women than in men. The prevalence of migraine varies as a function of age. Migraine is a disorder that is most prevalent between the ages of 25 and 55. Part of the reason the condition has such a big impact in the workplace is that it affects people during their peak productive years. Lipton RB, Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology. 1993;43(suppl 3):S6-S10.